StemCell Therapy

It's not exactly simple to provide tailored advice or information to the millions of participants in U.S. defined contribution plans. But with advancements in technology, new legislation and a retirement community striving to get people to sock more money away for their retirements, industry sources say retirement plans of the future in the U.S. will be shaped by customization.

"In accumulation, particularly the early years, a one-size target-date fund is pretty good for most people, but as you get closer to retirement and into retirement, individual circumstances and needs and wants and financial situation change," said Josh Cohen, Chicago-based head of institutional defined contribution at PGIM Inc., the investment management businesses of Prudential Financial.

Participants would benefit from learning whether they're on track to meet their particular retirement goals and hear what they need to do in order to make those goals a reality, Mr. Cohen said.

Advancements in record-keeper platform capabilities that are now able to "seamlessly pull and protect participant data" make further personalization possible for participants, according to Holly Verdeyen, Chicago-based director of defined contribution investments at Russell Investments.

"There's always been this realization that participant needs are highly personal, especially near retirement, but we just haven't had the ability to deliver that type of individualized advice to people on a mass scale, and now with the advancements in technology we're able to do that better than ever before," Ms. Verdeyen said.

Lew Minsky, Palm Beach Gardens, Fla.-based president and CEO of the Defined Contribution Institutional Investment Association, said customization will grow more prevalent in the coming years and thinks blockchain technology could play a major role. Last fall, DCIIA and the SPARK Institute, which represents retirement industry players such as record keepers, investment advisers, mutual fund companies and benefit consulting firms, held a forum on blockchain technology for the U.S. retirement system.

"We're still early days but you could definitely see an environment where, for example, there is a chain across the industry that has everybody's individual records on it and so all the information necessary for a pretty granular level of customization is available," Mr. Minsky said. "And it would just be about determining which providers within the chain needed what levels of information to be able to facilitate that customization."

And if getting people to save more and smarter is one part of the equation, getting them to save at all is the other. Recent federal and state legislation has opened the door for open multiple employer plans and state-sponsored automatic individual retirement account programs that are known as Secure Choice programs.

Industry stakeholders are confident these types of initiatives will help close the U.S. retirement savings gap. And in Washington, lawmakers are looking to build on the achievements of the Setting Every Community Up for Retirement Enhancement Act, the first retirement security package passed in more than a decade.

Rep. Richard Neal, D-Mass., chairman of the Ways and Means Committee, told Pensions & Investments after the SECURE Act passed in late December that he's working on legislation that will "essentially be the SECURE Act 2.0" and is aiming to move the Automatic Retirement Plan Act and the Retirement Plan Simplification and Enhancement Act with that package.

Mr. Neal in 2017 had introduced the Automatic Retirement Plan Act, which would require many employers to offer a 401(k) or 403(b) plan, and the Retirement Plan Simplification and Enhancement Act, which among other provisions, would exempt retirement savings below $250,000 from complicated required minimum distribution rules. He has yet to do so this Congress.

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Customization to play huge role in funds of tomorrow - Pensions & Investments

Its been a long, wet winter. Everybody has got colds, and now we are braced for a coronavirus epidemic. Boosting our immune system has rarely felt more urgent, but, beyond eating more tangerines and hoping for the best, what else can we do?

Sheena Cruickshank, a professor of immunology at the University of Manchester, has a shocking cold when we speak at a safe distance, over the phone. To know how to take care of your immune system, she says, first you need to understand the weapons in your armoury a cheeringly impressive collection, it turns out.

When you come into contact with a germ youve never met before, she says, youve got various barriers to try to stop it getting into your body. As well as skin, we have mucus snot is a really important barrier and a microbiome, the collective noun for the estimated 100tn microbes that live throughout our bodies, internally and externally. Some of these helpful bugs make antimicrobial chemicals and compete with pathogens for food and space.

Beneath these writhing swamps of mucus and microbes, our bodies are lined with epithelial cells which, says Cruickshank, are really hard to get through. They make antimicrobial products including, most relevant to coronavirus, antiviral compounds that are quite hostile.

If a pathogen breaches these defences, it has to deal with our white blood cells, or immune cells. One type, called macrophages, inhabit all our body tissue and, says Cruickshank, have all these weapons ready to go, but theyre not terribly precise. They report to the cleverer, adaptive white blood cells known as lymphocytes. They are the ones that remember germs, so if you meet that germ again, says Cruickshank, theyll just deal with it probably without you even knowing. Thats when youve got immunity and is the basis of vaccination. Its trying to bypass all the early stuff and create the memory, so you dont have to be sick.

Our immune systems may have blind spots. This might mean that our immune response doesnt recognise certain bugs, she says, or the bugs have sneaky evasion strategies. Personally, my immune system is not necessarily very good at seeing colds. But a healthy lifestyle will ensure your defences are as good as they get.

Seeing as our bodies contain more cells belonging to microbes, such as bacteria and yeasts, than human ones, lets start with the microbiome. We live in a symbiotic relationship with our gut bacteria, says Prof Arne Akbar, the president of the British Society for Immunology and a professor at University College, London. Having the right ones around, that we evolved with, is best for our health. Anything we do that alters that can be detrimental.

Not only do our microbes form protective barriers, they also programme our immune systems. Animals bred with no microbiome have less well developed immune responses. Older people, and those with diseases that are characterised by inflammation, such as allergies, asthma, rheumatoid arthritis and diabetes, tend to have less varied gut microbiomes.

To feed your gut flora, Cruickshank recommends eating a more varied diet with lots of high-fibre foods. Being vegetarian isnt a prerequisite for microbiome health, but the more plant foods you consume, the better. The microbiome really likes fibre, pulses and fermented foods, she adds.

Kefir yoghurt and pickles such as sauerkraut and kimchi are among the fermented delicacies now fashionable thanks to our increasing knowledge of the microbiome. But the evidence for taking probiotic supplements, she says, is mixed. Its not a dead cert that they will survive the journey through your digestive tract, or that they will hang around long enough if they do. Its more effective to change your diet, says Cruickshank.

The skin microbiome is important, too, but we know less about it. High doses of ultraviolet light (usually from the sun) can affect it negatively, weakening any protective functions (as well as triggering immune suppression in the skin itself). Overwashing with strong soaps and using antibacterial products is not friendly to our skin microbiomes. Combinations of perfumes and moisturisers might well also have an effect, says Cruickshank.

To be immunologically fit, you need to be physically fit. White blood cells can be quite sedentary, says Akbar. Exercise mobilises them by increasing your blood flow, so they can do their surveillance jobs and seek and destroy in other parts of the body. The NHS says adults should be physically active in some way every day, and do at least 150 minutes a week of moderate aerobic activity (hiking, gardening, cycling) or 75 minutes of vigorous activity (running, swimming fast, an aerobics class).

The advice for older people, who are more vulnerable to infection, is to do whatever exercise is possible. Anythings better than nothing, says Akbar. But a lifetimes exercise could significantly slow your immune system declining with age. In 2018, a study by University of Birmingham and Kings College London found that 125 non-smoking amateur cyclists aged 55 to 79 still had the immune systems of young people.

The other side of the coin, says Akbar, is elite athletes who become very susceptible to infections because you can exercise to a point where it has a negative impact on your immune system. This problem is unlikely to affect most of us unless, says Cruickshank, youre a couch potato and suddenly try and run a marathon, this could introduce stress hormones and be quite bad for your immune system.

One of the many happy side-effects of exercise is that it reduces stress, which is next on our list of immune-boosting priorities. Stress hormones such as cortisol can compromise immune function, a common example of which, says Akbar, is when chickenpox strikes twice. If you have had it, the virus never completely goes away. During periods of stress, he says, it can reactivate again and we get shingles.

Forget boozing through the coronavirus crisis, because heavy drinking also depletes our immune cells. Some studies have suggested that the first-line-of-defence macrophages are not as effective in people who have had a lot of alcohol, says Cruickshank. And theres been suggestions that high alcohol consumption can lead to a reduction of the lymphocytes as well. So if the bug gets into you, youre not going to be as good at containing and fighting it off.

Cruickshank says that vitamin D has become a hot topic in immunology. It is used by our macrophages, and is something that people in Britain can get quite low on in the winter. Necking extra vitamin C, however, is probably a waste of time for well-fed westerners. Its not that vitamin C isnt crucial to immune function (and other things, such as bone structure). All the vitamins are important, says Cruickshank, but vitamin C is water soluble, its not one that your body stores. Eating your five a day of fruits and vegetables is the best way to maintain necessary levels.

Exercising and eating well will have the likely knock-on effect of helping you sleep better, which is a bonus because a tired body is more susceptible to bugs. One study last year found that lack of sleep impaired the disease-fighting ability of a type of lymphocyte called T cells, and research is demonstrating the importance of our natural biorhythms overall.

Janet Lord, a professor at the University of Birmingham, recently showed that vaccinating people in the morning is more effective than doing so in the afternoon. Your natural biorhythms are, to some extent, dictated by sleep, says Akbar. If youve got a regular sleep pattern, you have natural body rhythms and everythings fine. If they go out of kilter, then youve got problems.

The seriousness of an infection largely depends on the dose you are hit with, which could in turn depend on how contagious the carrier is when they cough near you. Were constantly exposed to germs, and we only get sick from a handful of those, says Cruickshank.

If youre reasonably young and healthy, says Akbar, the mild benefits you may achieve from being extra good probably wont fend off a severe dose of coronavirus or flu. The likely scenario if you catch the infection is, he says, youll be sick for a while and you will recover.

From a public-health perspective, when nasty viruses such as coronavirus are doing the rounds, Akbars priority is not boosting already healthy peoples immune systems, but protecting the vulnerable people. Older people dont respond that well to the flu jab, though its better for them to have it than not. Its a general problem of immune decline with ageing.

When we get older, he says, the barrier function in the gut doesnt work that well, so you have something called leaky gut syndrome, where bugs creep into our bodies causing mild infections. This causes inflammation around the body, as does the natural accumulation of old zombie cells, called senescent cells, and inflammation compromises the immune response.

Akbar is working on developing drug treatments to reduce inflammation in older people but they are a way off yet. Age 65 is when, medically, one is considered older, but thats arbitrary, says Akbar. Some old people might get problems much earlier. And there are older people who are totally healthy.

In terms of coronavirus, says Cruickshank, its mostly spread by droplet transmission, as far as we can tell, so the biggest thing is hygiene. So wash your hands, and sneeze and cough into tissues, she suggests, between sniffles. No one can completely avoid getting sick, not even top immunologists.

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How to boost your immune system to avoid colds and coronavirus - The Guardian

Posted: Mar 6, 2020 / 11:57 PM EST / Updated: Mar 6, 2020 / 11:57 PM EST

BECKLEY, WV (WVNS) With all the viruses going around, many of us are looking for ways to strengthen our immune systems.

On Point Health and Wellness in Beckley has safe alternative methods to keep your family healthy.

According to owner and licensed acupuncturist, Kacy Korczyk, acupuncture can naturally boost immunity and help with inflammation by releasing neuromodulators in the brain. She said you can also relax in the salt cave, and breathe in the therapeutic salt in the air. It is both anti-bacterial and antiviral.

Its really something super easy and super affordable, said Korczyk. You literally just go sit in a room and breath in salt air, and it can work wonders for your sinuses and respiratory tract along with skin issues It can also help with muscle tension and sleep as well.

People can use the salt cave anywhere from two to three times a week to once a month depending on your needs.

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Alternative methods to boost your immune system - WVNS-TV

With the COVID-19 coronavirus spreading, should older adults be flying? (Photo: Getty)

If you are 65 years of age or older or have a chronic medical condition, you may want to think twice about air travel given the COVID-19 coronavirus (SARS-CoV2) situation. Think twice may include trying to recall if you actually have your own private jet.

If you dont have your own airplane, then consider the recommendations that the Centers for Disease Control and Prevention (CDC) website now has for those at higher risk for bad COVID-19 outcomes. As the CDC website explains, older adults and people who have severe chronic medical conditions like heart, lung or kidney disease seem to be at higher risk for more serious COVID-19 illness. Early data suggest older people are twice as likely to have serious COVID-19 illness. (If you want to learn more about why such illnesses tend to be more serious in older adults, Miriam Knoll, MD has previously written for Forbes on this topic.) Nowhere on the CDC web page does it explicitly tell older individuals or those with weaker immune systems to avoid air travel. Nevertheless, take a look at the actual recommendations:

These recommendations dont exactly scream that its OK to get on a commercial flight. After all, commercial flights that arent ghost flights tend to have crowds on them called passengers. Completely avoiding other passengers might require either riding on the wing or spending the entire flight in the bathroom chanting, dont come in here. Theres bad stuff in here. Plus, how can you keep space between yourself and others when you are so close to your neighbors that you cant quite tell which seat belt is whose? These CDC web page even says, avoid crowds, especially in poorly ventilated spaces. And spring breeze is probably not the first thing that you think of when on a commercial flight.

