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As coronavirus vaccines hurtle through development, scientists are getting their first look at data that hint at how welldifferent vaccines are likely to work. The picture, so far, is murky.

On May 18, US biotech firm Moderna revealed the first data from a human trial: its COVID-19 vaccine triggered an immune response in people, and protected mice from lung infections with the coronavirus SARS-CoV-2. The results which the company, based in Cambridge, Massachusetts, announced in apress release were widely interpreted as positive and sent stock prices surging. But some scientists say that because the data havent been published, they lack the details needed to properly evaluate those claims.

Tests of other fast-tracked vaccines show that they have prevented infections in the lungs of monkeys exposed to SARS-CoV-2 but not in some other parts of the body. One a vaccine being developed at the University of Oxford, UK, that is also in human trials protected six monkeys from pneumonia, but the animals noses harboured as much virus as did those of unvaccinated monkeys, researchers reported last week in a bioRxiv preprint. A Chinese group reported similar caveats about its own vaccines early animal tests this month.

Despite uncertainties, all three teams are pressing ahead with clinical trials. These early studies are meant mainly to test safety, but larger clinical trials designed to determinewhether the vaccines can actually protect humansfrom COVID-19 could report in the next few months.

Still, the early data offer clues as to how coronavirus vaccines might generate a strong immune response. Scientists say that animal data will be crucial for understanding how coronavirus vaccines work, so that the most promising candidates can be identified quickly and then refined. We might have vaccines in the clinic that are useful in people within 12 or 18 months, says Dave OConnor, a virologist at the University of WisconsinMadison. But were going to need to improve on them to develop second- and third-generation vaccines.

Modernas vaccine, which is being co-developed with the US National Institute of Allergy and Infectious Diseases (NIAID) in Bethesda, Maryland, began safety testing in humans in March. The vaccine consists of mRNA instructions for building the coronaviruss spike protein; it causes human cells to churn out the foreign protein, alerting the immune system. Althoughsuch RNA-based vaccinesare easy to develop, none has yet been licensed anywhere in the world.

In its press release, the company reported that 45 study participants who received one or two doses of the vaccine developed a strong immune response to the virus. Researchers measured virus-recognizing antibodies in 25 participants, and detected levels similar to or higher than those found in the blood of people who have recovered from COVID-19.

Tal Zaks, Modernas chief medical officer, said in a presentation to investors that these antibody levels bode well for the vaccine preventing infection. If you get to the level of people who had disease, that should be enough, Zaks said.

But its not at all clear whether the responses are enough to protect people from infection, because Moderna hasnt shared its data, says Peter Hotez, a vaccine scientist at Baylor College of Medicine in Houston, Texas. Im not convinced that this is really a positive result, Hotez says. He points to a May 15bioRxiv preprint3that found that most people who have recovered from COVID-19 without hospitalization do not produce high levels of neutralizing antibodies, which block the virus from infecting cells. Moderna measured these potent antibodies in eight trial participants and found their levels to be similar to those in recovered patients.

Hotez also has doubts about the Oxford teams first results, which found that monkeys produced modest levels of neutralizing antibodies after receiving one dose of the vaccine (the same regime that is being tested in human trials). It looks like those numbers need to be considerably higher to afford protection, says Hotez. The vaccine is a made from a chimpanzee virus that has been genetically altered to produce a coronavirus protein.

Hotez says that the vaccine being developed by Sinovac Biotech in Beijing seems to have elicited a more promising antibody response in macaque monkeys that received three doses, as reportedin a May 5 paper inScience. That vaccine is comprised of chemically inactivated SARS-CoV-2 particles.

No one yet knows the precise nature of the immune response that protects people from COVID-19, and the levels of neutralizing antibodies made by the monkeys in the Oxford Study might be enough to protect people from infection, says Michael Diamond, a viral immunologist at Washington University in St. Louis, Missouri, who is a member of Modernas scientific advisory board. If not, a second injection would probably boost levels appreciably. What we dont know is how long theyll last, he adds.

Still more questions hover over experiments showing that vaccines can protect animals from infection. Moderna said its vaccine stopped the virus replicating in the lungs of mice. The rodents had been infected with a version of the virus that was genetically modified to let it attack mouse cells, which are not ordinarily susceptible to SARS-CoV-2, according to Zakss presentation. But the mutation affects the protein that most vaccines, including Modernas, use to stimulate the immune system, and this could change the animals response to infection.

The Oxford monkeys were given an extremely high dose of virus after receiving the vaccine, says Sarah Gilbert, an Oxford vaccinologist who co-led the study with Vincent Munster, a virologist at NIAIDs laboratories in Hamilton, Montana. This could explain why the vaccinated animals had just as much SARS-CoV-2 genetic materials in their noses as control animals, even though the vaccinated monkeys didn't develop any signs of pneumonia. Administering high doses ensures that the animals are infected with the virus, but it might not replicate natural infections. The Oxford study did not measure whether the virus was still infectious, Diamond says, and the genetic material could represent virus particles inactivated by the monkeys immune response, or the viruses the researchers administered, rather than an ongoing infection.

Still, the result is a concern that raises the possibility that vaccinated people could still spread the virus, says Douglas Reed, an aerobiologist at the University of Pittsburgh Center for Vaccine Research in Pennsylvania. Ideally, you want a vaccine that would protect against disease and against transmission, so that we can kind of break the chain, he says.

One way to find out whether vaccines can prevent transmission would be to study them in animals that are naturally susceptible to the virus and seem capable of spreading it, such as ferrets and hamsters, says Reed. He and other researchers also point out that macaques display only mild symptoms of coronavirus infection, and they wonder whether vaccines should be trialled in animals that develop more severe disease.

Although assessing vaccines potential efficacy is difficult, the latest data are clearer on safety, say researchers. The Moderna vaccine caused few severe and no lasting health problems in trial participants. The vaccinated Oxford and Sinovac monkeys did not develop an exacerbated disease after infection a key fear, because an inactivated vaccine for the related coronavirus that causes SARS (severe acute respiratory syndrome) showed signs of this in macaques.

Stanley Perlman, a coronavirologist at the University of Iowa in Iowa City, says that the animal studies conducted so far can tell vaccine developers only so much. People are doing as best they can, he says. None of the data that hes seen should dissuade developers from pressing on with trials in humans to determine whether the vaccines work, he says.

Moderna will soon begin a phase II trial involving 600 participants. It hopes to begin a phase III efficacy trial in July, to test whether the vaccine can prevent disease in high-risk groups, such as health-care workers and people with underlying medical problems. Zaks said that further animal studies, including some in monkeys, were under way, and that it wasnt yet clear which animal would best predict whether and how the vaccine works.

The Oxford team has already enrolled more than 1,000 people in its UK trial. Some volunteers have received a placebo, so the trial could allow researchers to determine whether the vaccine works in humans over the coming months. The lack of safety problems in the teams monkey study was reassuring, Gilbert says.

We dont really need any more data from animal trials to continue, she says. If we get human efficacy, weve got human efficacy, and thats what matters.

This article is reproduced with permission and wasfirst publishedon May 19 2020.

Read more about the coronavirus outbreak from Scientific American here. And read coverage from our international network of magazines here.

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Coronavirus Vaccine Trials Have Delivered Their First Results--But Their Promise Is Still Unclear - Scientific American

DNA may not be lifes instruction book, but just a jumbled list of ingredients.

University of Maryland researcher develops potentially revolutionary framework for heredity and evolution in which inheritable information is stored outside the genome.

The common view of heredity is that all information passed down from one generation to the next is stored in an organisms DNA. But Antony Jose, associate professor of cell biology and molecular genetics at the University of Maryland, disagrees.

In two new papers, Jose argues that DNA is just the ingredient list, not the set of instructions used to build and maintain a living organism. The instructions, he says, are much more complicated, and theyre stored in the molecules that regulate a cells DNA and other functioning systems.

Jose outlined a new theoretical framework for heredity, which was developed through 20 years of research on genetics and epigenetics, in peer-reviewed papers in the Journal of the Royal Society Interface and the journal BioEssays. Both papers were published on April 22, 2020.

Joses argument suggests that scientists may be overlooking important avenues for studying and treating hereditary diseases, and current beliefs about evolution may be overly focused on the role of the genome, which contains all of an organisms DNA.

DNA cannot be seen as the blueprint for life, Jose said. It is at best an overlapping and potentially scrambled list of ingredients that is used differently by different cells at different times.

For example, the gene for eye color exists in every cell of the body, but the process that produces the protein for eye color only occurs during a specific stage of development and only in the cells that constitute the colored portion of the eyes. That information is not stored in the DNA.

In addition, scientists are unable to determine the complex shape of an organ such as an eye, or that a creature will have eyes at all, by reading the creatures DNA. These fundamental aspects of anatomy are dictated by something outside of the DNA.

Jose argues that these aspects of development, which enable a fertilized egg to grow from a single cell into a complex organism, must be seen as an integral part of heredity. Joses new framework recasts heredity as a complex, networked information system in which all the regulatory molecules that help the cell to function can constitute a store of hereditary information.

Michael Levin, a professor of biology and director of the Tufts Center for Regenerative and Developmental Biology and the Allen Discovery Center at Tufts University, believes Joses approach could help answer many questions not addressed by the current genome-centric view of biology. Levin was not involved with either of the published papers.

Understanding the transmission, storage and encoding of biological information is a critical goal, not only for basic science but also for transformative advances in regenerative medicine, Levin said. In these two papers, Antony Jose masterfully applies a computer science approach to provide an overview and a quantitative analysis of possible molecular dynamics that could serve as a medium for heritable information.

Jose proposes that instructions not coded in the DNA are contained in the arrangement of the molecules within cells and their interactions with one another. This arrangement of molecules is preserved and passed down from one generation to the next.

In his papers, Joses framework recasts inheritance as the combined effects of three components: entities, sensors and properties.

Entities include the genome and all the other molecules within a cell that are needed to build an organism. Entities can change over time, but they are recreated with their original structure, arrangement and interactions at the start of each generation.

That aspect of heredity, that the arrangement of molecules is similar across generations, is deeply underappreciated, and it leads to all sorts of misunderstandings of how heredity works, Jose said.

Sensors are specific entities that interact with and respond to other entities or to their environment. Sensors respond to certain properties, such as the arrangement of a molecule, its concentration in the cell or its proximity to another molecule.

Together, entities, sensors and properties enable a living organism to sense or know things about itself and its environment. Some of this knowledge is used along with the genome in every generation to build an organism.

This framework is built on years of experimental research in many labs, including ours, on epigenetics and multi-generational gene silencing combined with our growing interest in theoretical biology, Jose said. Given how two people who contract the same disease do not necessarily show the same symptoms, we really need to understand all the places where two people can be differentnot just their genomes.

The folly of maintaining a genome-centric view of heredity, according to Jose, is that scientists may be missing opportunities to combat heritable diseases and to understand the secrets of evolution.

In medicine, for instance, research into why hereditary diseases affect individuals differently focuses on genetic differences and on chemical or physical differences in entities. But this new framework suggests researchers should be looking for non-genetic differences in the cells of individuals with hereditary diseases, such as the arrangement of molecules and their interactions. Scientists dont currently have methods to measure some of these things, so this work points to potentially important new avenues for research.

In evolution, Joses framework suggests that organisms could evolve through changes in the arrangement of molecules without changes in their DNA sequence. And in conservation science, this work suggests that attempts to preserve endangered species through DNA banks alone are missing critical information stored in non-DNA molecules.

Jose acknowledged that there will be much debate about these ideas, and experiments are needed to test his hypotheses. But, he said, preliminary feedback from scientists like Levin and other colleagues has been positive.

Antony Joses generalization of memory and encoding via the entity-sensor-property framework sheds novel insights into evolution and biological complexity and suggests important revisions to existing paradigms in genetics, epigenetics and development, Levin said.

###

References:

A framework for parsing heritable information by Antony M. Jose, 22 April 2020, Journal of the Royal Society Interface.DOI: 10.1098/rsif.2020.0154

Heritable Epigenetic Changes Alter Transgenerational Waveforms Maintained by Cycling Stores of Information by Antony M. Jose, 22 April 2020, BioEssays.DOI: 10.1002/bies.201900254

Research in Antony Joses laboratory is supported by the National Institutes of Health (Award Nos. R01GM111457 and R01GM124356). The content of this article does not necessarily reflect the view of this organization.

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DNA May Not Be the Blueprint for Life Just a Scrambled List of Ingredients - SciTechDaily

People who test positive again for the coronavirus, despite having already recovered from COVID-19, arent being reinfected, a new study finds.

Reports of patients dischargedfrom hospitals in South Korea testing positive after their apparent recovery hadraised concerns that people could get infected by the virus in the short term morethan once or that the infection could come back. But diagnostic tests for the coronavirus that causes COVID-19 rely on detecting theviruss genetic material (SN: 4/17/20).A positive result does not indicate whether a person is shedding virusescapable of infecting cells which would signal an active infection.

Now, a May 19 report from theKorean Centers for Disease Control and Prevention shows that samples fromreinfected patients dont have infectious viruses. The finding hints that the diagnostic tests are picking upon the genetic material from noninfectious or dead viruses. That lack of infectious virus particles meansthese people arent currently infected and cant transmit the coronavirus toothers, the researchers say.

Its good news, says AngelaRasmussen, a virologist at Columbia University. It appears people are notbeing reinfected, and this virus is not reactivating.

In thestudy, researchers tried to isolate infectious coronaviruses from samples takenfrom 108 people who retested positive. All of those samples tested negative. When the scientists examined 23 of those patients for antibodiesagainst the coronavirus, almost all had neutralizing antibodies that can stop the virus from getting intocells (SN: 4/28/20). That immuneresponse may protect a person from getting reinfected, at least in the short term.

The team also tracked down790 contacts of 285 people who retested positive. Of those contacts, 27 testedpositive for the coronavirus. Twenty-four of those were cases that officialshad previously confirmed. Officials also identified three new cases, all ofwhom either had contact with the Shincheonji religious group which was hit particularly hard inthe early days of the pandemic or aconfirmed case in their family. No new cases appeared to stem from repeatpositive patients, a sign those patients arent contagious.

Now, we can largely stopworrying about reinfection and address the next big questions, Rasmussen says.How protective are immune responses in recovered patients, and how long doesimmunity last?

Scientists and journalists share a core belief in questioning, observing and verifying to reach the truth. Science News reports on crucial research and discovery across science disciplines. We need your financial support to make it happen every contribution makes a difference.

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New data suggest people arent getting reinfected with the coronavirus - Science News

If youve ever been a newlywed, you know the tingly euphoria of saying I do and starting a life with your spouse. This is romantic love, Western style. We often chalk it up to chemistry, an ill-defined connection of hearts and minds. Groundbreaking research at UC Santa Barbara finds we were closer than we knew.

For the first time, researchers have explored the neural and genetic connections to romantic love in newlyweds. By using functional magnetic resonance imaging (fMRI) and genetic analysis of 19 first-time newlyweds, Bianca Acevedo and her collaborators showed that romantic love maintenance is part of a broad mammalian strategy for reproduction and long-term attachment that is influenced by basic reward circuitry, complex cognitive processes and genetic factors.

In short, were hard-wired to sustain romantic love to maintain a successful marriage and the family unit, thanks to neurotransmitters like dopamine and a suite of genetic mutations.

This is the first study to examine the neural and genetic correlates of romantic love maintenance, said Acevedo, a research scientist at UC Santa Barbaras Department of Psychological & Brain Sciences and the lead author of After the Honeymoon: Neural and Genetic Correlates of Romantic Love in Newlywed Marriages in the journal Frontiers in Psychology.

