Innate Immune Response to SARS-CoV-2 Infection: From Cells to Soluble Mediators

Int J Mol Sci. 2021 Jun 29;22(13):7017. doi: 10.3390/ijms22137017.

Abstract

The vulnerability of humankind to SARS-CoV-2 in the absence of a pre-existing immunity, the unpredictability of the infection outcome, and the high transmissibility, broad tissue tropism, and ability to exploit and subvert the immune response pose a major challenge and are likely perpetuating the COVID-19 pandemic. Nevertheless, this peculiar infectious scenario provides researchers with a unique opportunity for studying, with the latest immunological techniques and understandings, the immune response in SARS-CoV-2 naïve versus recovered subjects as well as in SARS-CoV-2 vaccinees. Interestingly, the current understanding of COVID-19 indicates that the combined action of innate immune cells, cytokines, and chemokines fine-tunes the outcome of SARS-CoV-2 infection and the related immunopathogenesis. Indeed, the emerging picture clearly shows that the excessive inflammatory response against this virus is among the main causes of disease severity in COVID-19 patients. In this review, the innate immune response to SARS-CoV-2 infection is described not only in light of its capacity to influence the adaptive immune response towards a protective phenotype but also with the intent to point out the multiple strategies exploited by SARS-CoV-2 to antagonize host antiviral response and, finally, to outline inborn errors predisposing individuals to COVID-19 disease severity.

Keywords: SARS-CoV-2; innate immunity; soluble and cellular mediators.

Publication types

  • Review

MeSH terms

  • COVID-19 / immunology
  • COVID-19 / pathology*
  • COVID-19 / virology
  • Chemokines / metabolism
  • Cytokines / metabolism
  • Host-Pathogen Interactions
  • Humans
  • Immunity, Innate*
  • Killer Cells, Natural / cytology
  • Killer Cells, Natural / metabolism
  • Monocytes / cytology
  • Monocytes / metabolism
  • SARS-CoV-2 / isolation & purification
  • Severity of Illness Index

Substances

  • Chemokines
  • Cytokines