Mike Stobbe reported for the Associated Press that the White House overruled health officials who wanted to recommend that elderly and physically fragile Americans be advised not to fly on commercial airlines because of the new coronavirus. However, Katie Miller, the Press Secretary for Vice President Mike Pence, tweeted the following about this AP report:

Regardless of who actually said what or did what, it is hard to reconcile the current CDC recommendations with older adults taking a commercial flight. Thus, if you are 65 years or older, have a chronic medical condition like diabetes, heart disease, lung disease, or cancer, are on medications such as steroids that may weaken your immune system, or have some other reason why your immune system may not at peak condition, you may want to do whatever you can to avoid air travel. That includes canceling or postponing flights if feasible. Unless, of course, you have your own plane.

In fact, other aspects of the CDC recommendations essentially paint the general picture that older individuals and others with weaker immune systems should begin to distance themselves from others. That doesnt mean start acting aloof and cold and saying, bye, Felicia to everyone. Rather, it means maintaining more physical distance from others. If you are in the higher risk group, prepare to spend more time at home.

When you are older or have chronic medical medical conditions, the recommendation usually isnt too interact less with people. In fact, meeting new people can be a great way to cope with loneliness and other challenges. But these are not typical times. A potentially deadly and not yet well-understood infectious disease is spreading and the situation continues to evolve. Social distancing doesnt mean cut off all social ties. Technology now allows you to maintain and even grow social ties without always having to be physically next to each other. For example, you can start a massive amount of different hashtags or like everything that everyone says on Twitter. The CDC also isnt recommending that you become a hermit. Just make sure that face-to-face interaction is not literally face-to-face. Also, make sure that the people you do interact with in person are not sick and know what precautions to take to keep themselves and you from getting infected.

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Are You At Higher Risk For Serious COVID-19 Illness? Here Is What To Do - Forbes

WASHINGTON A team of scientists jostled for a view of the lab dish, staring impatiently for the first clue that an experimental vaccine against the new coronavirus just might work.

After weeks of round-the-clock research at the National Institutes of Health, it was time for a key test. If the vaccine revs up the immune system, the samples in that dish blood drawn from immunized mice would change color.

Minutes ticked by, and finally they started glowing blue.

Especially at moments like this, everyone crowds around, said Kizzmekia Corbett, an NIH research fellow leading the vaccine development. When her team sent word of the positive results, it was absolutely amazing.

Dozens of research groups around the world are racing to create a vaccine as COVID-19 cases continue to grow. Importantly, theyre pursuing different types of vaccines shots developed from new technologies that not only are faster to make than traditional inoculations but might prove more potent. Some researchers even aim for temporary vaccines, such as shots that might guard peoples health a month or two at a time while longer-lasting protection is developed.

Until we test them in humans, we have absolutely no idea what the immune response will be, cautioned vaccine expert Dr. Judith ODonnell, infectious disease chief at Penn Presbyterian Medical Center. Having a lot of different vaccines with a lot of different theories behind the science of generating immunity all on a parallel track really ultimately gives us the best chance of getting something successful.

First-step testing in small numbers of young, healthy volunteers is set to start soon. Theres no chance participants could get infected from the shots, because they dont contain the virus itself. The goal is purely to check that the vaccines show no worrisome side effects, setting the stage for larger tests of whether they protect.

First in line is the Kaiser Permanente Washington Health Research Institute in Seattle. It is preparing to test 45 volunteers with different doses of shots co-developed by NIH and Moderna Inc.

Next, Inovio Pharmaceuticals aims to begin safety tests of its vaccine candidate next month in a few dozen volunteers at the University of Pennsylvania and a testing center in Kansas City, Missouri, followed by a similar study in China and South Korea.

Even if initial safety tests go well, youre talking about a year to a year and a half before any vaccine could be ready for widespread use, stressed Dr. Anthony Fauci, director of NIHs National Institute of Allergy and Infectious Diseases.

That still would be a record-setting pace. But manufacturers know the wait required because it takes additional studies of thousands of people to tell if a vaccine truly protects and does no harm is hard for a frightened public.

I can really genuinely understand everybodys frustration and maybe even confusion, said Kate Broderick, Inovios research and development chief. You can do everything as fast as possible, but you cant circumvent some of these vital processes.

Behind-the-scenes in NIHs lab

The new coronavirus is studded with a protein aptly named spike that lets the virus burrow into human cells. Block that protein, and people wont get infected. That makes spike the target of most vaccine research.

Not so long ago, scientists would have had to grow the virus itself to create a vaccine. The NIH is using a new method that skips that step. Researchers instead copy the section of the virus genetic code that contains the instructions for cells to create the spike protein, and let the body become a mini-factory.

Inject a vaccine containing that code, called messenger RNA or mRNA, and peoples cells produce some harmless spike protein. Their immune system spots the foreign protein and makes antibodies to attack it. The body would then be primed to react quickly if the real virus ever comes along.

Corbetts team had a head start. Because theyd spent years trying to develop a vaccine against MERS, a cousin of the new virus, they knew how to make spike proteins stable enough for immunization, and sent that key ingredient to Moderna to brew up doses.

How to tell its a good candidate to test in people?

Corbetts team grew spike protein in the lab lots of it and stored it frozen in vials. Then with the first research doses of vaccine Moderna dubbed mRNA-1273, the NIH researchers immunized dozens of mice. Days later, they started collecting blood samples to check if the mice were producing antibodies against that all-important spike protein. One early test: Mix the mouse samples with thawed spike protein and various color-eliciting trackers, and if antibodies are present, they bind to the protein and glow.

Corbett said the work couldnt have moved so quickly had it not been for years of behind-the-scenes lab testing of a possible MERS vaccine that works the same way.

I think about it a lot, how many of the little experimental questions we did not have to belabor this time around, she said. When she saw the first promising mouse tests, I felt like there was a beginning of all of this coming full circle.

___

INOVIOS APPROACH

Inovios approach is similar -- again using genetic code, in this case packaged inside a piece of synthetic DNA that acts as the vaccine. One advantage Broderick cites for a DNA approach is that unlike many types of vaccines, it may not need refrigeration.

A MERS vaccine that Inovio designed the same way passed initial safety studies in people, paving the way for testing the new COVID-19 vaccine candidate. Inovio is doing similar animal testing to look for presumably protective antibodies.

While it gets ready for human safety tests, Inovio also is prepping for another piece of evidence whats called a challenge study. Vaccinated animals will be put in a special high-containment lab and exposed to the new coronavirus to see if they get infected or not.

___

PLACEHOLDER VACCINES?

Regeneron Pharmaceuticals is exploring a different approach: simply injecting people with coronavirus-fighting antibodies instead of teaching the body to make its own. This method could provide temporary protection against infection or work as a treatment for someone already infected.

Regeneron vaccinated mice genetically engineered to make human antibodies. From small blood samples, researchers culled hundreds of different antibodies, and now theyre teasing out which seem most potent against that notorious spike protein, said Christos Kyratsous, Regenerons chief of infectious disease research.

Regeneron developed this monoclonal antibody approach as a life-saving treatment for Ebola. Last year, it performed a successful safety test of experimental antibodies designed to fight MERS.

The difference between using antibodies as a treatment or a vaccine? Low-dose shots in the arm every few months might give enough antibodies to temporarily ward off infection, while treatment likely would require far higher doses delivered intravenously, Kyratsous said. Regeneron is pursuing both, and hopes to begin first-step safety testing in early summer.

The antibodies are the same, he said. We would like to have an antibody that is as flexible in administration as possible.

Whichever of these approaches, or others in the pipeline, pan out, NIHs Corbett said scientists one day hope to have vaccines on the shelf that could be used against entire families of viruses. One frustration when scientists have to start from scratch is that outbreaks too often are waning by the time vaccine candidates are ready for widespread testing.

This is the fastest we have gone, Fauci said of the NIHs vaccine candidate, although he warned it might not be fast enough.

Still, he called it quite conceivable that COVID-19 will go beyond just a season, and come back and recycle next year. In that case, we hope to have a vaccine.

___

The Associated Press Health and Science Department receives support from the Howard Hughes Medical Institutes Department of Science Education. The AP is solely responsible for all content.

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Behind the scenes, scientists prep for COVID-19 vaccine test - Northwest Herald

Coronavirus is far more deadly for men than women, with males 65 per cent more likely to die from an infection than females, new analysis shows.

The latest breakdown of figures from the World Health Organisation (WHO) and Chinese scientists shows that, of all suspected cases, 1.7 per cent of women who contract the virus will die compared with 2.8 per cent of men.

In confirmed cases, the infection is fatal for 4.7 per cent of men but just 2.8 per cent of women, even though the gender balance for those testing positive is roughly split in half.

Some experts believe the sex imbalance relates to a higher prevalance of smoking or chronic alcohol use among men, while others think men are more likely to have underlying health conditions such as heart disease and diabetes, making them more vulerable to an infection.

During the height of the Wuhan epidemic, 16 per cent of people receiving dialysis at Remnin Hospital contracted the disease, and 16 per cent died.

Although the overall global death rate is still being calculated, with estimates ranging from one to 3.8 per cent, the analysis by Worldometer shows it jumps hugely when people have health problems.

The risk of death rises to 10.5 per cent for people with cardiovascular disease, 7.3 per cent for diabetics, 6.3 per cent for those with chronic respiratory disease, six per cent for people with high blood pressure and 5.6 per cent for cancer sufferers.

However, Paul Hunter, professor of medicine at the University of East Anglia, believes women may simply have better immune systems and are biologically better at fighting off the virus.

"Some of the differences are probably due to men smoking more and being chronic abusers of alcohol, but also, women are intrinsically different to men in their immune response," he said.

"Sometimes that works in women's favour. Women seem to have more powerful immune systems, which means they suffer more from autoimmune disease like rheumatoid arthritis, when the immune system responds over-aggressively and ends up attacking the body.

"This happens in men far less frequently, but itappears to be a good thing for a number of infections and particularly influenza, and there is evidence women produce better antibody responses to the influenza vaccine than men."

Older men may be particularly at risk because the death rate rockets in the elderly.

While the chance of dying from the virus for anyone under 50 is less than 0.5 per cent, it jumps to 1.3 per cent after the age of 50 and then nearly trebles to 3.6 per cent after 60.

By the time someone reaches 70, their risk of dying has hit eight per cent, which then rises to 14.8 per cent for the over 80s, far and away the most vulnerable group.

On Thursday evening,NHS Berkshire confirmed that the first person to die in Britain was an "older patient with underlying health conditions".

The British man who died after contracting the virus on the Diamond Princess cruise ship, which was quarantined off the Japanese coast, was in his 70s.

Although many older people are often suffering from chronic disease which make them more vulnerable, the immune system itself begins to break down in later life.

Diseases that are largely harmless in youth, such as chicken pox, hide in the body and can become deadly shingles as people get older and their immunity begins to decline. The quality of antibodies produced also diminishes with age, preventing the body from clearing out viruses quickly and efficiently.

"Our immune systems start giving up the ghost," added Prof Hunter. "You're going to delay coming up with an antibody."

Yet young children seem to be oddly protected against coronavirus. So far there have been no deaths among the under 10s, and the disease is fatal for just 0.2 per cent of people aged between 10 and 40.

Dr Andrew Freeman, a reader in infectious diseases at Cardiff University, said: "I think, with children, it is likely that they are susceptible to infection but more likely get mild/asymptomatic infection.

"This does occur with some other viral infections such as Epstein-Barr virus infection which causes glandular fever in young adults, and also hepatitis A. We still have a lot to learn about this virus."

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Men far more likely to die from coronavirus than women, analysis shows - Telegraph.co.uk

USA TODAY answers a question you may be wondering: Is coronavirus worse than the flu? USA TODAY

You might be buying or making lots ofhand sanitizerto help protect yourself from the COVID-19 coronavirus, but health care professionals areasking you to do something a lot harder: Stop touching your face.

In addition to properly washing your hands, experts saykeeping your hands away from your eyes, nose and mouth will help protect you from the coronavirus orthe flu and other infections.

Easier said than done.

"Even health experts have trouble not touching their faces!" the Santa Clara County, California Public Health Department posted to Facebook on Thursday.

That followed an article bythe Washington Post pointing out thatSara Cody, the county's public health director, had licked her finger moments after urging the public not to touch their face.

Its just subconscious behavior," infection prevention expertConnie Steed told USA TODAY on Friday.

She said trying to break the habit has taken a big effort for her and her family.

But it's a habit worthbreaking.

Your face contains multiple pathways for infections to easily enter your body, and your hands can be contaminated without you knowing it.

You can clean your hands all day, but as soon as you start touching things again ...the germs on your hands increase, said Steed,the president of theAssociation for Professionals in Infection Control and Epidemiology.

Hand washing: You're probably washing your hands wrong and don't even know it

Watch: Boost your immune system by doing these things and fend off coronavirus, flu

If we could only see the germs on our hands, we'd find it a lot easier to keep them away from our face,Steed said.

Reducing how often you touch your face is just part of "common-sense basics" for avoiding all types of illnesses, not just the coronavirus currently causing widespread anxiety.

