SARS-CoV-2 Uses Nonstructural Protein 16 To Evade Restriction by IFIT1 and IFIT3
Craig Schindewolf, Kumari G. Lokugamage, Michelle N. Vu, Bryan A. Johnson, Dionna Scharton, Jessica A. Plante, Birte Kalveram, Patricia A. Crocquet-Valdes, Stephanea Sotcheff, Elizabeth Jaworski, R. Elias Alvarado, Kari Debbink, Matthew D. Daugherty, Scott C. Weaver, Andrew Routh, David H. Walker, Kenneth S. Plante, Vineet D. Menachery
Abstract
Similar to other coronaviruses, disruption of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) NSP16 function attenuates viral replication in a type I interferon-dependent manner. In vivo , our results show reduced disease and viral replication at late times in the hamster lung, but an earlier titer deficit for the NSP16 mutant (dNSP16) in the upper airway. In addition, our results confirm a role for IFIT1 but also demonstrate the necessity of IFIT3 in mediating dNSP16 attenuation.