The study showed that the maintenance of love is not only associated with activation of subcortical regions but also higher order centers of the brain, she said. Also, for the first time we provide evidence that the propensity to sustain romantic love may be affected by genetic variability. Specifically, the genes we examined are associated with pair-bonding behaviors including fidelity and sexual behaviors; and social behaviors such as trust, eye-gazing and attachment.

To test their hypothesis that romantic love is a developed form of the mammalian drive to find and keep mates, the researchers performed fMRI scans of the brains of the members of the study group 11 women and eight men. Participants were shown alternating images of their partners and a neutral acquaintance they knew well.

At the start of each session, the subjects were instructed to recall non-sexual events with the person whose face was displayed. While still in the scanner, participants rated their moods to verify that the evoked emotions corresponded to the target image.

The participants were tested around the time of marriage and a year later.

In addition, they provided saliva samples for testing of vasopressin, oxytocin and dopamine genes implicated in pair bonding in non-human mammals, such as voles.

Our findings showed robust evidence of the dopamine reward systems involvement in romantic love, Acevedo said. This system is interesting because it is implicated in motivation, energy, working for rewards, and is associated with corresponding emotions such as excitement, euphoria and energy, as well as frustration if the drive is thwarted.

Acevedos current research builds on her work on empathy and altruism and its correlates in the brain.

Empathy has its roots in social bonding, she explained. In our previous work we showed that although humans express sentiments such as empathy and altruism towards strangers and non-close others, brain responses to partners are stronger. Thus, there is specificity. Romantic love is somewhat different in that it may or may not include empathy or altruism, but in healthy partnerships it does.

For some romantics, it might seem a tad clinical to chalk up our feelings of love and commitment to biochemistry. Acevedo, however, said gene mutations and brain activity are only components of romance and belonging.

Humans are creative and clever, she said. Romantic love inspires people to know how to put a smile on their partners face. By making our partners happy we not only keep our relationships stable, but we also derive joy from such events.

In the brain, Acevedo continued, this is shown as increased reward activation when people are shown images of a partner smiling and they are told that something wonderful has happened to the partner. People know this intuitively. They know that romance goes a long way in finding and keeping a preferred mate. Thats why there is multibillion-dollar industry built on it from dating sites, to lingerie to Hallmark cards, chocolate and diamond rings.

And besides, our chemical impulses dont buy flowers or cook dinner.

Love is basic but complex, Acevedo said. We are wired to love, but it takes work to find and keep love alive."

Nancy L. Collins, a professor in UC Santa Barbaras Psychological and Brain Sciences, was a co-author of After the Honeymoon. She is also director of the UC Santa Barbara Close Relationship Lab. Other authors are Michael J. Poulin of the University of Buffalo and Lucy L. Brown of the Albert Einstein College of Medicine in New York.

The rest is here:
Are we wired for romance? - University of California

A girl in New Delhi gets a nasal swab to test for the new coronavirus. A rare Kawasaki diseaselike illness linked to the virus is sickening young people.

By Jennifer Couzin-FrankelMay. 21, 2020 , 4:10 PM

Sciences COVID-19 reporting is supported by the Pulitzer Center.

Three children at one London hospital in mid-April, followed the next day by three at anotherfor Elizabeth Whittaker, a pediatric infectious disease doctor at Imperial College London, those first cases raised an alarm. The youngsters had fevers, rashes, stomach pain, and, in some cases, heart problems, along with blood markers that characterize COVID-19 in adults, including one associated with clotting. But in most, nasal swabs failed to reveal any virus.

I dont understandthey look like they have coronavirus, Whittaker recalls thinking. Doctors nonetheless suspected a link. Within days, a survey turned up 19 additional cases across England, and an alert on 27 April asked doctors to be on the lookout for such symptoms in children. Soon after, dozens more cases surfaced in New York along with smaller clusters elsewhere, bolstering a connection to the pandemic. Reports of children on life support and some deaths put parents on edgeand were especially disheartening after earlier signs that COVID-19 largely spares children from serious illness.

It is another surprise from a virus that hasproffered many, and projects worldwide are gearing up to study it. They are combing the blood and sequencing the genomes of patientsand the virus, if it can be isolated from themto search for clues to what makes some children susceptible and how to head off the worst symptoms. Theres hope that whats learned from young patients might help the many adults in whom COVID-19 also triggers a grievous overreaction of the immune system.

In some respects, Its absolutely not shocking to see this, says Rae Yeung, a rheumatologist and immunologist at the Hospital for Sick Children, whose center treated 20 children over the past 3 weeks with similar symptoms.Many pathogens occasionally trigger a similar hyperactive immune response in children, known as Kawasaki disease. Its symptoms vary but include rash, fever, and inflammation in medium-size blood vessels. Children can suffer heart problems. In rare cases, blood pressure plummets and shock sets in.

Doctors disagree on whether the variant linked to COVID-19 is Kawasaki disease or something new, with some experts calling it multisystem inflammatory syndrome in children. But as with Kawasaki disease, most recover with treatment, including steroids and immunoglobulins, which calm the immune system.

In linking the inflammatory syndrome to COVID-19,Were going on more than just a hunch, says Jesse Papenburg, a pediatric infectious disease specialist at Montreal Childrens Hospital, in a city thats seen about 25 children with the condition. Kawasaki disease is rare, ordinarily affecting just one to three in every 10,000 children in Western countries, though its more common in children with Asian ancestry. The spikes recorded so far, in COVID-19 hot spots like northern Italy and New York City, track the novel coronavirus march around the world. And although a minority of these children test positive for SARS-CoV-2, a studypublished inThe Lancetby a team in Bergamo, Italy, reported that eight of 10 children with the Kawasaki-like illness had antibodies to the virus, indicating they had been infected. Positive antibody tests have been reported in sick children elsewhere, too.

It was obvious that there was a link, says Lorenzo DAntiga, a pediatrician at the Papa Giovanni XXIII Hospital who led the study. The new coronavirus can elicit a powerful immune response, which he thinks may explain why shock and a massive immune reaction called a cytokine storm are more common in the COVID-19linked cases than in textbook Kawasaki disease. And a time lag between infection and the Kawasaki-like illness could explain why many of the affected children show no evidence of the virus. The immune systems overreaction may unfold over weeks, though virus could also be hiding somewhere in the body.

Theres clearly some underlying genetic component that puts a small number of children at risk, says Tom Maniatis, founding director of Columbia Universitys Precision Medicine Initiative. New York state is investigating 157 cases, and Maniatis is also CEO of the New York Genome Center, which is pursuing whole-genome sequencing of affected children and their parents, as well as sequencing the virus found in children, with family consent. Finding genes that heighten risk of the illness or of developing a severe case could point to better treatments or help identify children who may take a sudden turn for the worse.

Genetics may also help explain a puzzle: why the illness hasnt been reported in Asian countries, even though Kawasaki disease is far more common in children with Asian ancestry. The virus own genetics may be important; an analysis last month indicatedthe predominant viral variant in New York was brought by travelers from Europe. Its also possible that the Kawasaki-like illness is so rare that it only shows up in COVID-19 hotbeds. The areas that have been hardest hit by coronavirus are the areas reporting this syndrome now, says Alan Schroeder, a critical care physician at Lucile Packard Childrens Hospital at Stanford University, which has seen one potentially affected child, a6-month-old baby, who healed quickly.

Yeung is pursuing ways to flag children with COVID-19 who are at risk of this complication. She co-leads an international consortium thats banking blood from affected children both before and after treatment and screening for various markers, including the cytokine molecules that indicate a revved-up immune system. They are also searching for gene variants known to predict poor outcomes in Kawasaki disease. Theres also core COVID stuff that needs to be measured, Yeung says, such as markers of heart function and levels of D-dimer, a protein fragment in the blood that indicates a tendency toward clotting and that surges in many sick adults.

Another project, called DIAMONDSand originally designed to improve diagnostics of pathogens based on patterns of immune response in children with fevers,is recruiting children across Europe with the Kawasaki-like complication, along with those who have run of the mill COVID-19 symptoms. Scientists will study blood for pathogensnot just SARS-CoV-2and the behavior of immune cells such as T cells and B cells.

We have to do a deep dive into the immunology of those patients, says Elie Haddad, a pediatric immunologist and scientist at the St. Justine University Hospital Center who,with Yeung and Susanne Benseler at Alberta Childrens Hospital, is leading Canadian research efforts on the new syndrome. These deep dives may also clarify the immune system chaos seen in many sick adults. Children are cleaner, Haddad points outtheyre less likely to have other health burdens, such as diabetes or high blood pressure, that can make it harder to tease out the virus impact on the immune system.

Its possible, too, that the illness affects adults as well but is harder to tease out from their other symptoms. A global effort studying COVID-19 in adults, called the International Severe Acute Respiratory and Emerging Infection Consortium, will look at adults clinical data and blood samples,Whittaker says, to see, is this a uniquely pediatric problem?

Eager as they are to understand this new face of the pandemic, doctors want to avoid overstating the hazards. We need to identify early and we need to intervene early in treating these children, Yeung says. But she also urges calm. The kids were seeing so far, she stresses, they respond to the treatments were giving.

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Doctors race to understand rare inflammatory condition associated with coronavirus in young people - Science Magazine

Have a question about coronavirus, also known as COVID-19?

We will ask the experts.

Send questions to tribdem@tribdem.com.

If a person had COVID-19 in the past, lets say in February, and takes the testagain in May, is the test going to show negative? In other words you could have hadcoronavirus in the past and it would test negative now?

So, the only way to find out if you had it in the past would be the antibody test, correct?

The answer:

Great questions, and it all comes back to testing and more frequent testing. Theres some very recent positive data out of South Korea which Ill discuss below.

Your questions refer to the different types of tests. One test is the molecular swab (Polymerase Chain Reaction PCR), which detects genetic RNA from SARS-CoV-2, also known as the COVID-19 virus. The other test is a blood IgG antibody, which determines if someone was previously infected, or was recently exposed to the virus 10-21 days ago.

If you had COVID-19 infection in February, the PCR swab test would probably be negative now, and the blood IgG antibody test would probably be positive (indicating prior infection). Recent data out of South Korea suggest that if the repeat PCR swab test is positive, that may be detecting dead virus, rather than indicating reinfection. And the positive IgG antibodies may provide some protection.

Because the pandemic is only a few months old, there is no data on long-term immune response.

Dr. David Csikos, chief medical officer, Chan Soon-Shiong Medical Center at Windber.

When older adults fly, canthey get tested upon arrival sothey dont need to be secluded for 14 days?

The answer:

The tests that are available on the market are antibody tests and SARS CoV-2 genome tests.

The antibody tests show if a person is having an adaptive or specific response to the virus; the genome test is indicative of an active infection, as viral RNA is present. These tests, particularly the genome test, give a snapshot of what is happening on that day.

Individualswho are exposed to SARS CoV-2 wont show symptoms for five to seven days, on average. A test upon landing would not be sufficient to say that the individual is not in the incubation period of COVID-19.

Theperson could have been exposed to the virus on the plane. This is why the 14-day quarantine is recommended.

Jill D. Henning, associate professor of biology, University of Pittsburgh at Johnstown.

My husband and I tested positive in March, then aftertwo weeks, we had no symptoms. We got retested last week and are both positive. Why would this happen?

The answer:

An excellent question that has relevant implications.

I assume the tests were molecular PCR (Polymerase Chain Reaction), which detects genetic RNA from the COVID-19 virus. If you and your husband dont have any symptoms or fever, this implies both are now asymptomatic carriers. It is not known how long you will remain a carrier without symptoms, and that may depend in part how long protective immunity will last.

I recommend you and your husband consider blood tests for IgG antibodies to SARS-CoV-2.

It is unknown if both are still contagious, and thats why its important to wear face masks in public and continue social distancing. While the evidence on reinfection is evolving, current data and experience from previous viruses without substantial seasonal mutation do not support this hypothesis.

Because the COVID-19 pandemic is only a few months old, there is no data on long-term immune response. It is also controversial when asymptomatic carriers may return back to work. I recommend both of you follow up with your primary care physician, and if necessary, consult an infectious disease specialist.

Dr. David Csikos, chief medical officer, Chan Soon-Shiong Medical Center at Windber.

I have read that scientists are working on testing community spread by testing water from the sewer.

Would it be possible to develop individual urine tests (akin to pregnancy testing)that could inform a person positive or negative for the virus on a daily basis?

The answer:

To my knowledge, there are only two kinds of tests for SARS CoV 2, a genomic RNA test and an antibody test. The RNA test is looking for viral genetic material in patients and the antibody test is looking for the presence of an immune response to the virus.

SARS CoV 2 has been detected in feces of infected patients, but it is not clear whether that virus is infectious. In addition, waste water has been shown to contain the virus, but standard municipal sanitation practices or use of a septic tank has been shown to inactivate the virus.

Urine contains waste products from the human body that can be dissolved in water. Hormones, sugar, vitamins and certain proteins can be found in urine. RNA and DNA can be found in urine as well.

Urine tests,such as those you mention in your question, require a high concentration of the substance to be in the urine.

A recent study out of China was able to detect SARS CoV 2 in urine of one patient out of 17 with confirmed disease. Other peer reviewed studies were unable to find viral RNA in urine. These studies used a technique called RT-PCR to detect the viral RNA. This technique amplifies minutely small quantities of viral RNA and brings the concentration up to detectable levels.

Who knows what the future holds? That is the beauty of science. But at present, we do not have the ability to detect the minuscule amount of viral RNA in urine without amplifying it first.

I am a cashier at Walmart. I had something similar to COVID-19 in December, however no breathing problems. Am I safe to visit my 2-week-old grandson? I shower, wash my hair and wear clean clothes and wash my hands when visiting. I also work daily, sanitize frequently and wash my hands every chance I can. I also wear a mask when working and visiting. Am I putting my grandson in danger?

The answer:

Social distancing is hard and it must be truly difficult when a new family member is born.

When we are first born and until we are about a year old, our immune systems are immature. The responses we build to microbes takes time and the littlest among us have not been around long enough to have the same responses that adults or even older children do. This makes infants more susceptible to infections.

In a recent study out of China, of more than 2,100 children with suspected or confirmed COVID-19 in between late December and early February showed that about 11% of infants had severe or critical illness. Children in other age groups had lower rates of severe or critical illness (about 7% for children ages 1 to 5, 4% for ages 6 to 10, 4% for ages 11 to 15).

Other studies are showing an inflammatory illness that may be linked to COVID-19. This response that is seen in children is severe and rare. It has to deal with an immune response that leads to a cytokine storm. Our innate response, the one we are born with, has the ability to make our blood vessels leaky in order to let white blood cells into our tissues where the infection is. It does this by releasing cytokines, proteins that allow the immune system to communicate with cells and tissue of the body. This response is usually localized, but in some children it becomes systemic causing the blood vessels all over the body to be leaky; this results in severe symptoms such as organ failure and shock.

From your question, it appears that you are doing things to reduce your risk of infection. If you feel that you had COVID-19 in December, I urge you to request an antibody test. This could help determine if you did have COVID-19.

With respect to visiting your newborn grandson, I support respecting the community directed stay-at-home orders. He is still developing his immune system and is in a risk group because of his age. You and your family can speak with the childs pediatrician to see what the case counts are in your area and then determine what level of risk is acceptable to you as a family.

Jill D. Henning, associate professor of biology, University of Pittsburgh at Johnstown.