Because it's a common habit most people do it all the time without realizing it. APIC estimates the average person touches their face23 times per hour, based on a small 2015 study.

It's something we start doing as young kids and most of us never stop, Steed said. Becoming self-aware of the problem is a good place to start.

That's what Verge journalistElizabeth Lopatto tried to do this week asshe attempted to count how often she touched her face in a day.

After a few hours she concluded "I am aborting the mission because I touch my face too often."

How-to guidesare popping upeverywhere.

One common thread: Try your best to do it less, but don't let it ruin your day. As one expert pointed out to the New York Times, stress is bad for your immune system and obsessing over breaking a common habit could create its own problems.

According Steed, there are a few simple things that may help:

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Health officials say not to touch your face. That's harder than it sounds even for them. - USA TODAY

On Monday, Donald Trump held a meeting in the White House to discuss his Administrations response to COVID-19, the novel coronavirus that has spread to every continent except Antarctica. At the time there had been more than a hundred and five thousand cases reported in at least eighty-three countries, leading to more than thirty-five hundred deaths. Seated around an oval table in the Cabinet Room were health experts from the Centers for Disease Control and Prevention, the Food and Drug Administration, and the National Institutes of Health, as well as pharmaceutical executives from Pfizer, Johnson & Johnson, Sanofi, and others. With more than a hundred cases already discovered in the U.S., which had resulted in six deaths (the virus has since infected nearly four hundred people in the U.S., and killed at least nineteen of them), Trump was concerned. But he was also confused, despite having had several previous briefings with the Administrations top health officials. Grasping for some good news, he pressed the executives to deliver a vaccine within a few months, at which point Anthony Fauci, the longtime director of the National Institute of Allergy and Infectious Diseases (N.I.A.I.D.), spoke up. A vaccine that you make and start testing in a year is not a vaccine thats deployable, he said. The earliest it would be deployable, Fauci added, is in a year to a year and a half, no matter how fast you go.

The virus seems to have been circulating in the United States, particularly in Washington State, for the past month, and more cases are expected. A person can be infected but asymptomatic, and therefore unknowingly infect other people. This limits the ability of public-health tools to contain its spread. Even still, a COVID-19 vaccine developed, licensed, and manufactured at a global scale in twelve months would be an unprecedented, remarkable, even revolutionary achievement. No other vaccine has come close to being developed that quickly. The fastest effort to date was during the Zika outbreak, in 2015, when one was ready for testing in about seven months, but the epidemic fizzled out before an approved vaccine could be sent through clinical trials. At the meeting on Monday, Trump said, I like the sound of a couple months better, if I must be honest.

John Shiver, the global head of vaccine research and development at the multinational pharmaceutical company Sanofi, which is developing a COVID-19 vaccine, was at the meeting with Trump. There was some confusion there, Shiver said, that certain officials did not understand that being in people, as in human trials, is not the same as having a product. Clinical trials are conducted on healthy people, which is inherently challenging. You certainly dont want a vaccine that can make it worse, Shiver said. There have been some vaccine candidates historically that could actually enhance the disease. Sanofi is working with the United States Biomedical Advanced Research and Development Authority, a sort of biomedical DARPA, to advance a COVID-19 vaccine based largely on the vaccine candidate it had developed for SARS. Shiver told me that the authority doesnt expect to have anything ready for human trials until much later this year. Its difficult, Shiver said, to see how, even in the case of an emergency, a vaccine could be fully ready for licensure in a year and a half.

The Coalition for Epidemic Preparedness Innovations (CEPI), an Oslo-based nonprofit organization, was established at Davos, in 2017, to help the world prepare for a disease X pandemic. One of its aims is to dramatically hasten the process of vaccine development. To create a viable, scalable vaccine takes vast amounts of funding and R. & D., Rachel Grant, the advocacy and communications director at CEPI, told me. It is a long and complex business. Its all doable, science can meet the challenges, but there is lots of attrition before any vaccine gets to the point of licensure. The problem is twofold. First, there may never be a market for a vaccine at the end of the development process, because the epidemic is contained, or never comes to pass. Then, traditionally, if there is an epidemic, it may take hold in a developing country where the costs of research and development cannot be recouped. The resources and expertise sit in biotech and pharma, and theyve got their business model, Grant said. Theyre not charities. They cant do this stuff for free.

CEPI, with funding from the government of Norway, the Gates Foundation, the Wellcome Trust, and several other countries (the United States is not among them), is trying to bridge the gap. The challenge of vaccine development is what CEPI was set up to solve, Grant told me, played out writ large in an episode like this. Since the novel coronavirus emerged, CEPI has ramped up its grant-making expenditures to more than nineteen million dollars. Two grant recipientsa Massachusetts-based biotech startup named Moderna and a lab at the University of Queensland, in Brisbane, Australiahave, remarkably, already developed a vaccine candidate that they will start testing in human trials in the next few months, and another biotech startup supported by CEPI is not far behind. But, ultimately, to get three different vaccines through the final phase of clinical testing, Nick Jackson, CEPIs head of programs and innovative technology, told me, will require an estimated two billion dollars.

Barney Graham is the deputy director of the Vaccine Research Center, at the N.I.A.I.D., in Bethesda, Maryland, which is collaborating with Moderna and other academic labs on a possible vaccine. Graham is one of the worlds experts on the structure of viruses and how they interact with human cells to make us sick. In the seven years before the COVID-19 virus appeared, one of Grahams projects had involved understanding the MERS coronavirus, in order to potentially develop a vaccine. (MERS, which can be transmitted from camels to humans, has been contained to the Middle East, and seems to spread mostly in confined spaces, like hospitals.) Theres several ways of delivering a protein to a human body that will make a vaccine-type response, he told me. Certain proteins, when injected into a human, are antigenic, provoking the bodys immune system to create antibodies. Traditionally, proteins are made in a microbrewery type of bioreactor, Graham saida common flu-virus vaccine, for instance, is grown in chicken eggsand it takes up to two years to get that protein ready. That is not fast enough if youre in a pandemic situation. Researchers have long been working on so-called vaccine-platform manufacturing technologies for future use. The idea is akin to creating a frozen-yogurt maker for vaccinessame machine, different flavors. With vaccine-platform technologies, the hope is that the way in which the vaccine is manufactured and delivered to the bodysuch as Modernas messenger-RNA (mRNA) technologywill transport any antigen and, therefore, theoretically protect against any infectious disease. You can make the RNA in the same way, purify it in the same way, release it in the same way, and yet make many different proteins, Graham said.

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How Long Will It Take to Develop a Coronavirus Vaccine? - The New Yorker

Coronavirus Can Quickly Progress to Severe Pneumonia and Even Death Due to Immune Hyperactivity Including Acute Respiratory Distress Syndrome (ARDS); CytoDyn's Trial Focuses on Patients Who Develop Mild-To-Moderate Respiratory Illness After Contracting Coronavirus

CytoDyn Negotiating to Expedite Setup of Treatment Clinics in New York and San Francisco

VANCOUVER, Washington, March 08, 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, announced today that the Company has submitted an investigational new drug (IND) application to the U.S. Food and Drug Administration (FDA) to conduct a Phase 2 clinical trial with leronlimab (PRO 140) as a therapy for patients who experience respiratory complications as a result of contracting the coronavirus disease 2019 (COVID-19).

Bruce Patterson M.D., CEO of IncellDX and advisor to CytoDyn explains: Leronlimab inhibits migration of Tregs, which can inhibit the innate immune response against pathogens, into areas of inflammation. Most importantly, the migration of macrophages and the release of inflammatory cytokines including TNF and IL-6 (cytokine storm) is what causes the profound damage in the lungs in some patients. Leronlimab binding to CCR5 changes the macrophages migration and cytokine production. Taken together, these activities may reduce the morbidity and mortality in moderate to severe cases of COVID-19. IncellDx has developed a suite of diagnostics to monitor these effects of leronlimab on the immune system in these critical patients.

Coronavirus deaths are linked to patients immune systems that have an inflammatory response to the virus causing Acute Respiratory Distress Syndrome (ARDS). With ARDS, the entire lung is affected, unlike pneumonia where often only part of the lung is affected, said Nader Pourhassan, Ph.D., president and chief executive officer of CytoDyn. Our scientists believe that our data in cancer patients indicated that leronlimabs role in blocking Tregs and macrophages demonstrates that leronlimab modulates the inflammatory response to more effectively provide effector function. With more than 840 patients treated with leronlimab in our clinical trials, we believe leronlimab could reduce the inflammation which contributes to ARDS, thereby potentially reducing morbidity and mortality rates in coronavirus patients. If we can show a similar response in our current Phase 2 trial, then leronlimab could have a powerful impact on improving the prognosis for coronavirus patients. With leronlimabs Fast Track designation from the FDA for the treatment of HIV and mTNBC (triple-negative breast cancer), we are expediting the initiation of this trial to address the rapid spread of this disease and are eager to test this proof of concept in clinical trials as a potential treatment for coronavirus, added Dr. Pourhassan.

The following is a brief summary of excerpts from the Companys Phase 2 clinical trial protocol:Indication for Use: Leronlimab is indicated for treatment of adult patients with mild-to-moderate symptoms of respiratory illness caused by coronavirus 2019 infection.Objective: The purpose of this study is to assess the safety and efficacy of leronlimab administered as weekly subcutaneous injection in subjects with coronavirus 2019 infection.Primary Outcome (Endpoint) Measure: Clinical Improvement based on change in total symptom score (for fever, myalgia, dyspnea and cough)Note: The total score per patient ranges from 0 to 12 points. Each symptom is graded from 0 to 3 [0=none, 1=mild, 2=moderate, and 3=severe].Trial Design: This is a Phase 2, single arm, open-label, multicenter study to evaluate the safety and efficacy of leronlimab (PRO 140) in patients with mild-to-moderate symptoms of respiratory illness caused by coronavirus 2019 infection. Leronlimab (PRO 140) will be administered subcutaneously as weekly dose of 700 mg.The study will have three phases: Screening Period, Treatment Period, and Follow-Up Period.Treatment Period: 4 weeks allowed windows.Inclusion Criteria:

About Coronavirus Disease 2019The coronavirus disease 2019 (COVID-19) was identified as the cause of an outbreak of respiratory illness first detected in Wuhan, China.1 The origin of COVID-19 is uncertain and it is unclear how easily the virus spreads. COVID-19 is thought to be transmitted 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. It is believed that symptoms of COVID-19 may appear in as few as two days or as long as 14 days prior to exposure, and that symptoms in patients have ranged from non-existent to severe and fatal. There are currently no known antiviral treatments effective at suppressing COVID-19.

About Leronlimab (PRO 140)The U.S. Food and Drug Administration (FDA) have 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 successfully 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 can 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.

In the setting of cancer, research has shown that CCR5 plays an important role in tumor invasion and metastasis. 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. Additional research is being conducted with leronlimab in the setting of cancer and NASH with plans to conduct additionalclinical studies when appropriate.

The CCR5 receptor appears to play a central role in modulating immune cell trafficking to sites of inflammation and may be important 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 further support the concept that the CCR5 receptor on engrafted cells is critical for the development of acute GvHD and that blocking this receptor from recognizing certain 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 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 key 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 in immune-mediated illnesses, such as GvHD and NASH. CytoDyn has successfully completed a Phase 3 pivotal trial with leronlimab in combination with standard anti-retroviral therapies in HIV-infected treatment-experienced patients. CytoDyn plans to seek FDA approval for leronlimab in combination therapy and plans to complete the filing of a Biologics License Application (BLA) in the first quarter of 2020 for that indication. CytoDyn is also conducting a Phase 3 investigative trial with leronlimab as a once-weekly monotherapy for HIV-infected patients and plans to initiate a registration-directed study of leronlimab monotherapy indication, which if successful, 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 with no reported drug-related serious adverse events (SAEs). Moreover, results from a Phase 2b clinical trial demonstrated that leronlimab monotherapy can prevent viral escape in HIV-infected patients, with some patients on leronlimab monotherapy remaining 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. 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

References:1.Novel Coronavirus 2019, Wuhan, China. (2020, January 24). Retrieved fromhttps://www.cdc.gov/coronavirus/2019-ncov/index.html

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CytoDyn Files IND and Protocol for Phase 2 Clinical Trial for Treatment of Patients with Coronavirus with Leronlimab (PRO 140) - GlobeNewswire

A pestilence isnt a thing made to mans measure, Albert Camus observed in The Plague. Therefore we tell ourselves that pestilence is a mere bogey of the mind, a bad dream that will pass away. Panic is exhausting. Only so many witches can be tossed into wells or rolls of toilet paper hoarded before knee-jerk anxiety progresses to a steady state of fear. Cities go dark, governments quarantine exposed populations, institutions begin shutting down, and, as we have seen with the erratic stock market, economies sputter. A population huddled indoors cant till the fields or man the pin factories. Oxen, asses, sheep, goats, pigs, and chickens and even dogs . . . were driven away and allowed to roam freely through the fields, Giovanni Boccaccio wrote in the Decameron. The crops lay abandoned.

