SARS-CoV-2 infection of airway cells causes intense viral and cell shedding, two spreading mechanisms affected by IL-13

• DOI: 10.1073/pnas.2119680119
• Publication Date: 2022-03-30T18:46:05Z
• Authors: Cameron B. Morrison; Caitlin E. Edwards; Kendall M. Shaffer; Kenza C. Araba; Jason A. Wykoff; Danielle R. Williams; Takanori Asakura; Hong Dang; Lisa C. Morton; Rodney C. Gilmore; Wanda K. O’Neal; Richard C. Boucher; Ralph S. Baric; Camille Ehre
• Keywords: 0301 basic medicine; 03 medical and health sciences; Interleukin-13; SARS-CoV-2; Respiratory System; COVID-19; Humans; Angiotensin-Converting Enzyme 2; Biological Sciences; Glycoproteins; 3. Good health

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.