Absence of Type I interferons has become a determinant of COVID-19 pneumonia. The absence of type I interferons in some COVID-19 patients may be due to genetic mutation or due to inactivation by auto-reactive antibodies.
The level of variance of COVID-19 symptoms in the population has driven researchers into studying these symptoms more in-depth. The findings of some of these studies shed light on why some people with COVID-19 develop severe disease and provide the reasons why more men than women die from COVID-19.
In a study of 1000 COVID-19 patients showing symptoms for lethal COVID-19 pneumonia, in more than 10 percent of the studied population the presence of auto-reactive antibodies that attack the immune system was confirmed, as opposed to the SARS-CoV-2 virus that causes the disease. Interestingly, a good number of these patients about 95% were men. Biochemical analysis conducted by experts revealed that auto-reactive antibodies inhibit the activity of type I interferon, a set of 17 proteins crucial for protection of cells and the body from viruses.
13 genes critical for the body’s immune defence against the virus were obtained from about 660 patients upon analysis rare genetic variations were found. Upto 3.5 percent or more of the people who developed COVID-19 pneumonia lacked a functioning gene and were unable to produce detectable type I interferons in response to infection with SARS-CoV-2.
Based on the research study, the absence of type I interferons appears to be a commonality among individuals who suffer from COVID-19 pneumonia.
The findings are the first published results from the COVID Human Genetic Effort. COVIDHGE is an international project consisting of more than 50 genetic sequencing hubs and hundreds of hospitals. The effort is co-led by Dr Helen Su, a senior investigator at the US National Institute of Allergy and Infectious Diseases (NIAID) and Dr Jean-Laurent Casanova, head of the St. Giles Laboratory of Human Genetics of Infectious Diseases at The Rockefeller University in New York, US.