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10.1007/s00430-022-00734-9

http://scihub22266oqcxt.onion/10.1007/s00430-022-00734-9
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suck abstract from ncbi


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pmid35366686      Med+Microbiol+Immunol 2023 ; 212 (2): 125-131
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  • Interferon antagonists encoded by SARS-CoV-2 at a glance #MMPMID35366686
  • Lee JH; Koepke L; Kirchhoff F; Sparrer KMJ
  • Med Microbiol Immunol 2023[Apr]; 212 (2): 125-131 PMID35366686show ga
  • 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.
  • |*COVID-19[MESH]
  • |*Interferons/genetics[MESH]
  • |Antiviral Agents/pharmacology/therapeutic use[MESH]
  • |Humans[MESH]
  • |Immunity, Innate[MESH]


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