Inflammasome activation in infected macrophages drives COVID-19 pathology.

ABSTRACT: Severe COVID-19 is characterized by persistent lung inflammation, inflammatory cytokine production, viral RNA and a sustained interferon (IFN) response, all of which are recapitulated and required for pathology in the SARS-CoV-2-infected MISTRG6-hACE2 humanized mouse model of COVID-19, which has a human immune system^1-20. Blocking either viral replication with remdesivir^21-23 or the downstream IFN-stimulated cascade with anti-IFNAR2 antibodies in vivo in the chronic stages of disease attenuates the overactive immune inflammatory response, especially inflammatory macrophages. Here we show that SARS-CoV-2 infection and replication in lung-resident human macrophages is a critical driver of disease. In response to infection mediated by CD16 and ACE2 receptors, human macro

SUBMITTER: Sefik E 

PROVIDER: S-EPMC9288243 | biostudies-literature | 2022 Jun

REPOSITORIES: biostudies-literature