SARS-CoV-2 Uses Nonstructural Protein 16 To Evade Restriction by IFIT1 and IFIT3-Reference-Cited by-同舟云学术

SARS-CoV-2 Uses Nonstructural Protein 16 To Evade Restriction by IFIT1 and IFIT3

Published:2023-02-28 Issue:2 Volume:97 Page:
ISSN:0022-538X
Container-title:Journal of Virology
language:en
Short-container-title:J Virol

Author:

Schindewolf Craig¹²,Lokugamage Kumari¹,Vu Michelle N.¹,Johnson Bryan A.¹,Scharton Dionna¹³,Plante Jessica A.¹³,Kalveram Birte¹⁴,Crocquet-Valdes Patricia A.⁵,Sotcheff Stephanea⁴,Jaworski Elizabeth⁴,Alvarado Rojelio E.¹⁶,Debbink Kari⁷,Daugherty Matthew D.⁸,Weaver Scott C.¹²³,Routh Andrew L.²⁴^ORCID,Walker David H.⁵⁹,Plante Kenneth S.¹²³,Menachery Vineet D.¹²³^ORCID

Affiliation:

1. Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, Texas, USA

2. Institute for Human Infections and Immunity, University of Texas Medical Branch, Galveston, Texas, USA

3. World Reference Center for Emerging Viruses and Arboviruses, University of Texas Medical Branch, Galveston, Texas, USA

4. Department of Biochemistry and Molecular Biology, University of Texas Medical Branch, Galveston, Texas, USA

5. Department of Pathology, University of Texas Medical Branch, Galveston, Texas, USA

6. Institute for Translational Sciences, University of Texas Medical Branch, Galveston, Texas, USA

7. Department of Microbiology and Immunology, Johns Hopkins University, Baltimore, Maryland, USA

8. Department of Molecular Biology, University of California, San Diego, California, USA

9. Center for Biodefense and Emerging Infectious Disease, University of Texas Medical Branch, Galveston, Texas, USA

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.

Funder

HHS | Centers for Disease Control and Prevention

HHS | NIH | National Institute of Allergy and Infectious Diseases

HHS | NIH | National Institute of General Medical Sciences

Publisher

American Society for Microbiology

Subject

Virology,Insect Science,Immunology,Microbiology

Link

https://journals.asm.org/doi/pdf/10.1128/jvi.01532-22

Reference50 articles.

1. Estimating excess mortality due to the COVID-19 pandemic: a systematic analysis of COVID-19-related mortality, 2020–21