Can you be a carrier ofCOVID-19 and not have any symptoms as in youre immune to the virus but still carry and spread the virus?

The answer:

Yes, there are asymptomatic carriers, however no one can truly determine the impact of asymptomatic cases on spread until theres more testing.

Can these people who are completely asymptomatic, who never develop any symptoms, transmit the infection? Thats still an open question, and no one knows for sure. Experts say these carriers without symptoms make it even more important for people to wear face masks in public.

Dr. David Csikos, chief medical officer, Chan Soon-Shiong Medical Center at Windber.

I was really sick with upper respiratory turned into bronchitis turned to pneumonia in late December to middle of February. Is it possible I had COVID?Would an antibody test still show antibodies if I did? I had almost all the symptoms.

The answer:

When did SARS CoV-2 emerge?

That is one of the big questions of 2020.

Science uses a method called the molecular clock to determine when new pathogens emerge.

SARS CoV-2 is an RNA virus. Ituses an enzyme to copy itself called RNA dependent RNA polymerase. This enzyme is sloppy in its copying. The rate of mistakes it makes is able to be tracked.

Using this technology, scientists at the Imperial College of London collaborated withthe World Health Organization to determine that SARS CoV-2 emerged between Nov. 6 and Dec. 13 in Wuhan, China. Couple the new respiratory virus with the ability to be anywhere in the world in 24 hours and ...

Testing can help sort out whether a person has recovered from COVID-19. The test that will determine if a person has had an immune response to the infection is the antibody test. IgG antibodies are present in a person aftershe or he has had an infection that resulted in an adaptive (specific) immune response.

If you are curious about your status, you can seek out an IgG antibody test. The more data that can be acquired about positive cases, in any stage, will help answer the question of when. It is possible, however, that we will never know when it emerged.

Jill D. Henning, associate professor of biology, University of Pittsburgh at Johnstown.

I am wondering how it could be possible to see my significant other during the coronavirus pandemic. We live separately, and I have been quarantined while he has continued to do basic things such as grocery shop and goes to work two times per week, always following recommended precautions. We are wondering if he were to do a PCR test for coronavirus RNA combined with an IgG and IgM antibody test, could this provide a sufficient picture upon which to base a decision to see one another, or not?

The answer:

Social distancing is so hard! All of us have someone we want to see.

In public health there is something called risk reduction. It refers to using strategies that minimize the risk or harm certain human behaviors come with for example, wearing a bicycle helmet when riding a bike. If you wear a helmet, you are less likely to have a traumatic brain injury if you wreck. You still ride the bike, just in a safer way.

With SARS CoV-2, becoming more lax on your social distancing is not the same as wearing a bicycle helmet when riding a bike. SARS CoV-2 is spread via airborne droplets by people who may not know they are sick yet. Even people who are practicing social distancing may not know they have been exposed because they could have come in contact with people who dont know they are infected yet.

Testing can help. The test for genomic RNA of SARS CoV-2 will let a person know ifhe or she is actively infected at that time. The antibody tests would show that you are in the first stages of an adaptive immune response (IgM) or that you are in the later stages or recovered from COVID-19 (IgG).

However, this is only a snapshot of the infection risk. It only says that at the time of the test, the individual is SARS CoV-2 free. If that individual goes out in the community the next day, he or she could be exposed to someone with the virus and become infected.

Until we have more testing,two-thirds of our population recovered, or a treatment is found, it is best to keep socially distant.

As always the risk assumption is yours; however, the recommendation is to maintain social distance.

Jill D. Henning, associate professor of biology, University of Pittsburgh at Johnstown.

Are drug users, especially intravenous, more likely to spread COVID-19 or other viruses and diseases than non-drug users?

The answer:

SARS CoV-2 is spread via respiratory droplets. Anyone can spread the infection if they have symptoms and we are seeing studies that show asymptomatic transmission in about 35% of individuals (recent studies from the New England Journal of Medicine).

Now is a good time to remind everyone that human behavior contributes to the spread of any infectious disease. When we consider COVID-19, we can reduce the spread by wearing a mask in public, washing our hands, and maintaining social distance.

Injection drug users are at a greater risk for blood-borne pathogens, such as Hepatitis and HIV, as well as having a greater risk for sepsis, a bacterial infection in the blood. As for other drug users, according to the National Institute of Allergy and Infectious Diseases, because SARS CoV-2 attacks the lungs it could be a serious threat to those who smoke tobacco or marijuana or who vape. People with opioid use disorder and methamphetamine use disorder may also be vulnerable due to those drugs effects on respiratory and pulmonary health.

In short, anything that decreases lung functioning can lead to more severe COVID-19 disease.

Jill D. Henning, associate professor of biology, University of Pittsburgh at Johnstown.

I am a nanny and was asked to enter the familys home wearing a mask. I assumed they (mom, dad and 41/2-year-old) would also be wearing masks. They did not. I wear one to protect them and vice-versa, correct?

The answer:

There are no formal guidelines on what should be done in this situation. Childcare is a necessity for many families, even if they are working from home. In this situation, I would recommend that you all (mom, dad, child and nanny) keep each other apprised of your health situation. Have a discussion about your exposures and risk factors for SARS CoV-2 (for example, do you live in a home with an essential worker) be truthful about each others movement (or lack there of) in the community. If you are nannying for another family, be sure to inform all parties involved.

After this conversation, decide together on a safety plan that makes everyone comfortable.

For example, everyone has their temperature taken daily before work starts. If symptoms become apparent, all are notified.

Maybe you have certain rooms that are for family only in the home, maybe you and the child remain in one area of the home.

Through working together as a unit, you can be sure to address all concerns and come to an agreement in which everyone feels safe.

Jill D. Henning, associate professor of biology, University of Pittsburgh at Johnstown.

The news keeps saying people under 18 rarely transmit the disease. However, what evidence is this based on? I read that children under 18 dont get the disease, or very mildly and dont transmit. But how many children have had the disease? How many children under 18 have actually been tested? If we do not have facts on children under 18 how can we say that they rarely get it and they do not transmit it?

The answer:

We dont have all the facts yet on how COVID-19 affects different populations, or know how many people have had the virus. And this is especially true with children.

It seems that children may not have symptoms that are severe, but we do know they get the virus. There have been a few cases (not locally) where kids are intubated, and respirators were used for children. Children can still pass the virus to their older family members who can have much more severe symptoms.

Everyone, including children, should follow the recommended precautions to prevent the spread of the virus.

Originally posted here:
Experts answer your COVID-19 questions: 'If a person had COVID-19 in the past, let's say in February, and takes the test again in May, is the test...

Aggressive public health measures tostem the tidal wave of coronavirus infections have left people isolated,unemployed and wondering when it will all end. Life probably wont gocompletely back to normal until vaccines against the virus are available,experts warn.

Researchers are working hard on thatfront. At least six vaccines are currently being tested in people, says EstherKrofah, chief executive of the FasterCures center at the Milken Institute in Washington,D.C. We expect about two dozen more toenter clinical trials by this summer and early fall. That is a huge number,Krofah said at an April 17 briefing. Dozens more are in earlier stages oftesting.

In unpublished, preliminary results of a test of one vaccine, inoculated people made as many antibodies against the coronavirus as people who have recovered from COVID-19 (SN: 5/18/20). The mRNA-based vaccine induces human cells to make one of the viruss proteins, which the immune system then builds antibodies to attack. That study was small, only eight people, but a second phase of safety testing has begun.

But vaccinestake time to test thoroughly (SN: 2/21/20). Even with acceleratedtimelines and talk of emergency use of promising vaccines for health care workersand others at high risk of catching the virus, the general public will likelywait a year or more to be vaccinated.

In the meantime, new treatments may helpsave lives or lessen the severity of disease in people who become ill.Researchers around the world are experimenting with more than 130 drugs to findout if any can help COVID-19 patients, according to atracker maintained by the Milken Institute.

Some of those drugs are aimed atstopping the virus, while others may help calm overactive immune responses thatdamage lungs and other organs. Although researchers are testing a battery ofrepurposed drugs and devising new ones, there is still a great deal ofuncertainty over whether the drugs help, or maybe even hurt.

The wait is frustrating, but theres still much doctors and scientists dont know about how this new coronavirus affects the body. Getting answers will take time, and finding measures to counter the virus that are both safe and effective will take even more. Early results suggest that the antiviral drug remdesivir can modestly speed recovery from COVID-19 (SN: 5/13/20). It is not a cure, but the drug may become the new standard of care as researchers continue to test other therapies.

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Antiviral drugs interfere with a viruss ability to replicate itself, though such drugs are difficult to create. Remdesivir is being tested in half a dozen clinical trials worldwide. The drug mimics a building block of RNA, the genetic material of the coronavirus (SN: 3/10/20). When the virus copies its RNA, remdesivir replaces some of the building blocks, preventing new virus copies from being produced, laboratory studies have shown.

Early results in COVID-19 patients given the drug outside of a clinical trial showed that 68 percent needed less oxygen support after treatment, as reported online April 10 in the New England Journal of Medicine (SN: 4/29/20). The drug went to very sick patients, including those who needed oxygen from a ventilator or through tubes in the nose. Other researchers have disputed those results, questioning the study methods and statistical analyses, which may have given an exaggerated impression of good outcomes. The studys authors say they have reanalyzed the data and still conclude that remdesivir has benefits.

Soon after, the U.S. National Instituteof Allergy and Infectious Diseases announced that hospitalized patients withCOVID-19 who got intravenous remdesivir recoveredmore quickly than those on a placebo: in 11 days versus 15. Those findingshad not been reviewed by other scientists at the time of the announcement. Thedug provides researchers with a baseline for comparing other treatments. Wethink its really opening the door to the fact that we now have the capabilityof treating, Anthony Fauci, director of the NIAID said April 29 in a newsbriefing at the White House.

Antiviral medications used against HIV are also being tested against COVID-19. The combination of lopinavir and ritonavir stops an HIV enzyme called the M protease from cutting viral proteins so that the virus can replicate itself. The SARS-CoV-2 virus produces a similar enzyme. But early results from a small study in China showed that the combination didnt stop viral replication or improve symptoms (SN: 3/19/20), and there were side effects.

For now, the Society of Critical CareMedicine recommendsagainst using the drugs, and the Infectious Diseases Society of Americasays patients should get the drugs onlyas part of a clinical trial. Several large trials may report results soon.

The HIV drugs may not work well against SARS-CoV-2, even though the viruses have similar M proteases: The coronaviruss enzyme lacks a pocket where the drugs fit in the HIV version of the enzyme.

This illustrates why antiviral drugs areso difficult to develop. Designing a drug requires knowing the 3-D structure ofthe viruss proteins, which can take months to years. But researchers arealready getting some close-up views of the new coronavirus. A team in Chinaexamined the structure of the coronaviruss M protease and designed smallmolecules that could block a part of the protein necessary to do its job. Theteam describedtwo such molecules, dubbed 11a and 11b, April 22 in Science.

In test tubes, both molecules stopped the virus from replicating in monkey cells. In mice, 11a stuck around longer in the blood than 11b, so the researchers tested 11a further and found it seemed safe in rats and beagles. More animal tests will probably be needed to show whether it stops the virus, then multiple stages of human tests will have to follow. The drug development and testing process often takes on average 10 years or more, and can fail at any point along the way.

Meanwhile, hundreds of thousands of people worldwide have already recovered from COVID-19, and many are donating blood that might contain virus-fighting antibodies. Clinical trials are under way to test whether antibodies from recovered patients blood plasma can help people fight off the virus (SN: 4/25/20, p. 6). More such trials are planned.

Stopping the virus is only half the problem. In some people seriously ill with COVID-19, their immune system becomes the enemy, unleashing storms of immune chemicals called cytokines. Those cytokines trigger immune cells to join the fight against the virus, but sometimes the cells go too far, causing damaging inflammation.

Some of the drugs used to calm cytokines in cancer patients (SN: 6/27/18, p. 22) may also help people with COVID-19 ride out the storm, says cancer researcher Lee Greenberger, chief scientific officer of Leukemia and Lymphoma Society. Several of those drugs are being tested against the coronavirus now.

Hydroxychloroquine, a drug approved totreat autoimmune disorders such as lupus and rheumatoid arthritis, became ahousehold word after President Trump touted it as a possible COVID-19treatment.

The drug is being tested in numerouslarge clinical trials around the world to see if it might help calm cytokinestorms in COVID-19 patients as well. But so far, there is no solid evidence thatit works either to prevent infection in people or to treat people who alreadyhave the disease.

And in some studies the drug has caused serious side effects, including causing irregular heartbeats, says Raymond Woosley, a pharmacologist at the University of Arizona College of Medicine in Phoenix. People with heart problems, low potassium or low oxygen levels in their blood are at higher risk of these side effects, he says. And those are exactly the kinds of patients who are most vulnerable to COVID-19. So, the very sickest COVID patients are those at most risk for these life-threatening arrhythmias and cardiac effects.

Results of some rigorous clinical trialsof hydroxychloroquine are expected this summer. Meanwhile, the U.S. Food andDrug Administration allows the drug to be used when no other treatment isavailable and patients cant join a clinical trial.

Todays enthusiasm for any drug thatseems promising feels familiar, says Woosley. He remembers the excitement overAZT, the first drug used to fight HIV in the 1980s. It wasnt the best drug tocombat the AIDS epidemic, and better ones came later. Likewise, the firsttreatments for COVID-19 might be better than nothing, but not the best we willultimately get.

Meanwhile, we wait.

With hundreds of clinical trials going on around the world, some answers may come soon. But for now, keeping the coronavirus contained will probably require aggressive testing, tracing and isolating contacts of people who have the virus and continued social distancing.

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As we wait for a vaccine, heres a snapshot of potential COVID-19 treatments - Science News

DUBLIN--(BUSINESS WIRE)--The "Global Genome Editing Market By Technique (CRISPR, Zinc Finger Nucleases, TALENs, Restriction enzymes, Others), By Applications (Synthetic Biology, Engineering Cell Line and Organisms, Others), By Source, By End-User, By Region, Forecast & Opportunities, 2025" report has been added to ResearchAndMarkets.com's offering.

The Global Genome Editing Market is expected to grow at a brisk rate during the forecast period owing to growing number of research activities for treatment of various chronic diseases using this technology. Further, increased government funding for genomics technology around the globe, growing preference for personalized medicine and increase in R&D expenditure are fueling the market growth of genome editing.

Genome editing is a way of making specific changes to the DNA of a cell or organism. It could be used to edit the genome of any organism. It uses a type of enzyme called an engineered nuclease' which cuts the genome in a specific place. After cutting the DNA in a specific place, the cell naturally repairs the cut. It finds application in large number of areas, such as mutation, therapeutics, and agriculture biotechnology. Moreover, rise in the number of chronic and infectious diseases is likely to fuel the market for genome editing in the coming years.

The Global Genome Editing market is segmented based on technique, applications, source, end-user and region. Based on applications, the market is segmented into synthetic biology, engineering cell line & organisms, therapeutic genome editing and others. Among them, the cell line engineering is expected to witness the highest growth rate in the coming years due to increase in the number of people suffering with genetic disorders and rising government funding for stem cell research.

Based on end-user, the Global Genome Editing Market is segmented into pharmaceutical & biotechnology companies, clinical research organization and research institutes. Pharmaceutical & biotechnology companies contribute to the largest share of revenue generation for the Global Genome Editing Market. Growing establishments of biotech and pharma companies in emerging economies and growing usage of gene editing technique in research activities undertaken by them to manufacture and develop drugs for rare diseases anticipated to fuel the market across the globe.

