A predominately pulmonary activation of complement in a mouse model of severe COVID-19.

ABSTRACT: Evidence from in vitro studies and observational human disease data suggest the complement system plays a significant role in SARS-CoV-2 pathogenesis, although how complement dysregulation develops in patients with severe COVID-19 is unknown. Here, using a mouse-adapted SARS-CoV-2 virus (SARS2-N501Y_MA30) and a mouse model of severe COVID-19, we identify significant serologic and pulmonary complement activation following infection. We observed C3 activation in airway and alveolar epithelia, and in pulmonary vascular endothelia. Our evidence suggests that while the alternative pathway is the primary route of complement activation, components of both the alternative and classical pathways are produced locally by respiratory epithelial cells following infection, and increased in pri

SUBMITTER: Szachowicz PJ 

PROVIDER: S-EPMC11185570 | biostudies-literature | 2024 Jun

REPOSITORIES: biostudies-literature