Cellular senescence as a source of SARS-CoV-2 quasispecies

FEBS J. 2023 Mar;290(5):1384-1392. doi: 10.1111/febs.16230. Epub 2021 Nov 8.

Abstract

In-depth analysis of SARS-CoV-2 biology and pathogenesis is rapidly unraveling the mechanisms through which the virus induces all aspects of COVID-19 pathology. Emergence of hundreds of variants and several important variants of concern has focused research on the mechanistic elucidation of virus mutagenesis. RNA viruses evolve quickly either through the error-prone polymerase or the RNA-editing machinery of the cell. In this review, we are discussing the links between cellular senescence, a natural aging process that has been recently linked to SARS-CoV-2 infection, and virus mutagenesis through the RNA-editing enzymes APOBEC. The action of APOBEC, enhanced by cellular senescence, is hypothesized to assist the emergence of novel variants, called quasispecies, within a cell or organism. These variants when introduced to the community may lead to the generation of a variant of concern, depending on fitness and transmissibility of the new genome. Such a mechanism of virus evolution may highlight the importance of inhibitors of cellular senescence during SARS-CoV-2 clinical treatment.

Keywords: COVID-19; SARS-CoV-2 quasispecies; cellular senescence.

Publication types

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

MeSH terms

  • COVID-19* / genetics
  • Cellular Senescence / genetics
  • Humans
  • Quasispecies
  • RNA
  • SARS-CoV-2 / genetics
  • Viruses* / genetics

Substances

  • RNA