| Literature DB >> 33757684 |
Silke Stertz1, Benjamin G Hale2.
Abstract
Pandemics are caused by novel pathogens to which pre-existing antibody immunity is lacking. Under these circumstances, the body must rely on innate interferon-mediated defenses to limit pathogen replication and allow development of critical humoral protection. Here, we highlight studies on disease susceptibility during H1N1 influenza and COVID-19 (SARS-CoV-2) pandemics. An emerging concept is that genetic and non-genetic deficiencies in interferon system components lead to uncontrolled virus replication and severe illness in a subset of people. Intriguingly, new findings suggest that individuals with autoantibodies neutralizing the antiviral function of interferon are at increased risk of severe COVID-19. We discuss key questions surrounding how such autoantibodies develop and function, as well as the general implications of diagnosing interferon deficiencies for personalized therapies.Entities:
Keywords: COVID-19; autoantibodies; disease severity; host genetics; influenza; interferon; pandemic virus
Year: 2021 PMID: 33757684 DOI: 10.1016/j.tim.2021.03.001
Source DB: PubMed Journal: Trends Microbiol ISSN: 0966-842X Impact factor: 17.079