Companies Mentioned

Objective of the Study:

Key Topics Covered:

1. Product Overview

2. Research Methodology

3. Executive Summary

4. Global Genome Editing Market Outlook

4.1. Market Size & Forecast

4.2. Market Share & Forecast

4.3. Market Attractiveness Index

5. Asia-Pacific Genome Editing Market Outlook

5.1. Market Size & Forecast

5.2. Market Share & Forecast

5.3. Market Attractiveness Index

5.4. Asia-Pacific: Country Analysis

6. Europe Genome Editing Market Outlook

6.1. Market Size & Forecast

6.2. Market Share & Forecast

6.3. Market Attractiveness Index

6.4. Europe: Country Analysis

7. North America Genome Editing Market Outlook

7.1. Market Size & Forecast

7.2. Market Share & Forecast

7.3. Market Attractiveness Index

7.4. North America: Country Analysis

8. South America Genome Editing Market Outlook

8.1. Market Size & Forecast

8.2. Market Share & Forecast

8.3. Market Attractiveness Index

8.4. South America: Country Analysis

9. Middle East and Africa Genome Editing Market Outlook

9.1. Market Size & Forecast

9.2. Market Share & Forecast

9.3. Market Attractiveness Index

9.4. MEA: Country Analysis

10. Market Dynamics

10.1. Drivers

10.2. Challenges

11. Market Trends & Developments

12. Competitive Landscape

12.1. Competition Outlook

12.2. Players Profiled (Leading Companies)

13. Strategic Recommendations

14. About Us & Disclaimer

For more information about this report visit https://www.researchandmarkets.com/r/tgb83z

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Outlook on the Worldwide Genome Editing Industry to 2025 - Featuring Pfizer, Bayer Crop Science & Editas Medicine Among Others -...

Surveys consistently report that people fear total blindness more than any other disability, and currently the major cause of untreatable blindness is retinal disease. The retina, a part of the brain that extends into the eye during development, initiates vision by first detecting light with the rod and cone photoreceptors. Four classes of retinal neurons then begin the analysis of visual images. Defects in the optical media that transmit and focus light rays onto the retina (lens and cornea) can usually be dealt with surgically, although such treatments are not available in some parts of the world, resulting in as many as 20 to 30 million legally blind individuals worldwide. Untreatable retinal disease potentially causes legal or total blindness in more than 11 million people in the United States alone, but progress in treatments raises the possibility of restoring vision in several types of retinal blindness (1).

Retinal neurons comprise bipolar and horizontal cells, which are second-order neurons that receive signals from the photoreceptors in the outer retina. Third-order amacrine and retinal ganglion cells are activated in the inner retina by bipolar cells. Axons from the ganglion cells form the optic nerve and carry the visual message to the rest of the brain (see the figure). The cells most susceptible to blinding retinal disease are the photoreceptors and ganglion cells. Whereas progress has been made in combating blindness caused by photoreceptor degeneration, little can be done currently to address ganglion cell loss, such as occurs in glaucoma.

The approach that has been most successful in restoring photoreceptor loss that results in complete blindness is the use of retinal prosthetic devices, with two now approved for clinical use (2). These devices electrically stimulate either bipolar or ganglion cells. They require goggles that have a camera that converts visual stimuli into electrical stimuli that activate the device, which in turn stimulates the retinal cells. Several hundred of these devices have been implanted in blind or virtually blind individuals, 70 to 80% of whom report improvement in quality of life. For those who are completely blind, the ability to experience again at least some visual function is viewed as a miracle.

There are substantial limitations to the devices, however. The best visual acuity attained so far is poor (20/500) and visual field size is limited, but many improvements, mainly technical, are being developed and tested, including the potential use of electronic low-vision devices to increase visual field size and acuity (3). Retinal prostheses are not useful for patients who are blind because of loss of ganglion cells and/or the optic nerve, but prostheses that bypass the retina and stimulate more central visual structures, including the lateral geniculate nucleus (the intermediary between retina and cortex) and visual cortex, are being developed and tested in humans (4). There remain considerable technical issues, but preliminary data indicate that such devices are feasible.

A second approach to treat photoreceptor degeneration and potential blindness, now in the clinic, is gene therapy (5). This involves injecting a viral construct into the eye that contains a normal gene to replace an abnormal one. Success so far has been limited to the treatment of Leber congenital amaurosis (LCA) type 2, a rare form of retinitis pigmentosa in which the gene whose product is required to form the correct isomer of vitamin A aldehyde, the chromophore of the visual pigments, is mutated. Little of the correct isomer is made in LCA patients, resulting in substantial loss of photoreceptor light sensitivity. This is reversed when viral constructs encoding the normal gene are injected deep into the eye between the photoreceptors and pigment epithelium.

Two factors make this approach feasible in LCA: The genetic defect is monogenic, and many of the photoreceptors in the patients remain alive, although compromised. Thus, how broadly feasible gene therapy will be for treating the enormous range of inherited retinal diseases now known to exist (300) remains to be seen. But at least a dozen other gene therapy trials on monogenic inherited eye diseases similar to LCA are under way (6). Other methods to manipulate genes are now available, including CRISPR-mediated editing of retinal genes. So far, the experiments have been mainly on isolated cells or retinas, but these powerful techniques are likely to have eventual clinical applications.

A variation on the use of gene therapy techniques is optogenetics, in which light-sensitive molecules are introduced into non-photosensitive retinal cells. This approach holds much promise for restoring vision to totally blind individuals whose photoreceptors have been lost. Using viruses to insert genes encoding light-sensitive molecules into bipolar and ganglion cells, as well as surviving photoreceptor cells that are no longer photosensitive, has been accomplished in animals and shown to restore some vision (7). Again, technical issues remain: The cells made light-sensitive require bright light stimuli, and the light-sensitive cells do not adapt. That is, whereas photoreceptors normally allow vision over as much as 10 log units of light intensity, the cells made light-sensitive respond only to a range of 2 to 3 log units. Various methods to overcome these limitations are now being developed, and at least one clinical trial is under way. Experiments to make cortical neurons sensitive to light or other stimuli that better penetrate the skullmagnetic fields or ultrasound, for exampleare also being developed and tested in animals.

Other promising approaches to restore vision are being explored. In cold-blooded vertebrates, retinal cells (in fish) and even the entire retina (in amphibians) can regenerate endogenously after damage. Regeneration of retinal cells in zebrafish is now quite well understood (8). The regenerated neurons come from the major glial cell in the retina, the Mller cell. After retinal damage, Mller cells reenter the cell cycle and divide asymmetrically to self-renew and produce a progenitor cell that proliferates to produce a pool of cells capable of differentiating into new retinal cells that repair the retina.

A number of transcription factors and other factors identified as being involved in retinal regeneration in zebrafish have been shown to stimulate some Mller cell proliferation and neuronal regeneration in mice. Regenerated bipolar and amacrine cells, as well as rod photoreceptors, have so far been identified in mouse retinas, and these cells are responsive to light stimuli (9, 10). Further, cells postsynaptic to the regenerated neurons are activated by light stimuli, indicating that the regenerated neurons have been incorporated into the retinal neural circuitry. So far, the regenerative capacity of mammalian Mller cells is limited, but directed differentiation of specific types of neurons with a mix of factors appears to be a possibility. Regrowth of ganglion cell axons after the optic nerve is disrupted is also under active investigation, and although the number of axons regrowing is low (10%), those that do regrow establish synaptic connections with their correct targets (11). Therefore, endogenous regeneration is still far from clinical testing, but substantial progress has occurred.

The retina lines the back of the eye and consists of rod and cone photoreceptors, as well as four types of neuron: second-order bipolar and horizontal cells and third-order retinal ganglion cells (RGCs) and amacrine cells. Mller glial cells fill the spaces between the neurons. The pigment epithelium, critical for photoreceptor function, underlies the retina. Photoreceptors and RGCs are most susceptible to blinding retinal disease. Progress in combating photoreceptor degeneration has been made, but there are few strategies to address RGC loss.

A long-studied area of research is transplantation of retinal cells, particularly photoreceptors, into diseased retinas. In experiments with mice, transplanted postmitotic rod photoreceptor precursor cells derived from embryonic retinas or from stem cells appeared to integrate into diseased retinas in reasonable numbers and to be functional. A surprising and unexpected complication in the interpretation of these experiments was recently discovered. Rather than integrating into diseased retinas, the donor cells appear to pass material (RNA or protein) into remaining host photoreceptor cells, rejuvenating them, and these appear to be most of the functional cells (12). The current evidence suggests that only a small proportion of the donor cells integrate, but progress in overcoming this setback is being made.

More success has been reported with stem cells induced to become pigment epithelial (PE) cells, which provide essential support for photoreceptors. A number of blinding retinal diseases relate to the degeneration of the PE cells, and replacement using such cellsin a suspension or on a scaffoldis being actively pursued. PE cells do not need to integrate synaptically with retinal cells; they simply need to contact the photoreceptor cells. This is achieved when PE cells are placed between the retina and the back of the eye. Early clinical trials suggest that the transplants are safe, but retinal detachment, a serious complication, can occur and efficacy has yet to be shown (13).

The finding that donor photoreceptor cells can help diseased host retinal cells to recover function suggests that certain substances can provide neuroprotection. Indeed, a substantial number of such neuroprotective molecules have been shown to affect retinal disease progression, especially degeneration of photoreceptor cells. No one factor has been shown to be effective generally, but two have received much attention. One, ciliary neurotrophic factor (CNTF), promotes photoreceptor survival in light-induced photoreceptor degeneration and in several other models of retinal degeneration (14). Some evidence suggests that CNTF acts primarily on Mller cells, but how it works, and on what cells, is still unclear. The other factor, rod-derived cone viability (RDCV) factor, has received less research attention, but with recent industrial support, it is now being advanced to the clinic. Current evidence indicates that RCDV factor protects cones after rod degeneration.

Two of the most common retinal diseases in developed countriesage-related macular degeneration (AMD), the leading cause of legal blindness (visual acuity of less than 20/200), and glaucoma, the leading cause of total blindnessare not monogenic diseases, and so genetic treatments for them are not obvious. Attempts to understand the etiology of these diseases are under way, but currently their underlying causes are still unclear. A difficulty presented by AMD is that no animal model is readily available, because it is a disease of the fovea, which mediates high-acuity vision. Except for primates, other mammals do not possess this small critical retinal area. Whereas large primates are not feasible for extensive cellular or molecular studies, small primates such as marmosets that have a fovea are potential models but have not been used much to date.

Other approaches for restoring vision have been suggested and have even yielded some progress. From both normal humans and those with an inherited retinal disease, skin biopsy cells can be induced to form tiny retinal eyecups called organoids (15). Containing all retinal cell types, these structures could be a source of retinal cells for studying retinal disease development and possible therapies, as well as for cell transplantation. A fovea has not been observed in any organoid so far, but this is not beyond the realm of possibility. Another suggested approach is to surgically transplant whole eyes into blind individuals. This appears feasible, but whether there is sufficient optic nerve regrowth remains an open question.

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Restoring vision to the blind - Science Magazine

'); jQuery('.cart-remove-box a').on('click', function(){ link = jQuery(this).attr('href'); jQuery.ajax({ url: link, cache: false }); jQuery('.cart-remove-box').remove(); setTimeout(function(){window.location.reload();}, 800); }); }); //jQuery('#ajax_loader').hide(); // clear being added addToCartButton.text(defaultText).removeAttr('disabled').removeClass('disabled'); addToCartButton.parent().find('.disabled-blocker').remove(); loadingDots.remove(); clearInterval(loadingDotId); jQuery('body').append(""); setTimeout(function () {jQuery('.add-to-cart-success').slideUp(500)}, 5000); }); } try { jQuery.ajax( { url : url, dataType : 'json', type : 'post', data : data, complete: function(){ if(jQuery('body').hasClass('product-edit') || jQuery('body').hasClass('wishlist-index-configure')){ jQuery.ajax({ url: "https://www.stemcell.com/meigeeactions/updatecart/", cache: false }).done(function(html){ jQuery('header#header .top-cart').replaceWith(html); }); jQuery('#ajax_loader').hide(); jQuery('body').append(""); setTimeout(function () {jQuery('.add-to-cart-success').slideUp(500)}, 5000); } }, success : function(data) { if(data.status == 'ERROR'){ jQuery('body').append(''); }else{ ajaxComplete(); } } }); } catch (e) { } // End of our new ajax code this.form.action = oldUrl; if (e) { throw e; } } }.bind(productAddToCartForm); productAddToCartForm.submitLight = function(button, url){ if(this.validator) { var nv = Validation.methods; delete Validation.methods['required-entry']; delete Validation.methods['validate-one-required']; delete Validation.methods['validate-one-required-by-name']; if (this.validator.validate()) { if (url) { this.form.action = url; } this.form.submit(); } Object.extend(Validation.methods, nv); } }.bind(productAddToCartForm); function setAjaxData(data,iframe,name,image){ if(data.status == 'ERROR'){ jQuery('body').append(''); }else{ if(data.sidebar && !iframe){ if(jQuery('.top-cart').length){ jQuery('.top-cart').replaceWith(data.sidebar); } if(jQuery('.sidebar .block.block-cart').length){ if(jQuery('#cart-sidebar').length){ jQuery('#cart-sidebar').html(jQuery(data.sidebar).find('#mini-cart')); jQuery('.sidebar .block.block-cart .subtotal').html(jQuery(data.sidebar).find('.subtotal')); }else{ jQuery('.sidebar .block.block-cart p.empty').remove(); content = jQuery('.sidebar .block.block-cart .block-content'); jQuery('').appendTo(content); jQuery('').appendTo(content); content.find('#cart-sidebar').html(jQuery(data.sidebar).find('#mini-cart').html()); content.find('.actions').append(jQuery(data.sidebar).find('.subtotal')); content.find('.actions').append(jQuery(data.sidebar).find('.actions button.button')); } cartProductRemove('#cart-sidebar li.item a.btn-remove', { confirm: 'Are you sure you would like to remove this item from the shopping cart?', submit: 'Ok', calcel: 'Cancel' }); } jQuery.fancybox.close(); jQuery('body').append(''); }else{ jQuery.ajax({ url: "https://www.stemcell.com/meigeeactions/updatecart/", cache: false }).done(function(html){ jQuery('header#header .top-cart').replaceWith(html); jQuery('.top-cart #mini-cart li.item a.btn-remove').on('click', function(event){ event.preventDefault(); jQuery('body').append('Are you sure you would like to remove this item from the shopping cart?OkCancel'); jQuery('.cart-remove-box a').on('click', function(){ link = jQuery(this).attr('href'); jQuery.ajax({ url: link, cache: false }); jQuery('.cart-remove-box').remove(); setTimeout(function(){window.location.reload();}, 800); }); }); jQuery.fancybox.close(); jQuery('body').append(''); }); } } setTimeout(function () {jQuery('.add-to-cart-success').slideUp(500)}, 5000); } // The EasySep Human B Cell Enrichment Kit is designed to isolate B cells from fresh or previously frozen peripheral blood mononuclear cells by negative selection. Unwanted cells are targeted for removal with Tetrameric Antibody Complexes recognizing non-B cells and dextran-coated magnetic particles. The labeled cells are separated using an EasySep magnet without the use of columns. Desired cells are poured off into a new tube.

For even faster cell isolations, we recommend the new EasySep Human B Cell Isolation Kit (17954), which isolates cells in just 9 minutes.