According to Cirium, an aviation-industry consulting firm, more than 200,000 flights in and out of China have been canceled, a 60 percent decline. In 2003, in the midst of SARS, global air travel was down 25 percent. Planes flew into Chek Lap Kok, Hong Kongs international airport, completely empty of passengers. Hong Kong, a city renowned for its shopping, became a retail ghost town. The eighth-of-a-mile walk from one Prada boutique in Hong Kongs Admiralty district to another Prada boutique in Central, usually a 30-minute journey due to all the jukes and spin moves required to avoid the throngs of mainland shoppers, was now a five-minute straight shot.

Concerned about the health of my staff at Time Asia, I consulted other managers at various subsidiaries of what was then the Time Warner empire. The local boss of CNN was in New York with his family and would be staying there for the duration of the outbreak. The head of Turner Entertainment Asia hadnt made any plans, but was eager to hear what I had in mind. Nothing was more fatal, Defoe had warned, then the supine negligence of the people themselves. Determined not to repeat the folly of Defoes Londoners, I did what managers everywhere do when they want to look like they know what they are doing: I convened a meeting. But when I suggested that anyone who had been in contact with a possible SARS case should stay away from the office, it became clear that everyone in the room already knew someone who might be infected. In fact, our circulation manager had dined the evening before at her father-in-laws apartment at Amoy Gardens. There was really nothing we could do, I realized, besides shutting down our publication. But that wasnt an option: We were a newsmagazine, and this was news.

Fear dissipates eventually, replaced by a more realistic sense of the risks. An epidemic, even one of a disease as seemingly easy to transmit as COVID-19, while burdening public-health systems and potentially deadly for the elderly and those with compromised immune systems, is eminently survivable by the majority of the population. This fact becomes obvious as people become sick, yet recover; doctors and nurses get a better handle on treatment; and most people go about their life and never succumb. In some ways we were lucky at Time Asia, because we had no choice but to continue visiting hospitals, talking with doctors, and interviewing virologists. We were worried, yes, but proximity to the professionals gave us clarity about the actual risks we were facing.

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The Pattern That Epidemics Always Follow - The Atlantic

Stronger immune systems are what we all need in order to successfully shield ourselves from being infected by harmful viruses and bacteria. Especially with the outbreak of the Coronavirus, this gives us even more reason to ensure that we build stronger immune systems. With or without the recent outbreak, we should be taking preventative measures in any case.

If we build stronger immune systems, our bodies will be more equipped to fend off viruses and bacterial attacks. To do this we must all practise good eating habits and choose food that builds stronger immune systems. This way you wont have to stress or panic as much as those who have weaker immune systems. Mainly because your body is ready for battle against any illnesses.

The point is not to panic but to instead focus on your own health. Not only does a strong immune system help fight infections caused by viruses, but it will also speed up the recovery process after an infection. Dont underestimate the power of your immune system. When youve got a strong one, it acts as your bodys defence against infectious organisms and other invaders.

For things first, what is the immune system? Basically it is a complex system in your body that is made up of a network of cells, tissues and organs that work together to protect the body. According to doctors, everyones immune system is different due to factors such as age, eating habits and lifestyle.

Therefore, it is important to make sure that your immune system is strong and fit to fight. Especially in times like these where unknown illnesses are on the loose. You need to look after your health and prioritize your protection. In fact, even if you think youre very healthy you should consider doing a few things to boost your immune system for additional protection against viruses. While there are no guarantees that taking these steps will help, they are very unlikely to hurt.

The most important tip from all health professionals:Wash. Your. Hands. Seems logical right? Well, just ensure youre doing it properly. And if you dont have any access to clean running water then you can also use hand sanitizer with at least 60 percent alcohol. There are also organic hand sanitizers available if youre worried about the environment.

Were going to share some useful tips to build stronger immune systems. Just be sure to remember to check in with your personal doctor or health professional before any change in your habits. Even if its just taking vitamin supplements or starting an exercise program.

Experts in health explain that one of the most important vitamins to build stronger immune systems is vitamin C. Why? Because when theres a lack of vitamin C it can make you more prone to getting sick.

Moreover, your body needs Vitamin B6, because it is vital in supporting biochemical reactions in the immune system. In addition to this, vitamin E is also a powerful antioxidant that aids the body in fighting off infections. This means that its very important to get enough vitamins for stronger immune systems. You should be able to do this with a healthy and balanced diet.

We think that in light of the current outbreak, it will work in your favor to consume food that boosts the immune system. You can start by making sure your diet includes green vegetables, kiwi fruits, lemons and oranges. In addition, you can also consume nuts like almonds and cashews, which are high in vitamins and antioxidants.

Youll be glad to hear that cooked poultry and shellfish are also important immune boosters due to the protein and zinc they provide. However, experts warn us to avoid consuming half-cooked or raw food for a while. Shellfish that are high in zinc include crab, clams, lobster and mussels. Take note of the daily recommended amount (11mg for men and 8mg for women). Too much zinc can inhibit the immune system.

Then it is also integral that you dont develop any vitamin D deficiencies. This may lead you to encounter poor bone growth, cardiovascular problems and a weak immune system. Therefore, you need to choose supplements that contain D3 (cholecalciferol) since its good for raising your blood levels of vitamin D. Nutritionists recommend a balanced diet comprising carbohydrates, proteins, fats, vitamins and minerals. And of course, drinking enough water is essential to building stronger immune systems.

Any health expert will inform you that a diet rich in colorful fruits and vegetables is important for the body. These foods help to replenish and build stronger immune systems. Moreover, fruits and vegetables contain Vitamin C, E and antioxidants that all enhance the immune system to fight against infections and pathogens.

Its best to eat a variety of citrus fruits and berries for a strong immune system. Then in terms of vegetables, consume bell peppers, broccoli and spinach. Just like anything though, be sure to consume these in moderation. Usually, people without any underlying health issues will not be affected by slightly higher intake. However, if you have a pre-existing health condition be cautious about dietary changes, especially if youve had any medical procedures done, for example to the heart, its best to consult a nutritionist for a customised regime.

You may also want to include more seeds into your diet. These are essential for boosting the immune system. For example, sunflower seeds contain phosphorous, magnesium and Vitamin B6. To get more vitamin E you can try including more avocados, dark leafy greens and nuts. Lots of research also points to eating more garlic, ginger, dark chocolate and green tea. These are highly beneficial to the body. Be sure to also include Vitamin D and probiotics from yogurt to build stronger immune systems. Essentially its best to stay away from any processed food.

Its also important to avoid high-sugar food and drinks as they may weaken your immunity, accumulate unnecessary fats or lead to other medical problems. To really maximise your healthy immune system, complement your healthy diet with regular and moderate amounts of exercise.

Never skimp on your sleep. Getting quality sleep will help build stronger immune systems. Why? Sleep helps your T cells stick to and attack infections. So when you miss out on sleep your T cells are less sticky and arent as strong in fighting off viruses.

Every person is different when it comes to sleep requirements. However, the general guidelines state that we need between 7 and 9 hours of solid sleep each night. If you have restless sleep, wake up every night or snore, you may want to talk to a doctor.

Whatever you do, just dont panic. This is because anxiety weakens the immune system. In fact, being stressed can cause your body to release extra cortisol, which over time can negatively affect sleep quality and your immune system. A well-rested body will build stronger immune systems. Apparently acupuncture is also very beneficial to building stronger immune systems.

The aim of the game is to do all that we can to build stronger immune systems, so we dont have to panic or stress too much about the risk of getting infected. Take care of yourselves.

To be healthy means to maintain an optimal balance of all the functions in your body. Eating good food is the best way to get the right balance of vitamins and minerals. Heres how.

Make Sure Immune System Is Strong And Fit To Fight. New Straits Times. https://www.nst.com.my/news/nation/2020/01/560946/make-sure-immune-system-strong-and-fit-fight

How to Boost Your Immune System to Help Avoid Coronavirus COVID-19. Alexandria Living. https://alexandrialivingmagazine.com/health-wellness/how-to-boost-immune-system-coronavirus-2020/

Play Good Defense With These 66 Ways to Boost Your Immune System During Flu Season. Parade. https://parade.com/992175/marysauer/how-to-boost-immune-system/

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Stronger Immune Systems Fight The Risk Of Infection - Longevity LIVE

I dont know about you but Im getting Coronavirus fatigue.

Like all news cycles, I feel like its run its course of being front page headline fodder. The glaring example of that was yesterdays No new cases headline. We are now reporting that there is nothing to report.

One of the key things Ive learned throughout all this is that not living in fear and instead working to support our immune systems is a very good idea. It sure beats the alternative, which is to panic.

Being proactive about being preventative applies to all healthcare, but we so often focus on the fixes at the bottom of the cliff, instead of dealing to it at the top. Yes, we should wash hands and clean communal surfaces, but also, we should be boosting our immune systems so the chances of us getting anything at all are reduced.

So how do we do that?

Well, according to what Ive read, by reducing stress (that includes reducing how much youre stressing about Coronavirus), by getting good sleep, by eating well, by regularly exercising - all the things we know we should do, but often forget to.

By reducing our consumption of social media, by acknowledging that not everything we read needs to be alarmist and taken at face value.

But also, did you know you can even boost your immune system by just being positive? Easier said than done a lot of the time, but still, its worth a shot.

I also think it benefits our kids too, who have enough to worry and be anxious about with global warming, the ice caps melting and everything else theyre taught to be afraid of. I dont know that parents panic buying toilet paper and donning face masks is the most reassuring thing for kids to see. Especially when its not necessary.

I was at the supermarket with my daughter yesterday and we saw about three people with face masks on while we were there. She asked me if they had Coronavirus, I told her probably not, but perhaps they just dont want it and theyre being extra careful.

She asked if we should have masks on. I said no. But you can see how panic leads to panic. I was panicking about the shopping itself, that if I saw toilet paper maybe I should snap it up because the panic buyers were making me panic that its running out!

My mother in law was up from Christchurch this weekend and she was bemused by it all, what she called a very Auckland thing. But its not just Auckland, there have been arrests and tasers and all out punch ups in Australia over panic buying, Tescos in the UK has had to start rationing, Italy went beserk emptying shelves, so were not alone.

But with our number of confirmed cases sitting globally speaking very low at five, I think its prudent we all take some positive action like trying to boost our immune systems, rather than fear-driven actions like panic buying hand sanitizer.

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Kate Hawkesby on coronavirus: We need to be proactive, not panicky - Newstalk ZB

Wayne W. Grody, Joshua L. Deignan, in Emery and Rimoin's Principles and Practice of Medical Genetics, 2013

This article is a revision of the previous edition article by Wayne W Grody, volume 1, pp 601626, 2007, Elsevier Ltd.

Molecular genetic testing has a unique range of indications, most of which are quite different from the uses of traditional clinical laboratory testing and even molecular biologic testing in other disease classes (e.g. infectious disease, cancer). The technical approaches as well as the psychosocial and ethical implications of molecular genetic tests may vary substantially depending on the reason for testing (e.g. diagnostic, carrier screening). Just as many of the applications are unique, so too the types of patient samples collected for molecular genetic testing may be different from those obtained for other types of clinical laboratory testing. In addition, the choice of technique will depend on the nature of the disease gene being studied (especially its size and mutational heterogeneity), the purpose of the test, and to some extent the condition of the specimen, and examples of specific conditions are discussed. Finally, high complexity laboratories performing molecular genetic testing need to be aware of the specific regulatory considerations involved.

Originally posted here:
Molecular Genetics - an overview | ScienceDirect Topics

Dr. Adrian R. Krainer, pioneer in neuromuscular disease treatment to be honored at June 8 symposium in New York City

The Feinstein Institutes for Medical Research has selected Adrian R. Krainer, PhD, St. Giles Foundation Professor at Cold Spring Harbor Laboratory, as the eighth awardee of the Ross Prize in Molecular Medicine. The prize is awarded annually through the Feinstein Institutes peer-reviewed, open-access journal, Molecular Medicine, and includes a $50,000 award that will be presented to Dr. Krainer on June 8 at the New York Academy of Sciences (NYAS) in Manhattan.

This press release features multimedia. View the full release here: https://www.businesswire.com/news/home/20200302005570/en/

Dr. Adrian R. Krainer (Credit: Cold Spring Harbor Laboratory)

The Ross Prize is made possible by the generosity of Feinstein Institutes board members Robin and Jack Ross. It is awarded to scientists who have made a demonstrable impact in the understanding of human disease pathogenesis and/or treatment and who hold significant promise for making even greater contributions to the general field of molecular medicine. Dr. Krainer is being recognized for his pioneering work in introducing antisense therapy in clinical use, and for its successful application to spinal muscular atrophy.

