Antibodies and T cells are among the most important elements of the immune defense against viruses.
The antibodies prevent viruses from entering the host cell. They also mark the infected cells for other players in the immune system, which are able to kill the infected cells.
Virus-specific T cells, on the other hand, can kill infected cells directly and highly efficiently.
In a recent study from Ruhr-Universität Bochum (RUB) and elsewhere, researchers tested specific antibodies and T cells occurring in recovered, seriously ill, and deceased COVID-19 patients.
They found comparable immune reactions. They suggest that people may have severe COVID-19 despite or even due to the strong immunity.
The study is published in Cell Reports Medicine. One author is Nina Babel.
Previous studies have done an analysis of these cell-killing SARS-Cov-2 specific T cells in patients with COVID-19.
The studies showed the detection of such cells in patients recovered from COVID-19 suggesting their protective antiviral effect.
On the other hand, some studies showed that an excessive immune response might be the cause of severe COVID-19. The role of SARS-Cov-2 specific T-cells in this exaggerated immune response is unclear.
In this study, the research team analyzed immune responses in COVID-19 patients during the disease progress.
They found that a strong T-cell and antibody response could be detected not only in patients with mild COVID-19 patients who had recovered from the virus infection.
Similar or even stronger immunity to SARS-Cov-2 was found in patients who had been critically ill and who suffered COVID-19-related lung failure.
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.
There was also no difference in the strength and functionality of the immune response between patients who still suffered from and those who had cleared a SARS-Cov-2 infection.
These results show that excessive SARS-Cov-2-specific T cell response can cause immuno-pathogenesis leading to COVID-19-related lung failure.
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