Advantages:

Fast, easy-to-use and column-free Up to 99% purity Untouched, viable cells

Magnet Compatibility:

EasySep Magnet (Catalog #18000)

The Big Easy EasySep Magnet (Catalog #18001)

Easy 50 EasySep Magnet (Catalog #18002)

EasyPlate EasySep Magnet (Catalog 18102)

EasyEights EasySep Magnet (Catalog #18103)

RoboSep-S (Catalog #21000)

Subtype:

Cell Isolation Kits

Sample Source:

Leukapheresis; PBMC

Selection Method:

Negative

Application:

Cell Isolation

Area of Interest:

Immunology

Document Type

Product Name

Catalog #

Lot #

Language

Yes. The EasySep kits use either a negative selection approach by targeting and removing unwanted cells or a positive selection approach targeting desired cells. Depletion kits are also available for the removal of cells with a specific undesired marker (e.g. GlyA).

Magnetic particles are crosslinked to cells using Tetrameric Antibody Complexes (TAC). When placed in the EasySep Magnet, labeled cells migrate to the wall of the tube. The unlabeled cells are then poured off into a separate fraction.

The EasySep procedure is column-free. That's right - no columns!

The Product Information Sheet provided with each EasySep kit contains detailed staining information.

Yes. RoboSep, the fully automated cell separator, automates all EasySep labeling and cell separation steps.

Yes. We recommend a cell concentration of 2x108 cells/mL and a minimum working volume of 100 L. Samples containing 2x107 cells or fewer should be suspended in 100 L of buffer.

Yes, the EasySep particles are flow cytometry-compatible, as they are very uniform in size and about 5000X smaller than other commercially available magnetic beads used with column-free systems.

No, but due to the small size of these particles, they will not interfere with downstream applications.

Yes; however, this may impact the kit's performance. The provided EasySep protocols have already been optimized to balance purity, recovery and time spent on the isolation.

Yes, the purity of targeted cells will increase with additional rounds of separations; however, cell recovery will decrease.

If particle binding is a key concern, we offer two options for negative selection. The EasySep negative selection kits can isolate untouched cells with comparable purities, while RosetteSep can isolate untouched cells directly from whole blood without using particles or magnets.

Read More

This product is designed for use in the following research area(s) as part of the highlighted workflow stage(s). Explore these workflows to learn more about the other products we offer to support each research area.

Research Area Workflow Stages for

Workflow Stages

Figure 1. FACS Histogram Results With EasySep Human B Cell Enrichment Kit

Starting with frozen mononuclear cells, the CD19+ cell content of the enriched fraction typically ranges from 95% - 99%.

D. G. W. Alanine et al.

The Plasmodium falciparum reticulocyte-binding protein homolog 5 (PfRH5) is the leading target for next-generation vaccines against the disease-causing blood-stage of malaria. However, little is known about how human antibodies confer functional immunity against this antigen. We isolated a panel of human monoclonal antibodies (mAbs) against PfRH5 from peripheral blood B cells from vaccinees in the first clinical trial of a PfRH5-based vaccine. We identified a subset of mAbs with neutralizing activity that bind to three distinct sites and another subset of mAbs that are non-functional, or even antagonistic to neutralizing antibodies. We also identify the epitope of a novel group of non-neutralizing antibodies that significantly reduce the speed of red blood cell invasion by the merozoite, thereby potentiating the effect of all neutralizing PfRH5 antibodies as well as synergizing with antibodies targeting other malaria invasion proteins. Our results provide a roadmap for structure-guided vaccine development to maximize antibody efficacy against blood-stage malaria.

K. Kwak et al.

Protective antibody responses to vaccination or infection depend on affinity maturation, a process by which high-affinity germinal center (GC) B cells are selected on the basis of their ability to bind, gather, and present antigen to T follicular helper (Tfh) cells. Here, we show that human GC B cells have intrinsically higher-affinity thresholds for both B cell antigen receptor (BCR) signaling and antigen gathering as compared with na{{i}}ve B cells and that these functions are mediated by distinct cellular structures and pathways that ultimately lead to antigen affinity- and Tfh cell-dependent differentiation to plasma cells. GC B cells bound antigen through highly dynamic actin- and ezrin-rich pod-like structures that concentrated BCRs. The behavior of these structures was dictated by the intrinsic antigen affinity thresholds of GC B cells. Low-affinity antigens triggered continuous engagement and disengagement of membrane-associated antigens whereas high-affinity antigens induced stable synapse formation. The pod-like structures also mediated affinity-dependent antigen internalization by unconventional pathways distinct from those of na{"{i}}ve B cells. Thus intrinsic properties of human GC B cells set thresholds for affinity selection."""

D. G. Gonzalez et al.

We examined the unique contributions of the cytokines IL-21 and IL-4 on germinal center (GC) B cell initiation and subsequent maturation in a murine model system. Similar to other reports, we found T follicular helper cell expression of IL-21 begins prior to T follicular helper cell migration into the B cell follicle and precedes that of IL-4. Consistent with this timing, IL-21 signaling has a greater influence on the perifollicular pre-GC B cell transition to the intrafollicular stage. Notably, Bcl6hi B cells can form in the combined absence of IL-21R- and STAT6-derived signals; however, these nascent GC B cells cease to proliferate and are more prone to apoptosis. When B cells lack either IL-21R or STAT6, aberrant GCs form atypical centroblasts and centrocytes that differ in their phenotypic maturation and costimulatory molecule expression. Thus, IL-4 and IL-21 play nonredundant roles in the phased progression of GC B cell development that can initiate in the combined absence of these cytokine signals.

Pé et al.

Type 1 diabetes (T1D) is characterized by a chronic, progressive autoimmune attack against pancreas-specific antigens, effecting the destruction of insulin-producing -cells. Here we show interleukin-2 (IL-2) is a non-pancreatic autoimmune target in T1D. Anti-IL-2 autoantibodies, as well as T cells specific for a single orthologous epitope of IL-2, are present in the peripheral blood of non-obese diabetic (NOD) mice and patients with T1D. In NOD mice, the generation of anti-IL-2 autoantibodies is genetically determined and their titre increases with age and disease onset. In T1D patients, circulating IgG memory B cells specific for IL-2 or insulin are present at similar frequencies. Anti-IL-2 autoantibodies cloned from T1D patients demonstrate clonality, a high degree of somatic hypermutation and nanomolar affinities, indicating a germinal centre origin and underscoring the synergy between cognate autoreactive T and B cells leading to defective immune tolerance.

Carroll VA et al.

HIV-1 infection is associated with increased risk for B-cell lymphomas. How HIV infection promotes the development of lymphoma is unclear, but it may involve chronic B-cell activation, inflammation, and/or impaired immunity, possibly leading to a loss of control of oncogenic viruses and reduced tumor immunosurveillance. We hypothesized that HIV structural proteins may contribute to lymphomagenesis directly, because they can persist long term in lymph nodes in the absence of viral replication. The HIV-1 transgenic mouse Tg26 carries a noninfectious HIV-1 provirus lacking part of the gag-pol region, thus constituting a model for studying the effects of viral products in pathogenesis. Approximately 15% of Tg26 mice spontaneously develop leukemia/lymphoma. We investigated which viral proteins are associated with the development of leukemia/lymphoma in the Tg26 mouse model, and performed microarray analysis on RNA from spleen and lymph nodes to identify potential mechanisms of lymphomagenesis. Of the viral proteins examined, only expression of HIV-1 matrix protein p17 was associated with leukemia/lymphoma development and was highly expressed in bone marrow before disease. The tumor cells resembled pro-B cells, and were CD19(+)IgM(-)IgD(-)CD93(+)CD43(+)CD21(-)CD23(-)VpreB(+)CXCR4(+) Consistent with the pro-B-cell stage of B-cell development, microarray analysis revealed enrichment of transcripts, including Rag1, Rag2, CD93, Vpreb1, Vpreb3, and Igll1 We confirmed RAG1 expression in Tg26 tumors, and hypothesized that HIV-1 matrix protein p17 may directly induce RAG1 in B cells. Stimulation of human activated B cells with p17 enhanced RAG1 expression in three of seven donors, suggesting that intracellular signaling by p17 may lead to genomic instability and transformation.

STEMCELL TECHNOLOGIES INC.S QUALITY MANAGEMENT SYSTEM IS CERTIFIED TO ISO 13485. PRODUCTS ARE FOR RESEARCH USE ONLY AND NOT INTENDED FOR HUMAN OR ANIMAL DIAGNOSTIC OR THERAPEUTIC USES UNLESS OTHERWISE STATED.

Internal Search Keywords: 19054|19054RF|19054C.2|19014|14054 |B cell isolation|Easy sep B cell

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EasySep Human B Cell Enrichment Kit

Phase 1 Clinical Study to Evaluate Multiple Doses of FT538 as Monotherapy for Acute Myeloid Leukemia and in Combination with Anti-CD38 Monoclonal Antibody Therapy for Multiple Myeloma

Off-the-shelf NK Cell Product Candidate Derived from Clonal Master iPSC Line Engineered with Three Functional Components to Enhance Innate Immunity

SAN DIEGO, May 20, 2020 (GLOBE NEWSWIRE) -- Fate Therapeutics, Inc. (FATE), a clinical-stage biopharmaceutical company dedicated to the development of programmed cellular immunotherapies for cancer and immune disorders, announced today that the U.S. Food and Drug Administration (FDA) has cleared the Companys Investigational New Drug (IND) application for FT538, the first CRISPR-edited, iPSC-derived cell therapy. FT538 is an off-the-shelf natural killer (NK) cell cancer immunotherapy that is derived from a clonal master induced pluripotent stem cell (iPSC) line engineered with three functional components to enhance innate immunity: a novel high-affinity, non-cleavable CD16 (hnCD16) Fc receptor; an IL-15/IL-15 receptor fusion (IL-15RF); and the elimination of CD38 expression. The Company plans to initiateclinical investigation of three once-weekly doses of FT538as a monotherapy in acute myeloid leukemia (AML) and in combination with daratumumab, a CD38-directed monoclonal antibody therapy, for the treatment of multiple myeloma.

We are very pleased to expand the clinical application of our proprietary iPSC product platform to multiple myeloma, where rates of relapse remain high, said Scott Wolchko, President and Chief Executive Officer of Fate Therapeutics. Clinical data suggest that deficiencies in NK cell-mediated immunity, which are evident even at the earliest stages of myeloma, continue to accumulate through disease progression. We believe administration of FT538 to patients can restore innate immunity, and that the anti-cancer effect of certain standard of care treatments, such as monoclonal antibodies, can be more effective when combined with the engineered functionality of FT538.

The three functional components of FT538 are designed to boost the innate immune response in cancer patients, where endogenous NK cells are typically diminished in both number and function due to prior treatment regimens and tumor suppressive mechanisms. In preclinical studies, FT538 has shown superior NK cell effector function, as compared to endogenous NK cells, with the potential to confer significant anti-tumor activity to patients through multiple mechanisms of action including:

The first-in-human, multi-center, dose-escalation Phase 1 clinical trial of FT538 is designed to determine the maximum tolerated dose (MTD) of three once-weekly doses of FT538 in up to 105 adult patients across four dose cohorts (100M cells per dose; 300M cells per dose; 900M cells per dose; and 1.5B cells per dose). The study will assess two treatment regimens: Regimen A as a monotherapy in patients with relapsed / refractory AML; and Regimen B in combination with daratumumab, an FDA-approved anti-CD38 monoclonal antibody, in patients with relapsed / refractory multiple myeloma who have failed at least two lines of therapy. In addition, the Company may initiate a third treatment regimen in combination with elotuzumab, an FDA-approved anti-SLAMF7 monoclonal antibody, in patients with relapsed / refractory multiple myeloma who have failed at least two lines of therapy starting at one dose level below the MTD of Regimen B. For all regimens, multiple indication- or dose-specific dose-expansion cohorts of up to 15 patients per cohort may be enrolled to further evaluate the clinical activity of FT538.

FT538 is the fourth off-the-shelf, iPSC-derived NK cell product candidate from the Companys proprietary iPSC product platform cleared for clinical investigation by the FDA. The Company has initiated clinical manufacture of FT538 at its GMP facility in San Diego, CA.

About Fate Therapeutics iPSC Product PlatformThe Companys proprietary induced pluripotent stem cell (iPSC) product platform enables mass production of off-the-shelf, engineered, homogeneous cell products that can be administered with multiple doses to deliver more effective pharmacologic activity, including in combination with cycles of other cancer treatments. Human iPSCs possess the unique dual properties of unlimited self-renewal and differentiation potential into all cell types of the body. The Companys first-of-kind approach involves engineering human iPSCs in a one-time genetic modification event and selecting a single engineered iPSC for maintenance as a clonal master iPSC line. Analogous to master cell lines used to manufacture biopharmaceutical drug products such as monoclonal antibodies, clonal master iPSC lines are a renewable source for manufacturing cell therapy products which are well-defined and uniform in composition, can be mass produced at significant scale in a cost-effective manner, and can be delivered off-the-shelf for patient treatment. As a result, the Companys platform is uniquely capable of overcoming numerous limitations associated with the production of cell therapies using patient- or donor-sourced cells, which is logistically complex and expensive and is subject to batch-to-batch and cell-to-cell variability that can affect clinical safety and efficacy. Fate Therapeutics iPSC product platform is supported by an intellectual property portfolio of over 300 issued patents and 150 pending patent applications.

Story continues

About Fate Therapeutics, Inc.Fate Therapeutics is a clinical-stage biopharmaceutical company dedicated to the development of first-in-class cellular immunotherapies for cancer and immune disorders. The Company has established a leadership position in the clinical development and manufacture of universal, off-the-shelf cell products using its proprietary induced pluripotent stem cell (iPSC) product platform. The Companys immuno-oncology product candidates include natural killer (NK) cell and T-cell cancer immunotherapies, which are designed to synergize with well-established cancer therapies, including immune checkpoint inhibitors and monoclonal antibodies, and to target tumor-associated antigens with chimeric antigen receptors (CARs). The Companys immuno-regulatory product candidates include ProTmune, a pharmacologically modulated, donor cell graft that is currently being evaluated in a Phase 2 clinical trial for the prevention of graft-versus-host disease, and a myeloid-derived suppressor cell immunotherapy for promoting immune tolerance in patients with immune disorders. Fate Therapeutics is headquartered in San Diego, CA. For more information, please visit http://www.fatetherapeutics.com.

Forward-Looking StatementsThis release contains "forward-looking statements" within the meaning of the Private Securities Litigation Reform Act of 1995 including statements regarding the advancement of and plans related to the Company's product candidates and clinical studies, the Companys progress, plans and timelines for the clinical investigation of its product candidates, the therapeutic potential of the Companys product candidates including FT538, and the Companys clinical development strategy for FT538. These and any other forward-looking statements in this release are based on management's current expectations of future events and are subject to a number of risks and uncertainties that could cause actual results to differ materially and adversely from those set forth in or implied by such forward-looking statements. These risks and uncertainties include, but are not limited to, the risk of difficulties or delay in the initiation of any planned clinical studies, or in the enrollment or evaluation of subjects in any ongoing or future clinical studies, the risk that the Company may cease or delay preclinical or clinical development of any of its product candidates for a variety of reasons (including requirements that may be imposed by regulatory authorities on the initiation or conduct of clinical trials or to support regulatory approval, difficulties in manufacturing or supplying the Companys product candidates for clinical testing, and any adverse events or other negative results that may be observed during preclinical or clinical development), the risk that results observed in preclinical studies of FT538 may not be replicated in ongoing or future clinical trials or studies, and the risk that FT538 may not produce therapeutic benefits or may cause other unanticipated adverse effects. For a discussion of other risks and uncertainties, and other important factors, any of which could cause the Companys actual results to differ from those contained in the forward-looking statements, see the risks and uncertainties detailed in the Companys periodic filings with the Securities and Exchange Commission, including but not limited to the Companys most recently filed periodic report, and from time to time in the Companys press releases and other investor communications.Fate Therapeutics is providing the information in this release as of this date and does not undertake any obligation to update any forward-looking statements contained in this release as a result of new information, future events or otherwise.