Dr. Krainer studies the mechanisms of RNA splicing, ways in which they go awry in disease, and the means by which faulty splicing can be corrected. Dr. Krainers research is focused in part on genes associated with spinal muscular atrophy (SMA), a neuromuscular disease that has been the leading genetic cause of death in infants. He worked on antisense approaches to correct mis-splicing, and in collaboration with Ionis Pharmaceuticals and Biogen, developed the first treatment for pediatric and adult SMA.

"I am very grateful and honored to receive this years Ross Prize," said Dr. Krainer. "My trainees and I feel privileged that our research has helped SMA patients. In keeping with the intent of this generous award, we will redouble our efforts to explore new ways to address unmet medical needs."

After a brief award presentation, a symposium will be held during which Dr. Krainer will discuss his research along with Michelle Hastings, PhD, director at Rosalind Franklin University of Medicine and Science, Edward Kaye, MD, CEO of Stoke Therapeutics, and Timothy Yu, MD, PhD, attending physician and assistant professor at Boston Childrens Hospital, who will discuss their latest research.

"Dr. Krainers remarkable discoveries have revolutionized the treatment of a devastating, crippling pediatric illness. His inventions are already giving children the ability to crawl, walk, and live their lives," said Kevin J. Tracey, MD, president and CEO of the Feinstein Institutes and editor emeritus of Molecular Medicine.

Dr. Krainer and his lab have also worked to shed light on the role of splicing proteins in cancer, particularly breast cancer, and on fundamental mechanisms of splicing and its regulation.

Past recipients of the Ross Prize are: Daniel Kastner, MD, PhD, the National Institutes of Healths (NIH) National Human Genome Research Institute (NHGRI) scientific director; Huda Y. Zoghbi, MD, professor, Departments of Pediatrics, Molecular and Human Genetics, Neurology and Neuroscience at Baylor College of Medicine; Jeffrey V. Ravetch, MD, PhD, the Theresa and Eugene M. Lang Professor and head of the Leonard Wagner Laboratory of Molecular Genetics and Immunology at The Rockefeller University; Charles N. Serhan, PhD, DSc, director of the Center for Experimental Therapeutics and Reperfusion Injury at Brigham and Womens Hospital, the Simon Gelman Professor of Anaesthesia at Harvard Medical School and professor at Harvard School of Dental Medicine; Lewis C. Cantley, PhD, the Meyer Director of the Sandra and Edward Meyer Cancer Center at Weill Cornell Medical College and New York-Presbyterian Hospital; John J. OShea, MD, scientific director at the National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS); and Dan R. Littman, MD, PhD, the Helen L. and Martin S. Kimmel Professor of Molecular Immunology in the Skirball Institute of Biomolecular Medicine at New York University School of Medicine.

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To learn more about the Ross Prize celebration and symposium, and to register for the event, please visit http://www.nyas.org/RossPrize2020. If you would like to nominate a candidate for the 2021 Ross Prize, please make a submission here.

About the Feinstein Institutes

The Feinstein Institutes for Medical Research is the research arm of Northwell Health, the largest health care provider and private employer in New York State. Home to 50 research labs, 2,500 clinical research studies and 5,000 researchers and staff, the Feinstein Institutes raises the standard of medical innovation through its five institutes of behavioral science, bioelectronic medicine, cancer, health innovations and outcomes, and molecular medicine. We make breakthroughs in genetics, oncology, brain research, mental health, autoimmunity, and are the global scientific leader in bioelectronic medicine a new field of science that has the potential to revolutionize medicine. For more information about how we produce knowledge to cure disease, visit feinstein.northwell.edu.

About Molecular Medicine

Molecular Medicine sits at the forefront of its field, rapidly disseminating discovery in the genetic, molecular, and cellular basis of physiology and disease across a broad range of specialties. With over two decades of experience publishing to a multidisciplinary audience, and continually celebrating innovation through the Ross Prize in Molecular Medicine and Anthony Cerami Award in Translational Medicine, the journal strives towards the design of better molecular tools for disease diagnosis, treatment, and prevention. Molecular Medicine is published by BMC, part of Springer/Nature, in partnership with The Feinstein Institutes for Medical Research.

About the New York Academy of Sciences

The New York Academy of Sciences is an independent, not-for-profit organization that since 1817 has been committed to advancing science, technology, and society worldwide. With more than 20,000 members in 100 countries around the world, the Academy is creating a global community of science for the benefit of humanity. The Academy's core mission is to advance scientific knowledge, positively impact the major global challenges of society with science-based solutions, and increase the number of scientifically informed individuals in society at large. Please visit us online at http://www.nyas.org.

About Cold Spring Harbor Laboratory

Founded in 1890, Cold Spring Harbor Laboratory (CSHL) has shaped contemporary biomedical research and education with programs in cancer, neuroscience, plant biology and quantitative biology. CSHL has been a National Cancer Institute designated Cancer Center since 1987. Home to eight Nobel Prize winners, the private, not-for-profit Laboratory employs 1,100 people, including 600 scientists, students and technicians. The Meetings & Courses Program annually hosts more than 12,000 scientists. The Laboratorys education arm also includes an academic publishing house, a graduate school and the DNA Learning Center with programs for middle and high school students and teachers. For more information, visit http://www.cshl.edu

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Ross Prize Awarded to Cold Spring Harbor Laboratory Professor - Yahoo Finance

Society neglecting needs of people with rare diseases, AKU moot told

Policymakers and stakeholders must pay greater attention to the challenges posed by rare diseases in Pakistan, said experts at a conference to mark Rare Disease Day 2020 at the Aga Khan University.

Worldwide, there are over 6,000 diseases classified as rare as they affect fewer than one in 2,000 people. In Pakistan, these diseases are not so rare because a major risk factor is prevalent: inter-family marriages which significantly raise the risk of their children suffering from genetic defects and disorders.

According to a press release issued by the AKU on Friday,

Dr Bushra Afroze, associate professor at the AKU and a clinical geneticist at the universitys teaching hospital, shared the story of Sadia Manzoor*, a girl from a small town in Sindh, to explain how the health care systems shortcomings were affecting those living with rare diseases.

Sadia was eight when the unusual symptoms started to appear. She began to lose her hair, fall over while walking, be inattentive in class and face difficulties in writing. As her problems appeared to be neurological, she was taken to a neurologist and erroneously diagnosed with a non-treatable disorder, preventing her from receiving timely treatment. When she started to experience additional symptoms such as the tendency to repeat words, she was thought to be crazy -- leading to more distress for her and her family.

Thankfully, her parents continued to feel that something was wrong and to search for help. They were finally referred to one of the countrys few genetics specialists in Karachi to learn that their daughter has remethylation defect in vitamin B12, a serious metabolic disorder. Sadia was prescribed disease-specific orphan drugs medication for a condition so rare that it is not feasible to mass produce that are very expensive. Such drugs have to be imported and are often in short supply, which in turn represents an emergency with potentially fatal consequences for Sadias family.

Sadia must have medication daily and will require continual monitoring and management of her condition. Her parents are very focused on helping her live as normal a life as possible with the result that Sadia is a happy child, attending school and enjoying her childhood.

Dr Afroze explained that providing quality care to children such as Sadia requires high-quality system-wide changes that can address several constraints: a lack of awareness; shortage of facilities, expertise and institutions as well as the geographic and economic inequities that people with rare diseases face. She quoted The Lancet Global Health Commission on High Quality Health Systems in the SDG Era 2018 report which stated that providing health services without guaranteeing a minimum level of quality was ineffective, wasteful and unethical.

Currently, there is a range of gaps in the arrangements to provide quality care for patients suffering from rare diseases. Narrowing these gaps will require collaboration between stakeholders across the spheres of research, healthcare, academia and government.

Quality is not a given, Dr Afroze said. Ensuring quality treatment for rare diseases will take vision, planning, investment, compassion, meticulous execution, and rigorous monitoring, from the national level to the smallest, remotest clinic.

As a first step, experts at the conference highlighted the importance of screening newborns for rare diseases. A simple blood test compulsory in China, Canada, the US, as well many countries in Asia and Europe can enable the prompt detection and treatment of such conditions. AKUs Professor Aysha Habib, chair of the conference, explained that tests that can screen for over 50 rare illnesses have been common in the developing world for over 50 years. In Pakistan less than one per cent of newborns are currently being screened for these diseases, since only a handful of private hospitals offer these services, and for a narrow range of just five rare diseases.

She added that more hospitals need to offer screening for rare diseases and called on the government to consider how such services could be scaled up through the public health insurance measures being introduced under the governments Ehsaas programme.

Speakers at the conference also spoke of the role of researchers in the field. At present, there are no national level studies or surveys on the prevalence of rare diseases. While there are a small number of patient registries for specific rare diseases, they exist in silos within hospitals. Data sharing between hospitals would not only enhance the accuracy of information (since a single patient travels to multiple doctors and could be recorded more than once) but would also help form a roster of patients that would enable treatment options to be explored through clinical trials. Efforts by the federal health ministry are also needed to support and streamline registries, speakers added.

Professor Habib noted that academics, clinicians and researchers need to create partnerships that would intensify the development of knowledge and skills in the field. She also highlighted the importance of patient advocacy groups in facilitating research and in fostering synergies between stakeholders.

Collaboration enables everyone to benefit from each others strengths, Professor Habib said. The challenge posed by rare diseases requires us to make the most of our existing resources while developing national and international partnerships that can meet the complex needs of those living with rare diseases that are currently being neglected.

The conference Reframe Rare in Pakistan: Breaking Silos and Bringing Synergies was preceded by two days of workshops that brought together genetic researchers, pathologists and child health specialists from public and private sector organisations across the country.

Other speakers at the event included Professor Shahid Mahmood Baig, head of Human Molecular Genetics at the National Institute for Biotechnology and Genetic Engineering and Professor Giancarlo La Marca, president of the Italian Society for Newborn Screening and Metabolic Diseases.

* The patients name has been changed to protect her identity.

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Society neglecting needs of people with rare diseases, AKU moot told - The News International

Sam Erickson followed his love of science to outer space one summer during an internship at NASA. He came away fascinated by seeing into deep space by interpreting interaction between matter and infrared radiation.

Now a full-fledged researcher at the University of Minnesotas College of Biological Sciences, the 25-year-old Alaska native is immersed in something far more earthly: killing carp. His fast-moving genetic engineering project is drawing attention from around the country as a potential tool to stop the spread of invasive carp.

I want to make a special fish, Erickson said in a recent interview at Gortner Laboratory in Falcon Heights.

In short, he plans to produce batches of male carp that would destroy the eggs of female carp during spawning season. The modified male fish would spray the eggs as if fertilizing them. But the seminal fluid thanks to DNA editing would instead cause the embryonic eggs to biologically self-destruct in a form of birth control that wouldnt affect other species nor create mutant carp in the wild.

His goal is to achieve the result in a controlled setting using common carp. From there, it will be up to federal regulators and fisheries biologists to decide whether to translate the technology to constrain reproduction of invasive carp in public waters.

What were developing is a tool, Erickson said. If we could make this work, it would be a total game-changer.

Supervised by University of Minnesota assistant professor Michael Smanski, Erickson recently received approval to accelerate his project by hiring a handful of undergraduate assistants. He also traveled last month to Springfield, Ill., to present his research plan to the 2020 Midwest Fish and Wildlife Conference.

Were pretty excited about where his project is at, said Nick Phelps, director of the Minnesota Aquatic Invasive Species Research Center at the U. Things are sure moving fast. Theres excitement and caution.

Ericksons research has received funding from Minnesotas Environment and Natural Resources Trust Fund. No breeding populations of invasive carp have been detected in Minnesota, but the Department of Natural Resources has confirmed several individual fish captures and the agency has worked to keep the voracious eaters from migrating upstream from the lower Mississippi River. Silver carp, bighead carp and other Asian carps pose a threat to rivers and lakes in the state because they would compete with native species for food and habitat.

Erickson views his birth control project as one possible piece in the universitys integrated Asian carp research approach to keep invasive carp out of state waters. Already the DNR has supported electric barriers and underwater sound and bubble deterrents at key migration points. Another Asian carp-control milestone was closing the Mississippi River lock at Upper St. Anthony Falls in Minneapolis in 2015.

Shooting star

Growing up in Anchorage, Erickson had never heard of Macalester College in St. Paul. But he visited the campus at the urging of a friend and felt like he fit in. He majored in chemistry and worked for a year at 3M in battery technology. But his interests tilted toward the natural world and how to better live in cooperation with nature, he said. Erickson met with Smanski about research opportunities at the university and was hired on the spot.

Smanski, one of the universitys top biological engineers, said carp is not an easy organism to work with and Erickson lacked experience in the field. But he hired the young researcher and assigned him to the carp birth control project because he seemed to have a rare blend of determination and intelligence.

I could tell right away when I was talking to him that he was like a shooting star, Smanski said. If you set a problem in front of him, he wont stop until he solves it Hes taken this farther than anyone else.

In two short years, Smanksi said, Erickson has mastered genetic engineering to the point that his research is starting to bear fruit.

With his new complement of research assistants, Erickson aims to clear his projects first major hurdle sometime this year. The challenge is to model his experiment in minnow-sized freshwater zebrafish. The full genetic code of zebrafish like common carp is already known.

