Functional landscape of SARS-CoV-2 cellular restriction
dc.contributor.author | Martin-Sancho, Laura | |
dc.contributor.author | Lewinski, Mary K | |
dc.contributor.author | Pache, Lars | |
dc.contributor.author | Stoneham, Charlotte A | |
dc.contributor.author | Yin, Xin | |
dc.contributor.author | Becker, Mark E | |
dc.contributor.author | Pratt, Dexter | |
dc.contributor.author | Churas, Christopher | |
dc.contributor.author | Rosenthal, Sara B | |
dc.contributor.author | Liu, Sophie | |
dc.contributor.author | Weston, Stuart | |
dc.contributor.author | De Jesus, Paul D | |
dc.contributor.author | O'Neill, Alan M | |
dc.contributor.author | Gounder, Anshu P | |
dc.contributor.author | Nguyen, Courtney | |
dc.contributor.author | Pu, Yuan | |
dc.contributor.author | Curry, Heather M | |
dc.contributor.author | Oom, Aaron L | |
dc.contributor.author | Miorin, Lisa | |
dc.contributor.author | Rodriguez-Frandsen, Ariel | |
dc.contributor.author | Zheng, Fan | |
dc.contributor.author | Wu, Chunxiang | |
dc.contributor.author | Xiong, Yong | |
dc.contributor.author | Urbanowski, Matthew | |
dc.contributor.author | Shaw, Megan L | |
dc.contributor.author | Chang, Max W | |
dc.contributor.author | Benner, Christopher | |
dc.contributor.author | Hope, Thomas J | |
dc.contributor.author | Frieman, Matthew B | |
dc.contributor.author | García-Sastre, Adolfo | |
dc.contributor.author | Ideker, Trey | |
dc.contributor.author | Hultquist, Judd F | |
dc.contributor.author | Guatelli, John | |
dc.contributor.author | Chanda, Sumit K | |
dc.date.accessioned | 2021-05-05T19:43:01Z | |
dc.date.available | 2021-05-05T19:43:01Z | |
dc.date.issued | 2021-04-13 | |
dc.identifier.uri | http://hdl.handle.net/10713/15589 | |
dc.description.abstract | A deficient interferon (IFN) response to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection has been implicated as a determinant of severe coronavirus disease 2019 (COVID-19). To identify the molecular effectors that govern IFN control of SARS-CoV-2 infection, we conducted a large-scale gain-of-function analysis that evaluated the impact of human IFN-stimulated genes (ISGs) on viral replication. A limited subset of ISGs were found to control viral infection, including endosomal factors inhibiting viral entry, RNA binding proteins suppressing viral RNA synthesis, and a highly enriched cluster of endoplasmic reticulum (ER)/Golgi-resident ISGs inhibiting viral assembly/egress. These included broad-acting antiviral ISGs and eight ISGs that specifically inhibited SARS-CoV-2 and SARS-CoV-1 replication. Among the broad-acting ISGs was BST2/tetherin, which impeded viral release and is antagonized by SARS-CoV-2 Orf7a protein. Overall, these data illuminate a set of ISGs that underlie innate immune control of SARS-CoV-2/SARS-CoV-1 infection, which will facilitate the understanding of host determinants that impact disease severity and offer potential therapeutic strategies for COVID-19. | en_US |
dc.description.uri | https://doi.org/10.1016/j.molcel.2021.04.008 | en_US |
dc.language.iso | en | en_US |
dc.publisher | Cell Press | en_US |
dc.relation.ispartof | Molecular Cell | en_US |
dc.rights | Copyright © 2021 Elsevier Inc. All rights reserved. | en_US |
dc.subject | BST2 | en_US |
dc.subject | ISG | en_US |
dc.subject | Orf7a | en_US |
dc.subject | SARS-CoV-2 | en_US |
dc.subject | innate immunity | en_US |
dc.subject | interferon | en_US |
dc.subject | viral evasion | en_US |
dc.title | Functional landscape of SARS-CoV-2 cellular restriction | en_US |
dc.type | Article | en_US |
dc.identifier.doi | 10.1016/j.molcel.2021.04.008 | |
dc.identifier.pmid | 33930332 | |
dc.source.country | United States |