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Antibodies that do not behave as they should, genetic mutations. These would be the causes of severe forms of Covid-19 in 10 and 3.5 percent of previously healthy patients, respectively. In both situations there would be reduced functionality of thetype I interferon, which is part of a large family of proteins called cytokines and is of great importance for the immune system. This was discovered by an investigation by Covid Human Genetic Effort (CovidHGE), an international consortium that involves more than 50 genetic sequencing centers and hundreds of hospitals and in which the Laboratory of Medical Genetics of the Tor Vergata University of Rome, the San Raffaele Institute of Milan and the Bambino Ges di Roma .
The results
The study was published in two articles in the journal Sciences and arises from the analysis of biological tissues of 987 seriously ill patients. The first publication explains that more than 10 percent of healthy people who develop severe forms of the disease have it. dysfunctional antibodies: they attack the immune system instead of the virus, preventing it from acting effectively against infection. The interferon in this case is neutralized by autoantibodies. The second article identifies 3.5 percent of seriously ill patients Genetic mutation predisposing, which causes a lower production of the key protein for the immune response to viruses.
The dysfunctions
The results convincingly suggest that type I interferon dysfunctions are often the cause of the most critical forms of Covid-19, explains Jean Laurent Casanova, director of the Human Genetics Laboratory of Infectious Diseases at Rockefeller University in New York and coordinator of both studies -. In theory at least, these are dysfunctions that can be treated with existing drugs and approaches.
The predisposition to serious forms.
Autoantibodies to interferon I are relatively rare in the general population: of 1,227 randomly selected healthy individuals, only four (0.33 percent) tested positive. Much less than 10 percent found in the critically ill sample. In most patients, positivity for these autoantibodies was detected in blood samples collected in the first days of infection. Researchers think that the antibodies were already present before contagion and, therefore, are a predisposing factor for severe forms. To confirm this hypothesis, its presence was also verified in the blood tubes collected in the days prior to infection.
Most affected patients
We believe that autoantibodies against interferon can explain a significant part of the most aggressive forms of Covid-19 and the way in which these forms are distributed in the general population, that is, affecting mostly men and older people, explains Lorenzo. Piemonti, director of the San Raffaele Diabetes Research Institute and associate professor of Endocrinology at Vita-Salute University, who contributed to the analysis and among the authors of the research. Not surprisingly, among patients with autoantibodies, 95 percent were male and more than 50 percent were over 65.
Not just Covid-19
There are also other examples of infectious diseases facilitated by the presence of autoantibodies that inhibit the action of the immune system. And research confirms the critical role of interferon ininnate immunity, which comes into play against an infection first and keeps it at bay while waiting for adaptive immunity to elicit a more specific response.
Possible therapies
The two studies are mutually reinforcing and suggest that intervening to restore the correct amounts of interferon I in the early stages of infection could be effective against the most severe forms of Covid-19, at least in a select group of patients, explains Fabio Ciceri. , vice principal. San Raffaele scientist and full professor of Hematology at Vita-Salute University. And it is precisely in this direction that it goes clinical study at baseline in our hospital, which tests the administration of beta interferon in seriously ill patients with Covid-19.
September 24, 2020 (change September 24, 2020 | 8:25 PM)
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