Innate immune evasion strategies of SARS-CoV-2

Nat Rev Microbiol. 2023 Mar;21(3):178-194. doi: 10.1038/s41579-022-00839-1. Epub 2023 Jan 11.


SARS-CoV-2, the virus responsible for the COVID-19 pandemic, has been associated with substantial global morbidity and mortality. Despite a tropism that is largely confined to the airways, COVID-19 is associated with multiorgan dysfunction and long-term cognitive pathologies. A major driver of this biology stems from the combined effects of virus-mediated interference with the host antiviral defences in infected cells and the sensing of pathogen-associated material by bystander cells. Such a dynamic results in delayed induction of type I and III interferons (IFN-I and IFN-III) at the site of infection, but systemic IFN-I and IFN-III priming in distal organs and barrier epithelial surfaces, respectively. In this Review, we examine the relationship between SARS-CoV-2 biology and the cellular response to infection, detailing how antagonism and dysregulation of host innate immune defences contribute to disease severity of COVID-19.

Publication types

  • Review
  • Research Support, Non-U.S. Gov't

MeSH terms

  • COVID-19*
  • Humans
  • Immune Evasion
  • Immunity, Innate
  • Interferon Type I* / pharmacology
  • Interferons
  • Pandemics
  • SARS-CoV-2


  • Interferons
  • Interferon Type I