Ericksons task is to make a small change to the DNA sequence of male zebrafish, kind of like inserting a DNA cassette into the fish, he said. During reproduction, the alteration will create lethal overexpression of genes in the embryonic eggs laid by females.

By analogy, Erickson said, the normal mating process is like a symphony with a single conductor turning on genes inside each embryo, Erickson said. But the DNA modification sends in a mess of conductors and the mixed signals destroy each embryo within 24 hours.

In the lab we have to make sure were causing the disruption with no off-target effects, he said. If we can do this in zebrafish, we hope to translate it. They are genetically similar to carp.

Ericksons upcoming experimentation with tank-dwelling live carp could be painfully slow because the fish only mate once a year. But hes working his way around that problem by altering lighting conditions and changing other stimuli in his lab to stagger when batches of fish are ready to reproduce.

The birth control process projected to be affordable for fisheries managers if it receives approval is already proven to work in yeast and insects. And Erickson said the same principles of molecular genetics have been used to create an altered, fast-growing version of Atlantic salmon approved for human consumption in the U.S.

Were not building a new carp from the bottom up but its kind of a whole new paradigm, so we have to get it done right, he said.

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Solution for a scourge? University of Minnesota scientist is progressing with carp-killer tool - Minneapolis Star Tribune

The quick sequencing of the SARS-CoV-2 genome and distribution of the data early on in the COVID-19 outbreak has enabled the development of a variety of assays to diagnose patients based on snippets of the viruss genetic code. But as the number of potential cases increases, and concerns rise about the possibility of a global pandemic, the pressure is on to enable even faster, more-accessible testing.

Current testing methods are considered accurate, but governments have restricted testing to central health agencies or a few accredited laboratories, limiting the ability to rapidly diagnose new cases, says epidemiologist and immunologist Michael Mina, the director of the pathology laboratory and molecular diagnostics at Brigham and Womens Hospital in Boston. These circumstances are driving a commercial race to develop new COVID-19 tests that can be deployed within hospitals and clinics to provide diagnostic answers in short order.

Globally, nearly 89,000 cases have now been reportedmore than 80,000 of these in Chinaalong with more than 3,000 deaths. The virus has been found in 64 countries, six of those in just the past day.

The full genome of the novel coronavirus was published on January 10 of this year, just weeks after the disease was first identified in Wuhan, China. A week later, a group of researchers led by German scientists released the first diagnostic protocol for COVID-19 using swabbed samples from a patients nose and throat; this PCR-based protocol has since been selected by the World Health Organization (WHO).

Not all countries have adopted the WHOs recommended diagnostic, including the US.

The assay was initially developed from genetic similarities between SARS-CoV-2 and its close relative SARS, and later refined using the SARS-CoV-2 genome data to target viral genes unique to the newly discovered virus. In particular, the test detects the presence of SARS-CoV-2s E gene, which codes for the envelope that surrounds the viral shell, and the gene for the enzyme RNA-dependent RNA polymerase.

Yvonne Doyle, the medical director and the director of health protection for Public Health England, tells The Scientist in an email that once a sample is received by a laboratory, it takes 2448 hours to get a result. Commenting on the tests accuracy, she says all the positive results to date in the United Kingdom, a total of 36 so far, have been confirmed with whole genome sequencing of the virus isolated from patient samples, and the analytical sensitivity of the tests in use is very high.

This approach also underpins COVID-19 laboratory testing in Australia, where 27 cases have so far been diagnosed, says medical virologist Dominic Dwyer, the director of public health pathology for NSW Health Pathology at Westmead Hospital in Sydney. We decided in the end to have a screening approach using the WHO primers that target the so-called E gene of the coronavirus, he says. If a screening test is positive, we then do some confirmatory testing which selects other targets of the virus genome.

The laboratory at Westmead Hospital also does a complete sequencing of every virus sample to look for possible new strains of SARS-CoV-2 and has shared some of those sequences in the international Global Initiative on Sharing All Influenza Data (GISAID) database for other researchers to study. The staff also cultures the virus and images it using electron microscopy. Thats not really a diagnostic test, but gives you some confirmation of what youre seeing in the laboratory, Dwyer says.

He adds that, so far, theres no suggestion of false positive findings, because every positive test has been confirmed with whole genome sequencing, viral culture, or electron microscopy. As for false negatives, he adds, it would be hard to know if any infected patients were mistakenly given the all-clear.

Not all countries have adopted the WHOs recommended diagnostic. The US Centers for Disease Control and Prevention (CDC), for instance, has developed its own assay that looks for three sequences in the N gene, which codes for the nucleocapsid phosphoprotein found in the viruss shell, also known as the capsid. The assay also contains primers for the RNA-dependent RNA polymerase gene. Dwyer says that the principles of testing are the same; its just the genetic targets that vary.

Mina says its not clear why the CDC chose to develop a different assay to that selected by the WHO and taken up by other countries. Was this actually based on superior knowledge that the CDC had, or was this more of an effort to just go our own route and have our own thing and feel good about developing our own test in the US versus the rest of the world? says Mina, who is also assistant professor of epidemiology at the Harvard School of Public Health. The CDC declined to respond to questions from The Scientist.

In the UK, testing for COVID-19 is being done by a range of accredited laboratories across the country. In the US, all laboratory testing for COVID-19 has until recently been done exclusively by the CDC. The turnaround time for a result has been 2472 hours. Mina argues that enabling hospitals to conduct their own on-site diagnostics could speed up the process. For instance, hospitals can generate flu results within an hour, Mina says, most commonly using assays that detect viral antigens. We spend a lot of money getting rapid turnaround tests in the hospital for flu, for example, because we have to know how to triage people.

The day or two or three that it takes to get COVID-19 results has had logistical ramifications for hospitals, Mina says. If we have a patient who we only suspect is positive, even if they are not positive, just the suspicion alone will lead us to have to find an isolation bed for them, he says.

There has been a move by the CDC to send out RT-PCR test kits to state health laboratories, says Molly Fleece, an infectious diseases physician at the University of Alabama at Birmingham. Hopefully, more laboratories around the country will be able to have access to these testing kits and be able to test specimens instead of having to send all the specimens to the CDC for testing, she says.

However, that plan hit a snag recently when one of the CDC kits reagents was found to be faulty. The agency has announced that the reagent is now being remanufactured.

There are now numerous companies working on commercial test kits in response to the rising diagnostic demands of the epidemic. Most are applying the same real-time PCR methods already in use, but others are taking a different approach. For instance, Mina and colleagues are trialling a diagnostic in partnership with Sherlock Biosciences, based in Cambridge, Massachusetts. The researchers are using CRISPR technology to tag the target SARS-CoV-2 sequences with a fluorescent probe.

Were not at that stage yet of rolling out the serology or antibody tests.

Dominic Dwyer,NSW Health Pathology at Westmead Hospital

In many ways its similar to real-time PCR but its just more sensitive and much more rapid, Mina says. Another CRISPR-based diagnostic protocol developed by researchers at the McGovern Institute at MIT uses paper strips to detect the presence of a target virus, and claims to take around one hour to deliver the result. It has not yet been tested on COVID-19 patient samples, and the institute has stressed the test still needs to be developed and validated for clinical use, for COVID-19 or any other viral disease. Meanwhile, Anglo-French biotech company Novacyte has announced the release of its real-time PCR diagnostic kit for COVID-19, which it says will deliver results in two hours.

A different diagnostics approach would be to devise blood tests for antibodies against the SARS-CoV-2 virus, a development that Mina says will be an important next step for monitoring the spread of the virus. Could we just start taking blood samples from people around the world and see how many people who had no symptoms or very minimal symptoms may have actually been exposed to this? Mina asks.

Dwyer says such approaches could help detect any false negatives that slip through the PCR-based protocols, but were not at that stage yet of rolling out the serology or antibody tests. Numerous groups are trying to isolate antibodies, some with more success than others. Researchers at Duke-NUS Medical School in Singapore have used antibody testing to demonstrate a link between two separate clusters of infections, and in patients who had cleared their symptoms at the time they were given the antibody test. Meanwhile, researchers in Taiwan are also working to identify a SARS-CoV-2 antibody that could be used for diagnostic testing, and they say such a test could deliver a result in a matter of minutes rather than hours.

Bianca Nogrady is a freelance science writer based in Sydney, Australia.

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How SARS-CoV-2 Tests Work and Whats Next in COVID-19 Diagnostics - The Scientist

When immunologist Dr. Wei Cao joined Baylor College of Medicine three-and-a-half years ago, her first project was to investigate how inflammation contributes to Alzheimers disease.

Alzheimers is the most common cause of dementia among older adults. The current understanding is that, in addition to having beta-amyloid plaques and tau protein tangles, the brains of patients with this condition have a marked inflammatory response, and that this inflammation might be more of a problem than protein aggregation itself, said Cao, associate professor of molecular and human genetics and the Huffington Center on Aging at Baylor.

Inflammation in Alzheimers disease involves the activation of two types of cells in the brain: the resident immune cells called microglia, and astrocytes, star-shaped cells that support neuronal functions. In addition, there are elevated levels of cytokines, molecules that are produced by immune cells to promote inflammation. But the question remained, how does chronic inflammation in brains with Alzheimers disease lead to neuronal dysfunction and the consequent neurodegeneration and dementia?

Amyloid plaques in the brains of people with Alzheimers disease have a heterogeneous composition; for instance, some may also contain sugars, lipids or nucleic acids. Previously, Cao and her colleagues found that amyloid fibrils with nucleic acids, but not those without them, triggered immune cells in the blood to produce type 1 interferon (IFN). IFN is a potent cytokine produced when immune cells sense nuclei acids, such as those that come from viral particles, in their environment. IFN triggers a beneficial inflammatory response that is the first line of defense against viral infections.

While it is best known for its ability to induce an antiviral state in cells, IFN is also involved in immune modulation and tissue damage associated with infectious, autoimmune and other conditions. But, until now, IFN has not been explicitly implicated in Alzheimers disease, Cao said.

In this project, we focused on what was going on in brains with Alzheimers disease, said Dr. Ethan R. Roy, a graduate student in the Graduate Program in Translational Biology and Molecular Medicine at Baylor while he was working on this project. We began by investigating whether microglia from the brain were able to respond to the amyloid/nucleic acid combination by producing IFN.

Roy looked at multiple Alzheimers mouse models in the lab of Dr. Hui Zheng, professor of molecular and human genetics and director of the Huffington Center on Aging, who also is co-principal investigator of the study. Roy found that almost all the animals brains in these models had plaques containing nucleic acids. The composition of these plaques had not been well characterized before, Roy said.

Interestingly, Cao, Roy and their colleagues found that the same mouse brains that had amyloid plaques with nucleic acids also showed a molecular signature mimicking an antiviral IFN response. Further experiments revealed that nucleic acids in the plaques activated brain microglia, which produced IFN that in turn triggered a cascade of inflammatory reactions that led to the loss of synapses, the junctions between neurons through which they communicate. Synapse loss is a key part of neurodegeneration and can lead to memory loss and eventually dementia.

It is well known that synapse loss is directly mediated by the complement system, which is part of the immune system. It comprises a group of proteins that work together to clear microbes and damaged cells, but it also is involved in inflammation.

Although we knew that complement activation triggered synapse loss, what we discovered was the chain of events that led to this outcome. The chain of events points to IFN-mediated pathways controlling complement activation, Cao said.

We were very excited to find that blocking the IFN-triggered cascade of reactions significantly dampened microglia activation and reduced synapse loss in our mouse models, further supporting the leading role of IFN in this process, Roy said.

This study provides a major advance in the understanding of a process that leads to neuronal damage, by connecting IFN, complement and synapse loss: IFN controls the expression of multiple components of the complement cascade and mediates synapse elimination in a complement-dependent manner.

The researchers looked into human brains with Alzheimers disease to see if they presented with characteristics that were similar to those they had observed in mouse models of the condition.

We found that human brains with Alzheimers disease have profound activation of the IFN pathway, suggesting that mechanisms similar to the one we found in mice may be involved in neuronal destruction in people with the disease, Roy said. Further studies need to be conducted to evaluate this hypothesis.

This is important because it would lead to a better understanding of how the disease occurs and suggest novel therapies for this incurable disease.

The accumulation of amyloid plaques in human brains is known to poorly correlate with the severity or duration of dementia. There are people without signs of dementia who harbor significant amounts of both amyloid plaques and tau tangles in their brains, but remarkably lack the robust microglial activation and inflammatory response that is associated with loss of synapses and neurons. On the other hand, the brains of people with dementia linked to Alzheimers disease present with amyloid plaques, tau tangles and inflammation that is involved in neurodegeneration.

Our findings in mouse models suggest that it is plausible that plaques that accumulate in Alzheimers disease patients and those in non-demented individuals differ in their content of nucleic acids. It is thus of great interest to examine more closely the molecular constituents of amyloid plaques in the brains of cognitively resilient individuals and compared them to those of Alzheimers disease cases, Cao said.