Contact:Christina TartagliaStern Investor Relations, Inc.212.362.1200christina@sternir.com

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Fate Therapeutics Announces FDA Clearance of IND Application for FT538, First CRISPR-edited, iPSC-derived Cell Therapy - Yahoo Finance

President Trump announced on Wednesday that the United States will pull out from the major 35-nation arms control treaty that allows nations to operate reconnaissance flights over other territoriesa critical agreement for building trust and maintaining peace between countries. The official withdrawal from the post-Cold War Open Skies agreement will reportedly happen in six months in accordance with the treatys exit policy. The move was prompted by several instances where Russia refused to comply with the pact, which poses a threat to the U.S. military and cybersecurity, The New York Times reports.

It will be the third major arms control agreement Trump has chosen to exitafter the Iran nuclear deal and the Intermediate Nuclear Forces treatyand reportedly indicates that he may also choose to pull out from the U.S.-Russia nuclear pact START. During the course of this review it has become abundantly clear that it is no longer in Americas interests to remain a party to the Open Skies treaty, a top U.S. official told Reuters.

Link:
Trump Moves to Withdraw From Yet Another Arms Control Treaty - The Daily Beast

Any company in Michigan that allows Donald Trump inside its facilities without wearing a face mask could face legal action, the states attorney general has warned ahead of the presidents Thursday visit. Trump is due in the state to look around a Ford facility in Ypsilanti that has been repurposed to make ventilators for coronavirus patients. The president has refused to wear a mask in public so farbut thats not something state officials will take lightly. Michigan Attorney General Dana Nessel told CNN early Thursday: Honestly, if [Trump] fails to wear a mask, hes going to be asked not to return to any enclosed facilities inside our state. She added: I think were going to take action against any company or any facility that allows him inside those facilities and puts our workers at risk. We simply cant afford it here in our state. Rep. Debbie Dingell (D-MI), who represents the district that includes the Ford plant, also told CNN: Leaders need to lead... I hope the president will follow the protocols because people will see the importance of wearing those masks. It matters. Michigan has been hard-hit by the pandemic, with more than 52,000 cases and more than 5,000 deaths.

See the article here:
Michigan Will Sue Companies That Let Trump Inside Unmasked, Warns State AG - The Daily Beast

Ontario Announces First Phase of Research Projects to Fight COVID-19Ontario-Based Solutions Contribute to the Global Effort against the Outbreak

Ontario is funding the following research on preventing, detecting and treating COVID-19. These projects focus on important areas of research, including vaccine development, diagnostics, drug trials and development, and social sciences.

A Randomized Open-Label Trial of CONvalescent Plasma for Hospitalized Adults with Acute COVID-19 Respiratory Illness (CONCOR-1)Donald Arnold, Principal InvestigatorMcMaster University

CONCOR-1 is a clinical trial that will collect blood plasma from individuals who have recovered from COVID-19, known as COVID-19 convalescent plasma. Convalescent plasma contains COVID-19 antibodies, proteins that help fight the virus. Convalescent plasma will be injected into patients currently fighting the infection, to test whether this is an effective treatment for the virus. This clinical trial will enrol patients 16 years of age and older admitted to hospital with COVID-19 and who require supplemental oxygen for respiratory illness.

Partners include 60 hospitals across Canada and three hospitals in New York City, the Canadian Blood Services and Hma-Qubec and the New York Blood Center.

Research and Deployment of Rapid High-Throughput Diagnostic Testing for COVID-19Marek Smieja, Principal InvestigatorSt Joseph's Healthcare Hamilton

This project will increase Ontario's COVID-19 testing capacity by deploying robotic liquid handling technology, specimen pooling, and efficient sample preparation, while reducing biological risk and ensuring reliable results. The Disease Diagnostics & Development group in the Research Institute of St Joe's Hamilton (RSJH) is collaborating with the Hamilton Regional Laboratory Medicine Program (HRLMP) and other clinical laboratories across the province to quickly develop, validate, and deliver high-throughput, COVID-19 testing, with the goal of testing up to 6,000 samples per lab daily.

Assay Development for SARS-CoV-2 Sero-SurveillanceJennifer Gommerman, Principal InvestigatorUniversity of Toronto

This study will provide a better understanding of the immune response to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the virus that causes COVID-19. This approach aims to measure the level and/or types of antibodies induced by SARS-CoV-2 infection in the blood of acute and convalescent patients. In addition, measuring these antibodies in the saliva of asymptomatic infected subjects identified through contact tracing will provide insights into what the early immune response to the virus looks like, and how this may correlate with clinical outcome. This knowledge, as well as the development of a robust serosurveillance platform, represents a powerful weapon in our fight against COVID-19.

Multivalent Antibody Scaffold to Deliver an Exceptionally Potent and Broad Antiviral Against SARS-CoV-2Jean-Philippe Julien, Principal InvestigatorThe Hospital for Sick Children

This project has the potential to develop a unique antibody-based molecule for protection and treatment against COVID-19. Molecular technology will allow these researchers to decipher the vulnerabilities of the virus with the goal of developing a potent and broad antiviral that neutralizes SARS-CoV-2 and prevents associated COVID-19 symptoms.

Developing Prophylactic Virus-Vectored Vaccines for COVID-19Byram Bridle, Leonardo Susta and Sarah Wootton (Co-Principal Investigators, University of Guelph); Darwyn Kobasa, National Microbiology Laboratory, Public Health Agency of Canada (Collaborator) University of Guelph

This research aims to develop a vaccination strategy for COVID-19. By developing avian avulavirus (AAvV-1) and adenovirus viral-vectored vaccines expressing the SARS-CoV-2 spike protein as a target antigen, researchers will test these vaccines in mice to identify a way to induce robust protective mucosal (respiratory, gastrointestinal and urogenital tract) and systemic immunity. Mucosal immunity plays a significant role in preventing pathogens from getting into the body. Systemic immunity clears any pathogens that bypass mucosal barriers. After optimization, these vaccines will be evaluated in a hamster challenge model at the National Microbiology Laboratory in Winnipeg.

The RAPID COVID Study - Application of Point-of-Care COVID-19 Testing to Optimize Patient Care, Resource Allocation and Safety for Frontline StaffDerek So, Principal InvestigatorUniversity of Ottawa Heart Institute

This study will determine the role of point-of-care testing (POC) as a tool to improve care of COVID-19 patients and conserve resources. A major obstacle facing hospitals during the COVID-19 outbreak is the inability to quickly diagnose who is infected with the virus. Delayed test results could mean that patients, who ultimately test negative, are treated for days utilising resources that could be better deployed elsewhere. An immediate diagnosis of COVID-19 among carriers could provide more expedient treatment, prevent clinical deterioration and help health care workers avoid unnecessary risk of exposure.

In collaboration with Spartan Biosciences, which has developed a novel point-of-care 45-minute bedside COVID-19 test, and a team of specialists from six centres in Ontario, this research will evaluate the efficacy of POC testing to determine when, how and to who it can be applied.

A Prospective, Observational Research Study on the Diagnosis of COVID-19 Infection from Stool Samples of Children and AdultsNikhil Pai, Jeff Pernica, Marek Smieja (Co-Principal Investigators)McMaster University

Through the development and use of a novel test to diagnose COVID-19 from stool samples, this team will assess up to 4,500 stool samples collected from outpatient clinics, emergency departments and inpatient wards across eight major Hamilton region hospitals and clinics. This work will improve COVID-19 disease detection in children and adults who lack respiratory symptoms, are asymptomatic, or are presumed to have "recovered" from past infection. The researchers hope to expand COVID-19 testing options across Canada and ultimately, better identify patients who carry high risk of community transmission than traditional respiratory testing alone.

Cellular Immuno-Therapy for COVID-19 Induced Acute Respiratory Distress Syndrome: The CIRCA-19 TrialDuncan Stewart, Principal InvestigatorOttawa Hospital Research Institute

Through a series of trials, this research will rapidly evaluate the safety and efficacy of using mesenchymal stromal/stem cells, or MSCs, to help treat patients with COVID-19 related acute respiratory distress syndrome (ARDS). Up to 25 percent of all patients admitted to hospital require admission to an intensive care unit, and as many as 40 percent develop severe difficulty breathing due to ARDS.

In total, 27 patients will undergo three sequential trials. The first trial, called the Vanguard study, is designed to quickly determine the optimal dosing strategy of MSCs derived from bone marrow to treat patients experiencing ARDS. The next two trials will use the optimal dose of cells determined by the Vanguard trial, but will administer MSCs derived from the umbilical cord, which is an abundant and readily available source.

Rapid Identification of Immunogenic and T-cell Epitopes to Enable Serologic Testing, Passive Immunotherapy, and Epitope Vaccine for COVID-19Shawn Li, Principal InvestigatorWestern University

To curb the COVID-19 outbreak caused by the SARS-CoV-2 virus, researchers are looking to solve three critical challenges as quickly as possible - detection, treatment, and vaccination. This project will address these challenges by developing a point-of-care blood test to identify infected individuals, including those without symptoms, devising strategies for the production of virus-neutralizing antibodies to treat the severely ill, and identifying viral epitopes to inform epitope-vaccine development.

The Impact of the Coronavirus Pandemic on Children with Medical Complexity Technology Dependency: A Novel Research Cohort StudyAudrey Lim, Principal InvestigatorMcMaster University

This study addresses how to effectively manage pediatric patients remotely by identifying the barriers and facilitators of virtual clinics. COVID-19 is placing strain on families of children with medical complexity, medical fragility and technology dependency. Many of these children are dependent on life sustaining technology such as tracheostomy, home mechanical ventilation, and/or enteral feeding tubes. Though accounting for less than 1 percent of all children in Ontario, this group is at increased risk of multiple and prolonged hospitalizations and poorer health outcomes. Normally, these children are seen at a hospital to address their multiple complex needs, however due to COVID-19, all in-person clinic appointments have been replaced by virtual clinics. Parental satisfaction with virtual clinic healthcare teams will also be assessed using a quality improvement tool developed for this study. This research has the potential to advance virtual medicine, beyond COVID-19.

Food Retail Environment Surveillance for Health and Economic Resiliency: FRESHER OntarioJason Gilliland, Principal InvestigatorWestern University

The Food Retail Environment Surveillance for Health & Economic Resiliency (FRESHER) project is a rapid response to the widespread closures of, and modified operating conditions for, many retail food outlets. The FRESHER project will examine the economic and social impacts of COVID-19 in Southwestern Ontario by identifying what businesses modified their operations, temporarily closed or permanently closed during the outbreak and how the outbreak has affected businesses and their employees. This study will help inform policies and programs that will maintain Ontario's food security, incentivize economic growth during the recovery period, and improve resiliency among businesses during future pandemics and emergencies.

Protective Immunity in Individuals Infected with COVID-19Ishac Nazy, Principal InvestigatorMcMaster University

The goal of this research is to determine the makeup, concentration, strength and viral properties of anti-SARS-CoV-2 antibodies to provide insights into the immune response of individuals infected with COVID-19. Working with Dr. Arnold (CONCOR-1 study on convalescent plasma therapy), this team will use samples from recovered patients to test whether antibodies exist, and if they are able to bind and neutralize the virus. This research will determine whether immunity is longstanding or if it wanes over time; and will inform researchers how immune-based treatments work to fight off the virus, including convalescent plasma or future vaccines.

Clinical Research on the Therapeutic Benefits of Annexin A5 in Severe COVID-19 PatientsClaudio Martin, Principal InvestigatorLawson Health Research Institute

There are currently no proven therapies to treat COVID-19. In the most severe cases, the disease is complicated by sepsis acute respiratory distress syndrome (ARDS), and multiorgan failure. Sepsis is a life-threatening condition caused by the body's response to an infection. While the body normally releases chemicals to fight an infection, sepsis occurs when the body's response to these chemicals is out of balance, triggering systemic inflammation that can damage multiple organs. Many critically ill COVID-19 patients develop sepsis 1-2 days before ARDS, suggesting that sepsis is a major contributor to the development of organ and respiratory failure.

This clinical trial will examine the effects of Annexin A5, in treating critically ill COVID-19 patients who develop sepsis. Annexin A5 is a human protein that has potent anti-inflammatory, anti-apoptotic (cell death prevention) and moderate anticoagulant (blood clot prevention) properties. The ultimate goal of the trial is to use Annexin A5 to treat sepsis and prevent respiratory and multi-organ failure.

Novel Coronavirus Antiviral Drug Discovery Using High-Throughput ScreeningJean-Simon Diallo, Principal InvestigatorOttawa Hospital Research Institute

Using a novel bio-sensor that detects drugs that disrupt the attachment of coronaviruses to cells, this research will test approximately 1,200 approved drugs to better understand their potential to prevent viral infection in cells and their ability to block the interaction between COVID-19 and its receptor. A second phase of this study will attempt to identify novel antivirals from a small (>220,000) molecule library.

Canada's COVID-19 Pandemic Response and Impact in Low-Income and Homeless or At-Risk for Homelessness Populations in Ottawa (Canada): A Mixed Method StudySmita Pakhale, Principal InvestigatorThe Ottawa Hospital Research Institute

Vulnerable populations face numerous social and health inequities that are exacerbated during times of crises. Lessons learned from previous public health crises suggest that inappropriate communication strategies jeopardize risk reduction for vulnerable populations. The objective of this research is to measure the impacts of COVID-19 public health emergency response efforts and communication strategies on Ottawa's low-income, homeless or at-risk for homelessness populations. The findings could help inform public health messaging strategies and pandemic approaches for vulnerable populations.

More:
Ontario Announces First Phase of Research Projects to Fight COVID-19 - Government of Ontario News

If these were normal circumstances, Yuki Bhambri would probably be back on the grind of the tennis tour trying to qualify for a Grand Slam again. It would be a far cry from his breakthrough 2018 season, where he crossed top 100 and played all four Majors, but at least he would be back and fighting on court.

However as things stand, the former India No 1 has not played a competitive match since October 2018 after battling a debilitating knee injury that wasnt correctly diagnosed for months and led to a layoff that is 18 months and counting now.

From a career-best ranking of 83 in April 2018 to losing his ranking and being tagged as inactive on the official ATP charts, it has been a period of difficulty and confusion for the 27-year-old, who has been a junior world No 1 and Grand Slam champion.

Its been a pain a struggle. The [past] 18 months have felt like five years. From not being able to really put any load on my knee, I think its a big achievement to be able to finally get back to playing tennis and do even the basic exercises, Bhambri told Scroll.in.

But even then, there are two ways to look at the long time away from the sport due to injury and now an extended break due to the coronavirus pandemic. The positive is, of course, a shutdown of the entire tennis tour means that the timeline for recovery is extended. Does he see this time off, although due to a negative reason, as beneficial?

Yes, it does for me and for everyone whos been out injured because you dont miss out on the tour. Everyone in the same situation, everyone comes back without hitting a tennis ball for months. Ill not be missing the Grand Slams or any events and it gives me time to come back. So for the few ones, like me, Roger Federer, Juan Martin del Potro, this is a good time. Of course, you dont want it to happen due to a pandemic, he added.

