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Med Microbiol Immunol
. 2022 Apr 2.
doi: 10.1007/s00430-022-00734-9. Online ahead of print.
Interferon antagonists encoded by SARS-CoV-2 at a glance
Jung-Hyun Lee # 1 2 , Lennart Koepke # 1 , Frank Kirchhoff 1 , Konstantin M J Sparrer 3
Affiliations
- PMID: 35366686
- DOI: 10.1007/s00430-022-00734-9
Abstract
The innate immune system is a powerful barrier against invading pathogens. Interferons (IFNs) are a major part of the cytokine-mediated anti-viral innate immune response. After recognition of a pathogen by immune sensors, signaling cascades are activated that culminate in the release of IFNs. These activate cells in an autocrine or paracrine fashion eventually setting cells in an anti-viral state via upregulation of hundreds of interferon-stimulated genes (ISGs). To evade the anti-viral effect of the IFN system, successful viruses like the pandemic severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) evolved strategies to counteract both IFN induction and signaling. In fact, more than half of the about 30 proteins encoded by SARS-CoV-2 target the IFN system at multiple levels to escape IFN-mediated restriction. Here, we review recent insights into the molecular mechanisms used by SARS-CoV-2 proteins to suppress IFN production and the establishment of an anti-viral state.
Keywords: COVID-19; Immune evasion; Innate immunity; Interferon; SARS-CoV-2.