SARS-CoV-2 infection triggers paracrine senescence and leads to a sustained senescence-associated inflammatory response.

ABSTRACT: Reports of post-acute COVID-19 syndrome, in which the inflammatory response persists even after SARS-CoV-2 has disappeared, are increasing¹, but the underlying mechanisms of post-acute COVID-19 syndrome remain unknown. Here, we show that SARS-CoV-2-infected cells trigger senescence-like cell-cycle arrest^2,3 in neighboring uninfected cells in a paracrine manner via virus-induced cytokine production. In cultured human cells or bronchial organoids, these SASR-CoV-2 infection-induced senescent cells express high levels of a series of inflammatory factors known as senescence-associated secretory phenotypes (SASPs)⁴ in a sustained manner, even after SARS-CoV-2 is no longer detectable. We also show that the expression of the senescence marker CDKN2A (refs. ^5,

SUBMITTER: Tsuji S 

PROVIDER: S-EPMC10154207 | biostudies-literature | 2022 Feb

REPOSITORIES: biostudies-literature