An aberrant immune-epithelial progenitor niche drives viral lung sequelae.

ABSTRACT: The long-term physiological consequences of respiratory viral infections, particularly in the aftermath of the COVID-19 pandemic-termed post-acute sequelae of SARS-CoV-2 (PASC)-are rapidly evolving into a major public health concern^1-3. While the cellular and molecular aetiologies of these sequelae are poorly defined, increasing evidence implicates abnormal immune responses^3-6 and/or impaired organ recovery^7-9 after infection. However, the precise mechanisms that link these processes in the context of PASC remain unclear. Here, with insights from three cohorts of patients with respiratory PASC, we established a mouse model of post-viral lung disease and identified an aberrant immune-epithelial progenitor niche unique to fibroproliferation in respiratory PAS

SUBMITTER: Narasimhan H 

PROVIDER: S-EPMC12456998 | biostudies-literature | 2024 Oct

REPOSITORIES: biostudies-literature