Proc Natl Acad Sci U S A
. 2022 Apr 19;119(16):e2119680119.
doi: 10.1073/pnas.2119680119. Epub 2022 Mar 30.
SARS-CoV-2 infection of airway cells causes intense viral and cell shedding, two spreading mechanisms affected by IL-13
Cameron B Morrison 1 , Caitlin E Edwards 2 , Kendall M Shaffer 1 , Kenza C Araba 1 , Jason A Wykoff 1 , Danielle R Williams 3 , Takanori Asakura 1 , Hong Dang 1 , Lisa C Morton 1 , Rodney C Gilmore 1 , Wanda K O'Neal 1 , Richard C Boucher 1 , Ralph S Baric 2 3 , Camille Ehre 1 4
Affiliations
- PMID: 35353667
- DOI: 10.1073/pnas.2119680119
Abstract
Significance Gaining insights into severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) high transmissibility and the role played by inflammatory mediators in viral proliferation are critical to investigating new therapeutic targets against COVID-19. Electron microscopy reveals important SARS-CoV-2 features, including the combination of large, rapidly released viral clusters and the massive shedding of epithelial cells packed with virions. Interleukin-13 (IL-13), a Th2 cytokine up-regulated in allergic asthma and associated with less severe COVID-19, protects against SARS-CoV-2 viral and cell shedding. Using gene expression analyses and biochemical assays, IL-13 is shown to affect viral entry, replication, and cell-to-cell transmission. Given the broad spectrum of COVID-19 clinical symptoms, it is important to elucidate intrinsic factors that modulate viral load and spreading mechanisms.
Keywords: IL-13 cytokine; SARS-CoV-2; asthma; human airway epithelial cells; infection.