Impact of the Presence of Anti-interferon Autoantibodies on the Viral Load in Severe Respiratory Infections

Type I interferons (IFN-I) production is induced by the detection of viral molecules, such as RNA or DNA viral strands, through pattern recognition receptors (PRR) present on many immune cell types. Despite a minimal concentration, IFN-I secretion activate the secretion, by neighbouring cells, of more than 700 proteins with antiviral properties (inhibition of viral replication, destabilization of virus membranes, etc.). IFN-I constitute therefore one of the major first line of defence established by the immune system in response to viral infection. Briefly, during the Coronavirus disease (COVID-19) pandemic, several teams including ours, highlighted a lack of IFN-I response in approximately one in five individuals presenting a severe form of COVID-19. Interestingly, within a large part of them, in vitro investigations revealed the presence of autoantibodies presenting neutralizing capacities against alpha and/or omega interferons This finding confirms the deleterious role of anti-IFN-I autoantibodies on the antiviral immune response and the key role of IFN-I pathway regarding defences against COVID-19 infection. Furthermore, those observations pave the way to interesting research that would allow understanding the underlying pathophysiological mechanisms of severe viral respiratory infection. The research hypothesis are: i) IFN-I deficiency could induce severe forms of viral infections which could lead to intensive care admission ii) IFN-I deficiency could increase viral l…

This description comes directly from the study's public registry record.

Louis CHAUVELOT, MD  ·  0472071762  ·  louis.chauvelot@chu-lyon.fr

Sophie ASSANT, MD  ·  0472678780  ·  sophie.assant@chu-lyon.fr

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