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A new study suggests immune responses to coronavirus in severely ill and critically ill patients are as strong or stronger than those of patients with milder illness. This adds to the evidence that the immune system itself is to blame for the most life-threatening form of the infection.

Immune cells known as T cells are responsible for recognizing pathogens, killing infected cells, and recruiting other branches of the immune system to combat infections.

However, according to the new study, T cell responses to the new coronavirus in critically ill patients appear to be just as robust as those with a less severe form of the illness.

The finding reinforces the conclusion that an inadequate immune response to SARS-CoV-2, the coronavirus that causes COVID-19, is not responsible for critical illness and death. Rather, an excessive immune response is to blame.

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The team of researchers, led by Marien Hospital Herne and Ruhr-Universitt Bochum in Herne, Germany, compared the T cell responses of 28 COVID-19 patients during the acute phase of the infection and after recovery in survivors.

Of these infections, 7 were categorized as moderate, 9 were severe, and 12 were critical.

The scientists measured the concentration of two T cell types in blood samples from each patient: helper T cells and killer or cytotoxic T cells.

They also analyzed the strength of these cells responses to three distinct parts of the virus: the three proteins that make up its spikes, its membrane, and the shell or nucleocapsid surrounding its nuclear material.

In addition, the team measured levels of cytokines immune signaling molecules that T cells produce to combat infection.

They found that in patients with critical illness, the scale of their immune responses was similar or even higher, compared with moderate or severe cases.

There were also no apparent associations between successful clearance of the virus or death and changes in T cell responses.

The total number of specific immune cells, as well as their functionality, was not better in patients who survived COVID-19 than in those who died from it, says Dr. Ulrik Stervbo, one of the authors.

The study features in the journal Cell Reports Medicine.

T cells migrate to a viral infection site, where they kill infected cells and select other parts of the immune system to neutralize the virus.

But these same T cells can also create a cytokine storm, which is responsible for a potentially fatal complication known as acute respiratory distress syndrome (ARDS).

Even though further studies will be necessary to understand the specific mechanism of COVID-19 development, our data suggest that excessive SARS-CoV-2-specific T cell response can cause [immune damage] leading to COVID-19-related lung failure, says lead author Prof. Nina Babel.

The new research adds to a growing body of evidence that excessive immune responses cause life-threatening COVID-19.

A major study published in June 2020 found that dexamethasone, a corticosteroid that suppresses the bodys immune response, saved the lives of around a third of all patients on ventilators over a 28-day period.

A more recent study, reported by Medical News Today, suggests that another kind of immune-suppressing drug, known as an interleukin-6 inhibitor, may help prevent severe COVID-19 infections from becoming life-threatening.

The authors of the new study acknowledge some limitations of their research.

They do not know exactly when patients in their research contracted the virus. Therefore, the slightly higher T cell response in critically ill patients may simply result from a longer period of infection.

In addition, they were unable to analyze the entire range of T cell subtypes and the cytokines they produce. So, it is possible that they missed protective or detrimental immune effects that impacted non-critical and critical patients differently.

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Critically ill patients have robust immunity to new coronavirus - Medical News Today

This entry was posted on September 10, 2020 at 2:57 am and is filed under Immune System. You can follow any responses to this entry through the RSS 2.0 feed. Both comments and pings are currently closed. |