The Indian has been spending time at home in Delhi, trying to get whatever fitness training he can at home with the tennis courts shut amid the nationwide lockdown but he knows its not enough.

Its difficult and different, no matter how much you train at home, its not the same. Youre obviously doing it for your career, for tennis and Im not able to play it and theres only a certain amount that you can really do at home. For me, its really just about being active and doing bits and pieces so that I dont have to start from scratch when I get back on the court, he added.

I was already following a bunch of exercises I need to for my knee rehab. But sometimes modifications are needed and Im in constant touch with my team. Theres only so much you know you can do but I think Ive been good enough in being active, said the Indian who is coached by Stephen Koon from the Impact Tennis Academy in Thailand.

Bhambri admitted that he is unsure if he would be a 100% if the tour were to restart.

Its pretty good but I am not match-fit. I made a lot of progress and if I had to, even right now Id give myself a 70% chance. I need to get out there and practice because I havent done anything in regards to my physical fitness for about over a year and a half now.

The body takes some time to get used to it again and for that Id have to be on the court I presume for at least a couple of months, to be able to get back to running and being able to take the load of a match. I had just started to do that and get into a routine when the lockdown happened. Once its over Ill get back to practice but looking at things, we may not have a tennis season this year he added.

As candid as Bhambri is while talking about the past few months, the toll becomes evident when he describes the excruciating details of his injury and the experimental treatment. He was injured in mid-2018 but it was only in September 2019 when he consulted with Dr Angel Ruiz Cortorro, who has worked with many top injured tennis players including Rafael Nadal, that Bhambri got a clear idea of the problem.

From what I understand of the diagnosis I have a small, partial tear in the medial part of my knee. Because it was tiny and in the middle of the tendon, no one could really figure it out and I was somewhere stuck in between because surgery would have been too big a step to repair it and the basic modern medication and therapy werent working. So I had to try different kinds of treatments, different injections to help heal the tendon, he said.

I was seeing doctors in the US and getting different opinions. But a few of them had the same idea, which was an experimental treatment called stem cell. This procedure was more advanced in Spain and there are very few countries that actually do it; they dont even do it in the States. Since I was getting different opinions, I decided to get in touch with Dr Cortorro just to have another opinion and went with him because hes the one who has treated a lot of tennis players who had knee trouble, Bhambri added.

The decision paid off because after almost a year of taking different injections and waiting for months to see if they made a difference, he finally made progress in late 2019. Around the new year is when I got back on court to hit the ball and I have seen improvement every week, which is a good sign.

Also read: Yuki Bhambri on building up the ammo to fire his way to the top

In his career so far, Bhambri is no stranger to injuries or fighting back from them, but even then one needs immense self-belief to be able to deal with this long and complicated rehab process.

There havent been too many positives, he laughed, but admitted that his success in 2017-18 was a reminder of what he is capable of.

I needed to keep reminding myself that I want to come back and continue playing to get back at the level I was at. I think having tasted success of finally playing the Slams, my first Wimbledon, winning a few matches at the Masters 1000 in Indian Wells and Miami, pushed me as well to try. Wanting to play those events again kept me going, he said.

Coming from a family of tennis players also helped the 27-year-old. His sister Ankita is the Indian Fed Cup coach while other sister Sanaa and cousin Prerna are all pro tennis players.

Theyre always on the lookout, helping out; specially both my sisters who have been helping with the research, making sure I am finishing training and not being lazy my parents coming in and asking if Ive iced my knee or not. So theyve all been actively involved and try to help it in whatever way they can, he said.

Read the original:
Indian tennis: For injury-plagued Yuki Bhambri, the lockdown is both a chance and another challenge - Scroll.in

Three arms of this trial will be leronlimab, remdesivir, and leronlimab + remdesivir

VANCOUVER, Washington, May 18, 2020 (GLOBE NEWSWIRE) -- CytoDyn Inc. (OTC.QB: CYDY), (CytoDyn or the Company), a late-stage biotechnology company developing leronlimab (PRO 140), a CCR5 antagonist with the potential for multiple therapeutic indications, today announced it will be submitting a protocol to the U.S. Food and Drug Administration (FDA) for a factorial design trial to compare effectiveness of leronlimab versus remdesivir and in combination with remdesivir for the treatment of COVID-19.

Leronlimab was administered to more than sixty patients with COVID-19 under emergency Investigational New Drug (eINDs) authorizations granted by the FDA. Preliminary results from this patient population led to CytoDyns Phase 2b/3 clinical trial for 390 patients, which is randomized, placebo-controlled with 2:1 ratio (active drug to placebo ratio). CytoDyn has also been granted a Phase 2 randomized clinical trial study in the U.S. for a Phase 2 randomized clinical trial for mild-to-moderate COVID-19 population in the U.S. CytoDyn plans to update the public regarding current eIND results later this week.

We believe the randomized head-to-head comparison of leronlimab to remdesivir and in combination will provide answers to the lingering question regarding effective treatment options for patients suffering from COVID-19. We look forward to working both in the United States and with potential international sites to help provide effective treatment options for COVID-19, said Jacob Lalezari, M.D., Chief Science Officer of CytoDyn.

Unfortunately, COVID-19 remains a global public health challenge, and its economic impact continues to devastate the world economy. With a second wave of potential cases threatening to surface in the fall and winter of 2020, it is more important than ever to be sure successful treatment options are available to protect the lives of patients. CytoDyn has assurance from its manufacturer that it will have available over 1 million vials this year and could ramp up production to 2-3 million vials this year alone, said, Nader Pourhassan, Ph.D., President and Chief Executive Officer of CytoDyn.

About Coronavirus Disease 2019CytoDyn is currently enrolling patients in two clinical trials for COVID-19, a Phase 2 randomized clinical trial for mild-to-moderate COVID-19 population in the U.S. and a Phase 2b/3 randomized clinical trial for severe and critically ill COVID-19 population in several hospitals throughout the country.

SARS-CoV-2 was identified as the cause of an outbreak of respiratory illness first detected in Wuhan, China. The origin of SARS-CoV-2 causing the COVID-19 disease is uncertain, and the virus is highly contagious. COVID-19 typically transmits person to person through respiratory droplets, commonly resulting from coughing, sneezing, and close personal contact. Coronaviruses are a large family of viruses, some causing illness in people and others that circulate among animals. For confirmed COVID-19 infections, symptoms have included fever, cough, and shortness of breath. The symptoms of COVID-19 may appear in as few as two days or as long as 14 days after exposure. Clinical manifestations in patients have ranged from non-existent to severe and fatal. At this time, there are minimal treatment options for COVID-19.

About Leronlimab (PRO 140) and BLA Submission for the HIV Combination TherapyThe FDA has granted a Fast Track designation to CytoDyn for two potential indications of leronlimab for deadly diseases. The first as a combination therapy with HAART for HIV-infected patients and the second is for metastatic triple-negative breast cancer.Leronlimab is an investigational humanized IgG4 mAb that blocks CCR5, a cellular receptor that is important in HIV infection, tumor metastases, and other diseases, including NASH.Leronlimab has completed nine clinical trials in over 800 people, including meeting its primary endpoints in a pivotal Phase 3 trial (leronlimab in combination with standard antiretroviral therapies in HIV-infected treatment-experienced patients).

In the setting of HIV/AIDS, leronlimab is a viral-entry inhibitor; it masks CCR5, thus protecting healthy T cells from viral infection by blocking the predominant HIV (R5) subtype from entering those cells. Leronlimab has been the subject of nine clinical trials, each of which demonstrated that leronlimab could significantly reduce or control HIV viral load in humans. The leronlimab antibody appears to be a powerful antiviral agent leading to potentially fewer side effects and less frequent dosing requirements compared with daily drug therapies currently in use.

The Company filed its BLA for Leronlimab as a Combination Therapy for Highly Treatment Experienced HIV Patients with the FDA on April 27, 2020, and submitted additional FDA requested clinical datasets on May 11, 2020. After the BLA submission is deemed completed, the FDA sets a PDUFA goal date. CytoDyn has Fast Track designation for leronlimab and a rolling review for its BLA, as previously assigned by the FDA, and the Company plans to request a priority review for the BLA. A priority review designation means the FDAs goal is to take action on the marketing application within six months of receipt (compared with 10 months under standard review).

In the setting of cancer, research has shown that CCR5 may play a role in tumor invasion, metastases, and tumor microenvironment control. Increased CCR5 expression is an indicator of disease status in several cancers. Published studies have shown that blocking CCR5 can reduce tumor metastases in laboratory and animal models of aggressive breast and prostate cancer. Leronlimab reduced human breast cancer metastasis by more than 98% in a murine xenograft model. CytoDyn is, therefore, conducting aPhase 1b/2 human clinical trial in metastatic triple-negative breast cancer and was granted Fast Track designation in May 2019.

The CCR5 receptor appears to play a central role in modulating immune cell trafficking to sites of inflammation. It may be crucial in the development of acute graft-versus-host disease (GvHD) and other inflammatory conditions. Clinical studies by others further support the concept that blocking CCR5 using a chemical inhibitor can reduce the clinical impact of acute GvHD without significantly affecting the engraftment of transplanted bone marrow stem cells. CytoDyn is currently conducting a Phase 2 clinical study with leronlimab to support further the concept that the CCR5 receptor on engrafted cells is critical for the development of acute GvHD, blocking the CCR5 receptor from recognizing specific immune signaling molecules is a viable approach to mitigating acute GvHD. The FDA has granted orphan drug designation to leronlimab for the prevention of GvHD.

About CytoDynCytoDyn is a late-stage biotechnology company developing innovative treatments for multiple therapeutic indications based on leronlimab, a novel humanized monoclonal antibody targeting the CCR5 receptor. CCR5 appears to play a critical role in the ability of HIV to enter and infect healthy T-cells.The CCR5 receptor also appears to be implicated in tumor metastasis and immune-mediated illnesses, such as GvHD and NASH. CytoDyn has successfully completed a Phase 3 pivotal trial with leronlimab in combination with standard antiretroviral therapies in HIV-infected treatment-experienced patients. CytoDyn filed its BLA in April 2020 to seek FDA approval for leronlimab as a combination therapy for highly treatment experienced HIV patients, and submitted additional FDA requested clinical datasets on May 11, 2020. CytoDyn is also conducting a Phase 3 investigative trial with leronlimab as a once-weekly monotherapy for HIV-infected patients. CytoDyn plans to initiate a registration-directed study of leronlimab monotherapy indication. If successful, it could support a label extension. Clinical results to date from multiple trials have shown that leronlimab can significantly reduce viral burden in people infected with HIV. No drug-related serious site injection reactions reported in about 800 patients treated with leronlimab and no drug-related SAEs reported in patients treated with 700 mg dose of leronlimab. Moreover, a Phase 2b clinical trial demonstrated that leronlimab monotherapy can prevent viral escape in HIV-infected patients; some patients on leronlimab monotherapy have remained virally suppressed for more than five years. CytoDyn is also conducting a Phase 2 trial to evaluate leronlimab for the prevention of GvHD and a Phase 1b/2 clinical trial with leronlimab in metastatic triple-negative breast cancer. More information is atwww.cytodyn.com.

Forward-Looking StatementsThis press releasecontains certain forward-looking statements that involve risks, uncertainties and assumptions that are difficult to predict. Words and expressions reflecting optimism, satisfaction or disappointment with current prospects, as well as words such as believes, hopes, intends, estimates, expects, projects, plans, anticipates and variations thereof, or the use of future tense, identify forward-looking statements, but their absence does not mean that a statement is not forward-looking. Forward-looking statements specifically include statements about leronlimab, its ability to have positive health outcomes, the possible results of clinical trials, studies or other programs or ability to continue those programs, the ability to obtain regulatory approval for commercial sales, and the market for actual commercial sales. The Companys forward-looking statements are not guarantees of performance, and actual results could vary materially from those contained in or expressed by such statements due to risks and uncertainties including: (i)the sufficiency of the Companys cash position, (ii)the Companys ability to raise additional capital to fund its operations, (iii) the Companys ability to meet its debt obligations, if any, (iv)the Companys ability to enter into partnership or licensing arrangements with third parties, (v)the Companys ability to identify patients to enroll in its clinical trials in a timely fashion, (vi)the Companys ability to achieve approval of a marketable product, (vii)the design, implementation and conduct of the Companys clinical trials, (viii)the results of the Companys clinical trials, including the possibility of unfavorable clinical trial results, (ix)the market for, and marketability of, any product that is approved, (x)the existence or development of vaccines, drugs, or other treatments that are viewed by medical professionals or patients as superior to the Companys products, (xi)regulatory initiatives, compliance with governmental regulations and the regulatory approval process, (xii)general economic and business conditions, (xiii)changes in foreign, political, and social conditions, and (xiv)various other matters, many of which are beyond the Companys control. The Company urges investors to consider specifically the various risk factors identified in its most recent Form10-K, and any risk factors or cautionary statements included in any subsequent Form10-Q or Form8-K, filed with the Securities and Exchange Commission. Except as required by law, the Company does not undertake any responsibility to update any forward-looking statements to take into account events or circumstances that occur after the date of this press release.

CYTODYN CONTACTSInvestors: Dave Gentry, CEORedChip CompaniesOffice: 1.800.RED.CHIP (733.2447)Cell: 407.491.4498dave@redchip.com

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CytoDyn to Prepare a Phase 3 Protocol to Submit to the FDA for a Three-Arm Comparative and Combination Trial of Leronlimab and Remdesivir -...

The study is anticipated to consist of approximately thirty patients with potential involvement of the NIH of Mexico in other CytoDyn trials

VANCOUVER, Washington, May 19, 2020 (GLOBE NEWSWIRE) -- CytoDyn Inc. (OTC.QB: CYDY), (CytoDyn” or the Company”), a late-stage biotechnology company developing leronlimab (PRO 140), a CCR5 antagonist with the potential for multiple therapeutic indications, today announced it will be coordinating with the NIH of Mexico and providing leronlimab for a trial for the severe/critical COVID-19 population in Mexico with the potential to collaborate on further CytoDyn COVID-19 trials.

CytoDyn is currently enrolling a Phase 2b/3 clinical trial for 390 patients, which is a randomized, placebo-controlled with 2:1 ratio (active drug to placebo ratio). CytoDyn is also enrolling a Phase 2 randomized clinical trial with 75 patients in the mild-to-moderate COVID-19 population. CytoDyn has been granted more than sixty emergency Investigational New Drug (eIND) authorizations by the U.S. Food and Drug Administration (FDA) and plans to provide clinical updates for this patient population later in the week.

We look forward to evaluating leronlimab as a treatment option for patients of COVID-19. We have seen the devastation of this disease on the citizens of Mexico and are looking forward to providing effective treatment options to mitigate the devastation of COVID-19,” said Dr. Gustavo Reyes Tern, head of the Coordinating Commission of National Institutes of Health and High Specialty Hospitals of Mexico, an organization that coordinates the main institutions of medical care and public research in the country.

The NIH of Mexico is committed to help alleviate human suffering and mortality of Mexican citizens. The Metropolitan Area of the Valley of Mexico has a population of approximately 21.5 million people and the contagious nature of COVID-19 is relentless. We look forward to working with the NIH of Mexico to rapidly commence with the proposed study. We also believe that this study results, along with the ongoing Phase 2 study, could establish a path for quick approval in Mexico for use of leronlimab in COVID-19 patients,” said Nader Pourhassan, Ph.D., President and Chief Executive Officer of CytoDyn.