This work also may provide new insights into the aging brain. Other work has shown that IFN also seems to participate in the normal aging process of the brain. Cao, Roy and their colleagues think it is also worthwhile to further explore the possibility of modulating IFN activity in aging populations.

Interested in all the details of this study? Find them in the Journal of Clinical Investigation.

Other contributors to this work include Baiping Wang, Ying-wooi Wan, Gabriel Chiu, Allysa Cole, Zhuoran Yin, Nicholas E. Propson, Yin Xu, Joanna L. Jankowsky, Zhandong Liu, Virginia M.-Y. Lee, John Q. Trojanowski, Stephen D. Ginsberg, Oleg Butovsky and Hui Zheng. The authors are affiliated with one or more of the following institutions: Baylor College of Medicine; Harvard Medical School; University of Pennsylvania School of Medicine; Nathan Kline Institute, N.Y., and New York University Langone Medical Center.

The study was funded by NIH grants AG05758, AG032051, AG020670, AG054111, NS092515, AG051812 and AG054672. Further support was provided by the Robert A. and Rene E. Belfer Family Foundation, BrightFocus ADR A20183775, Cure Alzheimers Fund and TBMM T32 training grant (ST32GM088129).

By Ana Mara Rodrguez, Ph.D.

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Connecting interferon, neuroinflammation and synapse loss in Alzheimer's disease - Baylor College of Medicine News

Ever since the earliest reports of a pneumonia-like illness spreading within Hubei province in China, the resemblance to the SARS outbreak of 2002-2003 has been uncanny: probable origins in the wild-animal markets of China; an illness that in some people resembles the common cold or a flu, but in others leads to pneumonia-like symptoms that can cause respiratory failure; community transmission that often occurs undetected; super-spreader events; and reported vertical transmission in high-rises or other living spaces where the waste systems are improperly engineered or drain catch-basins are dry, allowing aerosolized particles to pass from one floor of a building to another (see The SARS Scare for an in-depth description of the epidemiology and virology of the SARS outbreak of 2002-2003 and the four independent zoonotic transmissions of 2003-2004).

UPDATED 3-04-2020 at 12:57p.m. See below.

At first, this latest outbreak was referred to as a novel coronavirus, then in the media as COVID-19 (formally, the name for the disease in an infected person who has become sick, a distinction analogous to that between a person who is HIV positive and one who has developed AIDS). Now that the virus has been characterized and its relationship to SARS firmly established, its designation is SARS-CoV-2severe acute respiratory syndrome coronavirus 2.

Will public-health measures be sufficient to contain its spread? How infectious is it? What is the incubation period? Is this a pandemic? What role does the immune-system response play in the progression of the disease? Which populations are most at risk? Can scientists develop a vaccine, and how quickly? These are some of the questions that scientists worldwide are asking, and that a collaboration among Harvard University and Chinese researchers will address as part of a $115-million research initiative funded by China Evergrande Group, which has previously supported Universitygreen-buildings research at the Graduate School of Design, research onimmunologic diseases, and work inmathematics. (See below for the University press release describing the initiative.)

Harvard Magazinespoke with some of the researchers involved in fighting the first SARS outbreak, and those who will be collaborating with Chinese colleagues, in what is already a worldwide effort to control SARS-CoV-2.

Michael Farzan 82, Ph.D. 97, who in 2002 was an assistant professor of microbiology and molecular genetics at Harvard Medical School (HMS) studying the mechanism that viruses use to enter cells, was the first person to identify the receptor that SARS used to bind and infect human cells. SARS-CoV-2 is a close cousin to SARS, and uses the same human receptor, ACE2, reports Farzan, who is now co-chair of the department of immunology and microbiology at Scripps Research. The ACE2 receptor is expressed almost exclusively in the lungs, gastrointestinal tract, and the kidneys, which explains why the disease is so effectively transmitted via both the respiratory and fecal-oral routes.

But there are subtle differences in the new virus behind the current outbreak, he explained in an interview. The viruss receptor binding domainthe part that attaches to the human receptorhas undergone a lot of what we call positive selection, meaning there has been a good deal of evolutionary pressure on that region from natural antibodies, probably in bats or some other animal host that is a reservoir for this disease. So while the virus retains its ability to bind ACE2, Farzan explains, it no longer binds the same antibodies. That is unfortunate, because as the first SARS epidemic wound down, HMS professor of medicine Wayne Marasco had identified a single antibodyfrom what was then a 27-billion antibody librarythat blocked the virus from entering human cells. (Marasco is actively testing new antibodies, hoping to find one that will have the same effect on SARS-CoV-2. For more on Marascos work, see below.) Still, we are not starting from square one, says Farzan.

In animal studies,Remdesivir [a new and experimental antiviral drug] has seemed to work against SARS-like viruses, he says. Its effectiveness will probably hinge on getting it early enough, in the same way that the antiviral drug Tamifluis most effective against the seasonal flu when given to patients early in the course of infection.

And there is a reasonable hope that a vaccine canbe developed, Farzan adds, because the part of the virus that binds the human receptor is exposed and accessible, making it vulnerable to the immune systems antibodies. In addition, the viral genome is relatively stable. That means SARS CoV-2 wont evolve much over the course of an epidemic, so a vaccine that is relatively protective at the beginning of an epidemic will remain effective until its end.

Another reason for optimismdespite the long road to deploying any vaccine in humansis that the science that allows researchers to understand the viruss structure, life cycle, and vulnerabilities is progressing far more rapidly today than during the first SARS outbreak 17 years ago. So, too, is the understanding of the human immune response to the virus, and of the most effective public-health strategies based on the epidemiology of the disease.

When epidemiologists assess the severity of an epidemic, they want to know how effectively the disease can propagate in a population. The first measure they attempt to calculate is the reproductive number (R0)the number of people that an infected individual will in turn infect in an unexposed population, in the absence of interventions. When the reproductive number is greater than 1 (meaning each infected person in turn infects more than one other person), more and more people become infected, and an epidemic begins. Public-health interventions are therefore designed to lower the rate of transmission below 1, which eventually causes the epidemic to wind down. The second number epidemiologists focus on is the serial intervalhow long it takes one infected person at a particular stage of the disease to infect another person to the point of the same stage of the disease. The serial interval thus suggests how rapidly the disease can spread, which in turn determines whether public-health officials can identify and quarantine all known contacts of an infected individual to prevent their retransmitting the disease to others.

Epidemiologist Marc Lipsitch will be one of several Harvard scientists collaborating with Chinese colleagues to fight SARS-CoV-2Photograph by Kent Dayton

Marc Lipsitch, a professor of epidemiology at the Harvard Chan School of Public Health (HSPH), and director of the schoolsCenter for Communicable Disease Dynamics, helped lead one of the two teams that first calculated the reproductive number of SARS in the 2002-2003 outbreak. SARS had an R0 of 3, he recalls: each case led to three others. In that outbreak, about 10 percent of those who became sick died. The good news is that SARS CoV-2 appears to have a much lower R0 than SARS, ranging from the high ones to low twos, and only 1 percent to 2 percent of those who become sick have died. On the other hand, the serial intervalstill being worked outappears to be shorter, meaning the new virus has the potential to spread faster.

In the current epidemic, Lipsitch notes a further concern: the fact that the incubation-period distribution and the serial-interval distribution are almost identical. Thats a mathematical way of saying that people can start transmitting the virus even when they are pre-symptomatic, or just beginning to exhibit symptoms. That makes tracing and quarantining contacts of infected individualsa classic, frontline public-health measurenearly impossible.

Tracing, quarantining, and other public-health interventions, such as distancing measures (closing workplaces or asking employees to work from home, for example) proved sufficient to defeat SARS in the early 2000s. But with SARS-CoV-2, public-health measures alone may prove inadequate. Controlling this version of SARS may require antivirals, stopgap antibody therapies, and ultimately, vaccines, deployedtogetherwith robust public-health containment strategies.

Unfortunately, SARS-CoV-2 is almost certainly already a pandemic, Lipsitch continues: demonstrating sustained transmission in multiple locations that will eventually reach most, if not all places on the globe. The disease appears to be transmitting pretty effectively, probably in Korea, probably in Japan, and probably in Iran. He now estimates that 20 to 60 percent [figures updated 03-04-2020 at 12:57 p.m.]of the adult global population will eventually become infected.

That said, Infected is different from sick, he is careful to point out. Only some of those people who become infected will become sick. As noted above, only about 1 percent to 2 percent of those who have becomesickthus far have died, he says. But the number of people who areinfectedmay be far greater than the number of those who are sick. In a way, he says, thats really good news. Because if every person who had the disease was also sick, then that would imply gigantic numbers of deaths from the disease.

I'm very gratified, Lipsitch continues, to see that both China and Harvard recognize the complementarity between public health and epidemiology on the one hand, and countermeasure-development on the other hand. We can help target the use of scarce countermeasures [such as antivirals or experimental vaccines] better if we understand the epidemiology; and we will understand the epidemiology better if we have good diagnostics, which is one of the things being developed in this proposal. These approaches are truly complementary.

In the short term, Lipsitchwho has sought to expand the modeling activities of the Center for Communicable Disease Dynamics to better understand the current outbreaks epidemiologysays, It would be great toexpand collaborations with Chinese experts. Longer term, I see a really good opportunity for developing new methods for analyzing data better, as we have in previous epidemics. After the first SARS outbreak, for example, epidemiologists developed software for calculating the reproductive number of novel diseases; that software now runs on the desktop computers of epidemiologists around the world. And in 2009, during an outbreak of swine flu in Mexico, Lipsitch and others developed a method for using the incidence of the disease among awell-documented cohort of travelerswho had left Mexico, to estimate the extent of the disease among amuch larger and less well surveyedpopulation of Mexican residents.

What they found then was that the estimated number of cases in Mexican residents likely exceeded the number of confirmed cases by two to three orders of magnitude. The same method is being used to assess the extent of SARS-CoV-2 in China right nowso far without any hiccups. In the Mexican case, Lipsitchreports, the estimates suggested that severe cases of the disease were uncommon, since thetotal numberof cases was likely much larger than the number ofconfirmedcases. So I think we have learned from each epidemic how to do more things. And in between them, you solidify that less visible, less high-profile research that builds the foundation for doing better the next time. His group, for example, has been developing ways to make vaccine trials faster and better once a vaccine candidate exists.

A vaccine is the best long-term hope for controlling a disease like SARS-CoV-2. Higgins professor of microbiology and molecular genetics David Knipe, who like Lipsitch will participate in the newly announced collaboration, works on vaccine delivery from a molecular perspective. Knipe has developed methods to use the herpes simplex virus (HSV) as a vaccine vector and has even made HSV recombinants that express the SARS spike proteinthe part of the virus that binds the human ACE2 receptor. He now seeks to make HSV recombinants that express the new coronavirus spike protein as a potential vaccine vector.

But Knipe also studies the initial host-cell response to virus infection, which is sometimes called the innate immune response. And he has used HSV vectors that expressed the first SARS spike protein to study how it activates innate immune signaling. That is important because inSARS 1, initial symptoms lasted about a week, but it was the second phasecharacterized by a massive immune-system response that began to damage lung tissuethat led to low levels of oxygen saturation in the blood, and even death.The inflammation in the lungs is basically a cytokine storm, an overwhelming and destructive immune response thats the result of innate signaling, Knipe explains. So were going to look at that with the new coronavirus spike protein, as well. This could help to determine the actual mechanism of inflammation, and then we can screen for inhibitors of that that might be able to alleviate the disease symptoms.

The idea, he says, is to stop theinflammatoryresponse now killing people in the respiratory phase of the disease by targeting the specific molecular interaction between the virus and the host cell. This, he explains, aligns with one of the principal initial goals of the collaboration, which is to support research both in China and at Harvard to address the acute medical needs of infected individuals during the current crisis.

Another form of frontline defense against the virus is antibody therapy. In an epidemic, this type of therapy is usually administered as a prophylaxis to first responders at high risk of infection, or as treatment to patients who are already sick or to people who might be harmed by a vaccine, such as pregnant women, the elderly, or those with co-morbidities. Wayne Marasco, an HMS professor with a lab at the Dana Farber Cancer Institute, was the first to develop antibody therapies against SARS and MERS, a related coronavirus, in 2014. What he learned in those outbreaks was that using only a single antibody to bind the viruss receptor binding domainthe part of the virus that attaches to the human receptoris not enough to prevent escape through mutations that neutralize the therapy. You have to use combinations of antibodies to block the escape pathways, he explains. But the combinations have to be carefully designed to avoid the risk that the virus will evolve a gain of functionor the virus coming out of the patient is more pathogenic than the virus you started to treat.

During the MERS outbreak, Marasco led the Defense Advanced Research Projects Agencys 7-Day Biodefense program.DARPA would drop an unknown pathogen off at our doorstep, Marasco says, and we had seven days to develop a therapeutic that could be manufactured at scale. A second DARPA-funded project focused on reducing the cost of therapies to less than $10 a dose. The government has made efforts to streamline that process to get the production sped up and the cost decreased, he notes, although the efforts are independent of regulatory approval, which has a life of its own.

