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Global Statistics

All countries
695,781,740
Confirmed
Updated on September 26, 2023 9:04 pm
All countries
627,110,498
Recovered
Updated on September 26, 2023 9:04 pm
All countries
6,919,573
Deaths
Updated on September 26, 2023 9:04 pm

Global Statistics

All countries
695,781,740
Confirmed
Updated on September 26, 2023 9:04 pm
All countries
627,110,498
Recovered
Updated on September 26, 2023 9:04 pm
All countries
6,919,573
Deaths
Updated on September 26, 2023 9:04 pm

Critically ill patients have robust immunity to new coronavirus

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live updates on the current COVID-19 outbreak and visit our coronavirus hub for more advice on prevention and treatment.

The team of researchers, led by Marien Hospital Herne and Ruhr-Universität 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 body’s 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.

For live updates on the latest developments regarding the novel coronavirus and COVID-19, click here.


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