About Coronavirus Disease 2019 CytoDyn is currently enrolling patients in two clinical trials for COVID-19, a Phase 2 randomized clinical trial for mild-to-moderate COVID-19 population in the U.S. and a Phase 2b/3 randomized clinical trial for severe and critically ill COVID-19 population in several hospitals throughout the country.

SARS-CoV-2 was identified as the cause of an outbreak of respiratory illness first detected in Wuhan, China. The origin of SARS-CoV-2 causing the COVID-19 disease is uncertain, and the virus is highly contagious. COVID-19 typically transmits person to person through respiratory droplets, commonly resulting from coughing, sneezing, and close personal contact. Coronaviruses are a large family of viruses, some causing illness in people and others that circulate among animals. For confirmed COVID-19 infections, symptoms have included fever, cough, and shortness of breath. The symptoms of COVID-19 may appear in as few as two days or as long as 14 days after exposure. Clinical manifestations in patients have ranged from non-existent to severe and fatal. At this time, there are minimal treatment options for COVID-19.

About Leronlimab (PRO 140) and BLA Submission for the HIV Combination Therapy The FDA has granted a Fast Track” designation to CytoDyn for two potential indications of leronlimab for deadly diseases. The first as a combination therapy with HAART for HIV-infected patients and the second is for metastatic triple-negative breast cancer. Leronlimab is an investigational humanized IgG4 mAb that blocks CCR5, a cellular receptor that is important in HIV infection, tumor metastases, and other diseases, including NASH. Leronlimab has completed nine clinical trials in over 800 people, including meeting its primary endpoints in a pivotal Phase 3 trial (leronlimab in combination with standard antiretroviral therapies in HIV-infected treatment-experienced patients).

In the setting of HIV/AIDS, leronlimab is a viral-entry inhibitor; it masks CCR5, thus protecting healthy T cells from viral infection by blocking the predominant HIV (R5) subtype from entering those cells. Leronlimab has been the subject of nine clinical trials, each of which demonstrated that leronlimab could significantly reduce or control HIV viral load in humans. The leronlimab antibody appears to be a powerful antiviral agent leading to potentially fewer side effects and less frequent dosing requirements compared with daily drug therapies currently in use.

The Company filed its BLA for Leronlimab as a Combination Therapy for Highly Treatment Experienced HIV Patients with the FDA on April 27, 2020, and submitted additional FDA requested clinical datasets on May 11, 2020. After the BLA submission is deemed completed, the FDA sets a PDUFA goal date. CytoDyn has Fast Track designation for leronlimab and a rolling review for its BLA, as previously assigned by the FDA, and the Company plans to request a priority review for the BLA. A priority review designation means the FDA’s goal is to take action on the marketing application within six months of receipt (compared with 10 months under standard review).

In the setting of cancer, research has shown that CCR5 may play a role in tumor invasion, metastases, and tumor microenvironment control. Increased CCR5 expression is an indicator of disease status in several cancers. Published studies have shown that blocking CCR5 can reduce tumor metastases in laboratory and animal models of aggressive breast and prostate cancer. Leronlimab reduced human breast cancer metastasis by more than 98% in a murine xenograft model. CytoDyn is, therefore, conducting a Phase 1b/2 human clinical trial in metastatic triple-negative breast cancer and was granted Fast Track designation in May 2019.

The CCR5 receptor appears to play a central role in modulating immune cell trafficking to sites of inflammation. It may be crucial in the development of acute graft-versus-host disease (GvHD) and other inflammatory conditions. Clinical studies by others further support the concept that blocking CCR5 using a chemical inhibitor can reduce the clinical impact of acute GvHD without significantly affecting the engraftment of transplanted bone marrow stem cells. CytoDyn is currently conducting a Phase 2 clinical study with leronlimab to support further the concept that the CCR5 receptor on engrafted cells is critical for the development of acute GvHD, blocking the CCR5 receptor from recognizing specific immune signaling molecules is a viable approach to mitigating acute GvHD. The FDA has granted orphan drug” designation to leronlimab for the prevention of GvHD.

About CytoDyn CytoDyn is a late-stage biotechnology company developing innovative treatments for multiple therapeutic indications based on leronlimab, a novel humanized monoclonal antibody targeting the CCR5 receptor. CCR5 appears to play a critical role in the ability of HIV to enter and infect healthy T-cells. The CCR5 receptor also appears to be implicated in tumor metastasis and immune-mediated illnesses, such as GvHD and NASH. CytoDyn has successfully completed a Phase 3 pivotal trial with leronlimab in combination with standard antiretroviral therapies in HIV-infected treatment-experienced patients. CytoDyn filed its BLA in April 2020 to seek FDA approval for leronlimab as a combination therapy for highly treatment experienced HIV patients, and submitted additional FDA requested clinical datasets on May 11, 2020. CytoDyn is also conducting a Phase 3 investigative trial with leronlimab as a once-weekly monotherapy for HIV-infected patients. CytoDyn plans to initiate a registration-directed study of leronlimab monotherapy indication. If successful, it could support a label extension. Clinical results to date from multiple trials have shown that leronlimab can significantly reduce viral burden in people infected with HIV. No drug-related serious site injection reactions reported in about 800 patients treated with leronlimab and no drug-related SAEs reported in patients treated with 700 mg dose of leronlimab. Moreover, a Phase 2b clinical trial demonstrated that leronlimab monotherapy can prevent viral escape in HIV-infected patients; some patients on leronlimab monotherapy have remained virally suppressed for more than five years. CytoDyn is also conducting a Phase 2 trial to evaluate leronlimab for the prevention of GvHD and a Phase 1b/2 clinical trial with leronlimab in metastatic triple-negative breast cancer. More information is at http://www.cytodyn.com.

Forward-Looking Statements This press release contains certain forward-looking statements that involve risks, uncertainties and assumptions that are difficult to predict. Words and expressions reflecting optimism, satisfaction or disappointment with current prospects, as well as words such as believes,” hopes,” intends,” estimates,” expects,” projects,” plans,” anticipates” and variations thereof, or the use of future tense, identify forward-looking statements, but their absence does not mean that a statement is not forward-looking. Forward-looking statements specifically include statements about leronlimab, its ability to have positive health outcomes, the possible results of clinical trials, studies or other programs or ability to continue those programs, the ability to obtain regulatory approval for commercial sales, and the market for actual commercial sales. The Company’s forward-looking statements are not guarantees of performance, and actual results could vary materially from those contained in or expressed by such statements due to risks and uncertainties including: (i) the sufficiency of the Company’s cash position, (ii) the Company’s ability to raise additional capital to fund its operations, (iii) the Company’s ability to meet its debt obligations, if any, (iv) the Company’s ability to enter into partnership or licensing arrangements with third parties, (v) the Company’s ability to identify patients to enroll in its clinical trials in a timely fashion, (vi) the Company’s ability to achieve approval of a marketable product, (vii) the design, implementation and conduct of the Company’s clinical trials, (viii) the results of the Company’s clinical trials, including the possibility of unfavorable clinical trial results, (ix) the market for, and marketability of, any product that is approved, (x) the existence or development of vaccines, drugs, or other treatments that are viewed by medical professionals or patients as superior to the Company’s products, (xi) regulatory initiatives, compliance with governmental regulations and the regulatory approval process, (xii) general economic and business conditions, (xiii) changes in foreign, political, and social conditions, and (xiv) various other matters, many of which are beyond the Company’s control. The Company urges investors to consider specifically the various risk factors identified in its most recent Form 10-K, and any risk factors or cautionary statements included in any subsequent Form 10-Q or Form 8-K, filed with the Securities and Exchange Commission. Except as required by law, the Company does not undertake any responsibility to update any forward-looking statements to take into account events or circumstances that occur after the date of this press release.

CYTODYN CONTACTS Investors: Dave Gentry, CEO RedChip Companies Office: 1.800.RED.CHIP (733.2447) Cell: 407.491.4498 dave@redchip.com

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CytoDyn and the Mexican National Institutes of Health Participate in a Collaborative Study of Leronlimab for the Treatment of Severe/Critical COVID-19...

Magnifier Research has offered the latest report titled Global Canine Arthritis Treatment Market Size, Status and Forecast 2020-2026 which facilitates clients with the changing trends in various markets, regions, and consumers in the global market. The report exhibits on current market analysis scenario, upcoming as well as future opportunities, revenue growth, pricing, and profitability. It gives business summary which includes an examination of the current and past market, analysis of major players dominating the global Canine Arthritis Treatment market, their revenue, their business summary, product segmentation, as well as market size, share, growth, trends analysis, segment and forecasts from 2020-2026.

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Global Canine Arthritis Treatment Market 2020 Manufacturer Landscape, Revenue and Volume Analysis and Segment Information upto 2026 - Cole of Duty

University Health System physicians say each scent offers a unique effect.

SAN ANTONIO Over the past few months most of us have gotten used to wearing masks, whether it is in the grocery store, outside, or for some at all times, and in many cases it just isn't comfortable.

Dr. Jan Patterson, the Medical Director of the Integrative Medicine Program and an Infectious Disease Physician at University Health System, and Professor of Medicine and Infectious Diseases at UT Health San Antonio, spoke to KENS 5 about the study among UHS where they found essential oils to improve mask comfort.

"When COVID happened we realized we had to shift some of our focus to the staff with universal masking which we are very grateful for because it helps us protect each other," she said. "We started in early April with our hospital staff and went to different departments. We are doing both clinical staff and non-clinical staff. More recently weve open it up to patients, some of our patients who are in the clinics who are here for quite a while for infusions and so forth. We would like to try it and see if it makes a difference for them as well."

Rebekah Kendrick, a nurse specializing in pain management told us, "People are feeling different effects from wearing these all day so we wanted to offer them something that might alleviate some of those complaints. Essential oils are really becoming a new thing, so theres new interest in it."

Some of the most common mask complaints include anxiety, fatigue, poor mental focus, headaches, and shortness of breath. Dr. Patterson said, "We know that essential oils, not only do they smell good, but they can affect us very positively in terms of our mood."

The oils go directly to the brain through the olfactory nerve or smell nerve, and they can also affect the respiratory system by opening up the lungs, making breathing easier. The doctors say each scent does something different.

The doctors told us, "Lavender would be great for that to help alleviate some of the anxiety with that and mental focus. The orange oil, we call it happy oil, which is a very happy and calming oil. The lemon oil is brightening and cleansing. People get their headaches relieved through peppermint oil and it can help with mental focus fatigue and breathing. Eucalyptus it's a strong oil we like to say it opens the mind as well as the lungs."

Dr. Patterson spoke about how you apply the oil and said, "Once we choose an oil we simply get a very small drop and put it on the outer edge of the inner mask."

But the ones you get online could be stronger and have a more pleasant effect than the ones you get at the grocery store

Dr. Patterson said, "The ones you get at the grocery store or drugstore or at a lower price point, so sometimes they are diluted and have synthetics in them but you may still get a positive affect. We wanted to use some very pure oils that are what we call therapeutic grade, because we think it has a better affect because they are purer and they last longer.

Dr. Kendrick added, "We have a lot of different options that can help make it a little more of a pleasant experience."

Dr. Patterson also told us how the study they are conducting works. She said, "The survey simply ask things like whats bothering you and how is the mask affecting your anxiety level your mood your fatigue your mental focus. We go through that survey and we help them choose an essential oil that we think is best for them."

Make sure to start with one drop and if you need more add one at a time.

For more information about family health call 210-358-3045. You can also find the rest of Wear The Gown stories, just go to WearTheGown.com.

The rest is here:
Wear The Gown: Using essential oils to improve mask comfort - KENS5.com

A quiz.

Q. You are walking on one side of a sidewalk. Someone strolling toward you veers within six feet of you. You dont have any room to move but the other person does. You call out through your mask, Six feet!

The correct action for that person is:

a. Pretend not to hear and stay the course.

b. Give you the finger and swerve a little.

c. Create some distance by moving away.

The right answer is c.

As some of our COVID-19 pandemic lockdown rules in Illinois are easing and the spring weather is bringing us outside more frequently to walk, run and bike, Ive been navigating the new normal while social distancing. There is no best practices manual for this.

Im a speed walker. I aim at five miles a day. As I roam around, Ive made it a point to observe social or physical distancing behavior who among us tries to observe the six feet; who doesnt; and whether lapses appear willful or the result of being oblivious. Ive become a student of the various tactics people are using and developing some of my own.

Without getting into the heavier political issues associated with wearing masks and social distancing as President Donald Trump ignores both I want to share my evolving rules of the road for folks finding themselves sharing the same sidewalks, paths and streets.

In writing this column, I consulted with two specialists at Northwestern University working on caution fatigue behavior during this pandemic: Dr. Melinda Ring, executive director of the Osher Center for Integrative Medicine, and her colleague, Jacqueline Gollan, associate professor of psychiatry and behavioral sciences at the Asher Center for the Study and Treatment of Depressive Disorders at the Feinberg School of Medicine.

Caution fatigue, Ring said, is a loss of interest in following the recommended guidelines due to mental or physical exhaustion.

Gollan told me in an email, Caution fatigue can influence our ability to comply (with) the new rules. This occurs when people show low motivation or energy to comply with safety guidelines. We may become impatient with the warnings, or we dont believe the warnings to be real or relevant (or) we interpret the risk incorrectly. We may stop safety behaviors, like washing our hands and social distancing.

Caution fatigue occurs because we become desensitized to warnings or risk. Initially, when we hear pandemic warnings, we become fearful and take action. But being intensely fearful is highly taxing on the brain. We adjust psychologically to reduce the fear and desensitize to the pandemic information.

And with that, here are the Sweet Outdoor Rules of the Road:

1. Its on me.

Social distancing is key to avoiding the spread of COVID-19. There are all sorts of persuasion messaging and advertising campaigns ongoing to convince people to stay six feet apart. Yet people dont. Maybe its a spatial dissonance thing? A political statement? Youthful rebellion? Entitlement? Free floating hostility? Ignorance? Doesnt matter why.

Since I care more than you may do about this six-feet thing, its on me to get out of your way.

In general, what we know is, Ring said, you cant change another persons behavior. You can only change your own.

2. Make peace with doing the easiest thing to create the six feet: cross the street, take a turn, whatever. Remember we are living in difficult times.

We are seeing a rise in depression, anxiety, PTSD, Ring said. Add to that people struggling with financial and relationship burdens.

3. Maintain situational awareness. Do not stop in the middle of a sidewalk or path to read your email or chat on the phone. Move off the sidewalk or path.

4. Its also on you.

When you are walking, running or biking behind someone who doesnt know you are there, it is your responsibility to create the six feet of space. Slow down, which, for heavens sake, is not the end of the world. Please call out something like on your left so I can scramble out of your way.

5. End the blockades. Dont be a sidewalk hog. No, you cant always walk or run three abreast with a dog if the path is crowded. Single file.

6. Distance shaming can backfire. Reserve calling out six feet when there is no alternative.

It sounds like a mother scolding a kid, Ring said.

7. Signal. This is for walkers. Sidewalk hogs get a warning when you stick out your arm to create some safe distance and flap it up and down a little. The nonverbal cue is effective in getting folks to fall into single file. Yes, I look a little crazy.

Many folks are great. I zig, they zag, and it works out. Dont get worked up. Said Ring, take some deep belly breaths beneath your mask and move on.

Continued here:
Exercising while social distancing: Rules of the road for walking, running and biking - Chicago Sun-Times