Marasco currently collaborates with an international team that can perform studiesincluding some that cant be done at Harvardthanks to ready access to a Biosafety Level 4 laboratory and to non-human primates for testing. The team is working to develop antibody therapies effective against SARS-CoV-2, but Marasco cautions that the situation is pretty worrisome with a disease that has a long latency period when people show no symptoms, and when public-health officials cannot identify source cases (as in Italy and in the single case of apparent community transmission in California reported February 26).

The problem in getting ahead of this now, he continues, is funding. Government resources are generally a redistribution of funds that have previously been granted to projects such as the Ebola outbreak in West Africa, or come as administrative supplements to preexisting grants. But with the pace of this epidemic, a lack of resources is limiting what can get done and how quickly it can be accomplished. Beyond the creation of therapeutics, there are all kinds of epidemiologic considerations that require rapid funding, from investigating modes of transmission to field testing for infection.

In the near term, the way to treat masses of patients, he says, is to take blood plasma from someone who has recovered and administer it to an infected person. The convalescents antibodies then fight the infection. The FDA would never approve it, he notes, but it does work. Ultimately, the treatment of choiceand the most cost-effective approach, he says, will be a vaccine.

In the last days of 2019 and the first days after the New Year, we started hearing about a pneumonia-like illness in China, says Dan Barouch, an HMS professor of medicine and of immunology known for his anti-HIV work, whose lab has developed a platform for rapid vaccine development. (During the Zika virus outbreak of 2016, for example, his group was the first to report, within a month, a vaccine protective in animal models.) When the genome of the virus was released on Friday, January 10, we started reviewing the sequence that same evening, working through the weekend. By Monday morning, we were ready to grow it.

His concern about this latest outbreak was that the rate of spread seemed to be very rapid. In addition, the outbreak had the clinical features of an epidemic. We reasoned that this might make it difficult to control solely by public-health measures, he says, particularly because the virus can be transmitted by asymptomatic individuals. Thus, if the epidemic is still spreading toward the end of this year or early 2021, by which point a vaccine might be available, Barouch explains, such a remedy could prove essential. Historically, when viral epidemics don't self-attenuate, the best method of control is a vaccine.

Although Barouchs Beth Israel Deaconess Medical Center lab is working on DNA and RNA vaccines, a new technology that has the potential to cut vaccine development times in half, large-scale manufacturing using so-called nucleotide vaccines is unproven. That's why I think there needs to be multiple parallel vaccine efforts, he emphasizes. Ultimately, we don't know which one will be the fastest and most protective. At the moment, he reports, there are at least a half dozen scientifically distinct vaccine platforms that are being developed and he believes that vaccine development for this pathogen will probably go faster than for any other vaccine target in human history.

Ever since I graduated from medical school, he points out, there have been new emerging or re-emerging infectious disease outbreaks of global significance with a surprising and disturbing sense of regularity. There is Ebola. There was Zika. There were SARS, MERS; the list keeps growing. With climate change, increasing globalization, increasing travel, and population shifts, the expectation is that epidemics will not go away, and might even become more frequent.

In this global context, Barouch emphasizes the importance of a collaborative response that involves governments, physicians, scientists in academiaandin industry, and public-health officials. It has to be a coordinated approach, he says. No one group can do everything. But I do think that the world has a greater sense of readiness this time to develop knowledge, drugs, and therapeutics very rapidly. The scientific knowledge that will be gained from the vaccine efforts [will] be hugely valuable in the biomedical research field, against future outbreaks, and in the development of a vaccine to terminate this epidemic.

University provost Alan Garber, a physician himself, adds that Global crises of such magnitude demand scientific and humanitarian collaborations across borders. Harvard and other institutions in the Boston area conduct research on diagnostics, virology, vaccine and therapeutics development, immunology, epidemiology, and many other areas.With its tremendous range of expertise and experience, our community can be an important resource for any effort to address a major global infectious disease outbreak. Our scientists and clinicians feel an obligation to be part of a promising collaboration to overcome the worldwide humanitarian crisis posed by this novel virus.

UPDATED 3-03-2020 AT 12:10 p.m.TO INCLUDE A REPORT FROM THE MEETING WITH CHINESE COLLEAGUES

In a closed-door meeting that took place Monday, March 2, 2020, at Harvard Medical School, nearly 80 Boston-area scientists gathered to discuss with colleagues from China participating via video link how to respond to COVID-19 disease and the SARS-CoV-2 virus that causes it. This was the first meeting to take place as a result of the collaboration with scientists at theGuangzhou Institute of Respiratory Health announced on Monday, February 24.In attendance locally were experts from Harvard Medical School (HMS), the Harvard T.H. Chan School of Public Health, the HMS-affiliated hospitals, the Ragon Institute, Boston University, the Broad Institute, MIT, the Wyss Institute, as well as representatives from industry. The workshop, convened by HMS dean George Q. Daley, was a planning session to map out the process for coordinating on collaborative projects, designed to allow the participants to meet, form working groups by research area, and determine next steps.

The collaboration harnesses the strengths of the Boston scientific and biomedical ecosystem, the events organizers said in a statement, with the critical experience of Chinese scientists, who are providing on-the-ground insight into diagnostics and care for patients on the frontlines.

This public health crisis, they continued, is an opportunity to catalyze an unprecedented level of collaboration among various scientific efforts across Boston and Cambridge to address both the acute, most pressing challenges of this particular epidemic but also to establish a framework for future collaborations and create a more nimble rapid-response system for other epidemics.

The meeting was organized according to areas of research interest, need, and opportunity including:

The meeting demonstrated the need to establish a collaborative regional response capacity, not only for this outbreak, but for other future emerging infectious diseases, said the organizers. They are now working to create an organizational structure that will formalize the working groups in each of the above areas, and allow for the optimal deployment of resources including disciplinary and clinical expertise, shared core facilities, and funding.

The official Harvard press release follows:

Harvard University Scientists to Collaborate with Chinese Researcherson Development of Novel Coronavirus Therapies, Improved Diagnostics

At a glance:

Since its identification in December, the novel coronavirus has quickly evolved into a global threat, taking a toll on human health, overwhelming vulnerable health care systems and destabilizing economies worldwide.

To address these challenges, Harvard University scientists will join forces with colleagues from China on a quest to develop therapies that would prevent new infections and design treatments that would alleviate existing ones.

The U.S. efforts will be spearheaded by scientists at Harvard Medical School, led by DeanGeorge Q. Daley, working alongside colleagues from the Harvard T.H. Chan School of Public Health. Harvard Medical School will serve as the hub that brings together the expertise of basic scientists, translational investigators and clinical researchers working throughout the medical school and its affiliated hospitals and institutes, along with other regional institutions and biotech companies.

The Chinese efforts will be led by Guangzhou Institute of Respiratory Health and Zhong Nanshan, a renowned pulmonologist and epidemiologist. Zhong is also head of the Chinese 2019n-CoV Expert Taskforce and a member of the Chinese Academy of Engineering.

Through a five-year collaborative research initiative, Harvard University and Guangzhou Institute for Respiratory Health will share $115 million in research funding provided by China Evergrande Group, aFortuneGlobal 500 company in China.

We are confident that the collaboration of Harvard and Guangzhou Institute of Respiratory Health will contribute valuable discoveries to this worldwide effort, said Harvard University President Lawrence Bacow. We are grateful for Evergrandes leadership and generosity in facilitating this collaboration and for all the scientists and clinicians rising to the call of action in combating this emerging threat to global well-being.

Evergrande is honored to have the opportunity to contribute to the fight against this global public health threat, said Hui Ka Yan, chair of the China Evergrande Group. We thank all the scientists who responded so swiftly and enthusiastically from the Harvard community and are deeply moved by Harvard and Dr. Zhongs teams dedication and commitment to this humanitarian cause. We have the utmost confidence in this global collaborative team to reach impactful discoveries against the outbreak soon.

While formal details of the collaboration are being finalized, the overarching goal of the effort is to elucidate the basic biology of the virus and its behavior and to inform disease detection and therapeutic design. The main areas of investigation will include:

With the extraordinary scale and depth of relevant clinical and scientific capabilities in our community, Harvard Medical School is uniquely positioned to convene experts in virology, infectious disease, structural biology, pathology, vaccine development, epidemiology and public health to confront this rapidly evolving crisis, Daley said. Harnessing our science to tackle global health challenges is at the very heart of our mission as an institution dedicated to improving human health and well-being worldwide.

We are extremely encouraged by the generous gesture from Evergrande to coordinate and supportthe collaboration and by the overwhelmingly positive response from our Harvard colleagues, said Zhong, who in 2003 identified another novel pathogen, the severe acute respiratory syndrome (SARS) coronavirus and described the clinical course of the infection.

We look forward to leveraging each of our respective strengths to address the immediate and longer-term challenges and a fruitful collaboration to advance the global well-being of all people, Zhong added.

Harvard University ProvostAlan M. Garbersaid outbreaks of novel infections can move quickly, with a deadly effect.

This means the response needs to be global, rapid and driven by the best science. We believe that the partnershipwhich includes Harvard and its affiliated institutions, other regional and U.S.-based organizations and Chinese researchers and clinicians at the front linesoffers the hope that we will soon be able to contain the threat of this novel virus, Garber said. The lessons we learn from this outbreak should enable us to respond to infectious disease emergencies more quickly and effectively in the future.

Read the original here:
Harvard and Guangzhou Institute of Respiratory Health Team to Fight SARS-CoV-2 - Harvard Magazine

Close inspection: A neuronal tract that connects the brains hemispheres is absent or thinner in people with TBR1 mutations (bottom) than in controls (top).

People with mutations in a gene called TBR1 have unusual features in several brain regions, along with autism traits and developmental delay, according to a new study1.

TBR1 encodes a protein that is involved in brain development. It controls the expression of several other autism-linked genes that lay out the structure of the cerebral cortex, the brains outer layer and locus of higher cognition.

Studies in mice have suggested that deletion or mutation of TBR1 results in structural abnormalities in the brain2. The layers of the cerebral cortex in these mice may be disorganized, and connections in the amygdala a structure involved in processing emotions may be missing.

However, few studies have examined how TBR1 mutations affect people.

Mutations in the gene have been linked to intellectual disability and autism, but more subtle features have not been well documented, says lead investigator Sophie Nambot, a clinician who specializes in medical genetics at the Centre Hospitalier Universitaire Dijon Bourgogne in France.

Previous research documented about 13 people with TBR1 mutations, but the reports included minimal information about outward characteristics, and few include brain-scan data, Nambot says.

The new study adds 25 previously unreported individuals to the literature, along with detailed descriptions of their physical, neurological and genetic features. The findings were published in January in the European Journal of Human Genetics.

It greatly increases the number of individuals and types of mutations in the TBR1 gene that are associated with developmental disorders, says John Rubenstein, professor of psychiatry at the University of California, San Francisco, who was not involved in the study.

Nambots team identified people with TBR1 mutations by contacting national and international health networks, such as GeneMatcher and DECIPHER. They ultimately recruited 25 people, ranging in age from 2 to 29 years, at 22 sites.

Scientists at the centers gathered information about these individuals development and autism traits, such as communication difficulties, lack of eye contact and restricted interests.

All 25 have intellectual disability or moderate-to-severe developmental delays; 19 show autism traits.

The researchers also scanned the individuals genomes to identify small and large mutations in TBR1. Combining their data with those from previous studies, the team identified 29 different single-nucleotide variants.

Magnetic resonance images from seven of the people revealed previously unidentified structural differences in their brains, Nambot says. These differences are in the cerebral cortex; the anterior commissure, a neuronal tract that connects the two hemispheres of the brain; and the hippocampus, an area involved in learning and memory.

In two of the people, the ridges in the cerebral cortex are unusually broad and thick, and in three people, the hippocampus is malformed.

The hippocampal problems are very likely to affect learning and memory, says Robert Hevner, director of neuropathology at the University of California, San Diego. The findings may explain why people with TBR1 mutations have developmental delays, he says. They also support prior studies suggesting that TBR1 affects a type of cell that helps organize the cortex and the hippocampus during fetal development.

Notably, in all seven people, the anterior commissure is thin or absent.

Research in mice demonstrates a similar phenomenon, says Yi-Ping Hsueh, distinguished research fellow in neuroscience at the Institute of Molecular Biology in Taiwan, who was not involved in the new study. In 2014, Hsuehs team found the anterior commissure to be partially missing in mice lacking one copy of TBR1, resulting in social and cognitive problems2.

Unlike mouse studies, however, the new study does not quantify volume differences in brain structures, which makes it difficult to gauge what should be considered atypical, Hsueh says.

The researchers caution that their sample is small, especially given the range of TBR1 mutations present. Still, they say, their findings may help scientists classify genetic subtypes of autism.

Continue reading here:
Mutations in top autism gene linked to changes in brain structure - Spectrum