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Too strong immune response to blame for severe COVID-19 course

The immune system of the body fights Viruses primarily with Antibodies and T lymphocytes. The antibodies bind to certain virus receptors and thus prevent the viruses from entering Cells can penetrate. At the same time, the infected cell is marked for other actors in the immune system so that they can kill the cell. Virus-specific T lymphocytes, on the other hand, can kill infected cells directly.

In studies that have been carried out in the past few weeks, these have been found to be cell killing SARS-Cov-2-specific T cells in patients with the by the novel Coronavirus induced disease Covid-19 analyzed. The results showed that such cells were mainly found in people who had survived Covid-19 disease. Scientists explain that this suggests that these cells have a protective antiviral effect. On the other hand, some studies would suggest that too strong an immune system response could be the cause of the severe Covid-19 courses. However, the role of the SARS-Cov-2-specific T cells in this excessive immune response is unclear.

The strength of the immune response is crucial

In contrast to previously assumed, the dreaded arises Lung failure In the case of severe courses of Covid-19, not because the immune response is too weak. On the contrary. An overreaction of the immune system seems to contribute to this lung failure. Researchers of the Marien-Hospital Herne and the virology of Ruhr-University Bochum (RUB) as well as the Infectious Diseases and Anesthesia Clinics and the Institute for Virology of University Medicine Essen have carried out extensive studies on this.

Under the direction of Prof. Dr. Nina Babel, head of the Center for Translational Medicine at the RUB-Klinikum Marien-Hospital Herne, the scientists have specific antibodies and T cells in the course of the Covid-19 disease, both in patients with a mild course of the disease, in those who are seriously ill and later deceased patient examined. They found that the immune responses were comparable.

In the study published in the journal Cell Reports Medicine was published, the researchers analyzed immune responses in patients in the course of Covid-19 disease. “We wanted to investigate the role of T cells and antibodies in controlling infection and disease,” explains Nina Babel. “The novelty of our study is that we have analyzed SARS-Cov-2-specific T cells and antibodies with regard to the course of the disease and virus clearance. We were able to determine that a strong T cell and antibody response was not only detectable in patients with a mild course of Covid-19 or after a virus infection was defeated. ” Patients with the most severe courses and lung failure caused by Covid-19 would have shown comparable or even stronger immunity to SARS-Cov-2.

Further studies needed

“During the course of the disease, the number of specific immune cells and their functionality were no better in patients who survived Covid-19 than in those who died from it,” says Dr. Ulrik Stervbo, laboratory manager at the Center for Translational Medicine. There was also no difference in the strength and functionality of the immune response between the patients with existing and survived SARS-Cov-2 infection.

“Although further studies are needed to understand the specific mechanism of Covid-19-associated lung failure, our data indicate that an excessive SARS-Cov-2-specific T-cell immune response triggers immunopathogenesis and thus makes it life-threatening Course leads ”, emphasizes study director Nina Babel. “The results of current studies on the successful use of immunosuppressive therapies for Covid-19 support this hypothesis”, summarizes Prof. Dr. Timm Westhoff, Director of the Medical Clinic I of the Marien Hospital in Herne.

Originalveröffentlichung:
Constantin J. Thieme, Moritz Anft et al.: A robust T cell immunity towards spike, membrane, and nucleocapsid SARS-CoV-2 proteins is not associated with recovery in critical COVID-19 patients, in: Cell Reports Medicine, 2020, DOI: 10.1016/j.xcrm.2020.100092: https://www.cell.com/cell-reports-medicine/fulltext/S2666-3791(20)30118-X

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