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Covid-19: 10% of critically ill patients produce antibodies that boycott the immune response | Coronavirus

There are certainly other factors, but scientists seem to have found another reason that could explain why some patients with covid-19 show more severe symptoms of the disease. In an article published this week in the journal Science, a team of researchers claims to have found genetic variants associated with the production of a certain type of antibody that compromise the immune response to infection in 10% of critically ill patients. Another study in the same journal also shows that there are certain genetic changes linked to a specific molecule that may explain 3.5% of the most severe cases of covid-19.

In addition to factors that had previously been identified as being older and having associated pathologies, scientists have now realized that there are genetic changes that are shared by these patients with more severe manifestations and that appear to ‘boycott’ the disease. immune system response, further aggravating the condition of these people. “The clinical outcome after infection with SARS-CoV-2 varies from silent infection to fatal covid-19,” note the authors of one of the articles which identifies yet another risk factor for a severe manifestation of covid-19. One of the studies involved 659 patients with pneumonia and death from covid-19 and 534 asymptomatic patients and looked for mutations in genes that are associated with the immune system’s response to the influenza virus.

By testing some of the rare variants with 13 loci (fixed places on a chromosome where a particular gene or genetic marker is located), the scientists identified mutations in 23 patients (3.5%), aged 17 to 77 years. “We show that human fibroblasts with mutations that affect this pathway are vulnerable to SARS-CoV-2,” they write, concluding that these “innate immunity errors” may be “at the basis of covid pneumonia. -19 potentially fatal in patients without previous serious infection ”. The authors note that this genetic “defect” primarily affects men, which is surprising given that autoimmune diseases affect women more. THE

Another study published in the same journal by the same international consortium of scientists begins with the same warning about the different manifestations of the disease: “The inter-individual clinical variability during infection with SARS-CoV-2 is immense”, insist the researchers. In this case, the researchers report “that at least 101 of 987 patients with life-threatening covid-19 pneumonia” had some type of antibody that counteracts the effect of a molecule that functions to trigger an alert when the body is invaded by a virus ”.

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Furthermore, these specific antibodies were not found in 663 people with asymptomatic or mild SARS-CoV-2 infection and were only present in 4 of the 1,227 healthy people involved in this work. In the group of 101 patients, aged 25 to 87, who produce these antibodies which boycott the body’s defense, 95 were men. In other words, the authors note that this genetic “defect” primarily affects men, which is surprising given that autoimmune diseases affect women more.

“This discovery will change the treatment of some patients”, explains Carlos Rodríguez-Gallego, immunologist at the University Hospital of Gran Canaria Doutor Negrín and co-author of the studies, quoted in a press article by El País. The researcher also adds to the same journal as the team “He is already studying how to conduct clinical trials to identify patients who produce these antibodies and perhaps treat them with other types of antibodies to neutralize the problem.”

Of course, there may be many other “genetic defects” that may be associated with greater severity in the manifestation of covid-19. In fact, this is one of the main goals of the international COVID Human Genetic Effort consortium, which in addition to wanting to identify what may be failing in the response of patients at serious risk of this infection, also research the changes that seem to make certain individuals resistant to it. infection. In other words, seek to know our strengths and weaknesses in molecular, cellular and immunological mechanisms to fight more effectively against this virus.

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