Type I and Type III Interferons Restrict SARS-CoV-2 Infection of Human Airway Epithelial Cultures
Abigail Vanderheiden, Philipp Ralfs, Tatiana Chirkova, Amit A. Upadhyay, Matthew G. Zimmerman, Shamika Bedoya, Hadj Aoued, Gregory M. Tharp, Kathryn L. Pellegrini, Candela Manfredi, Eric J. Sorscher, Bernardo A. Mainou, Jenna L Lobby, Jacob E. Kohlmeier, Anice C. Lowen, Pei‐Yong Shi, Vineet D. Menachery, Larry J. Anderson, Arash Grakoui, Steven E. Bosinger, Mehul S. Suthar
Abstract
The current pandemic of respiratory illness, COVID-19, is caused by a recently emerged coronavirus named SARS-CoV-2. This virus infects airway and lung cells causing fever, dry cough, and shortness of breath. Severe cases of COVID-19 can result in lung damage, low blood oxygen levels, and even death. As there are currently no vaccines approved for use in humans, studies of the mechanisms of SARS-CoV-2 infection are urgently needed. Our research identifies an excellent system to model SARS-CoV-2 infection of the human airways that can be used to test various treatments. Analysis of infection in this model system found that human airway epithelial cell cultures induce a strong proinflammatory cytokine response yet block the production of type I and III IFNs to SARS-CoV-2. However, treatment of airway cultures with the immune molecules type I or type III interferon (IFN) was able to inhibit SARS-CoV-2 infection. Thus, our model system identified type I or type III IFN as potential antiviral treatments for COVID-19 patients.