Show simple item record

dc.contributor.authorMartin-Sancho, Laura
dc.contributor.authorLewinski, Mary K
dc.contributor.authorPache, Lars
dc.contributor.authorStoneham, Charlotte A
dc.contributor.authorYin, Xin
dc.contributor.authorBecker, Mark E
dc.contributor.authorPratt, Dexter
dc.contributor.authorChuras, Christopher
dc.contributor.authorRosenthal, Sara B
dc.contributor.authorLiu, Sophie
dc.contributor.authorWeston, Stuart
dc.contributor.authorDe Jesus, Paul D
dc.contributor.authorO'Neill, Alan M
dc.contributor.authorGounder, Anshu P
dc.contributor.authorNguyen, Courtney
dc.contributor.authorPu, Yuan
dc.contributor.authorCurry, Heather M
dc.contributor.authorOom, Aaron L
dc.contributor.authorMiorin, Lisa
dc.contributor.authorRodriguez-Frandsen, Ariel
dc.contributor.authorZheng, Fan
dc.contributor.authorWu, Chunxiang
dc.contributor.authorXiong, Yong
dc.contributor.authorUrbanowski, Matthew
dc.contributor.authorShaw, Megan L
dc.contributor.authorChang, Max W
dc.contributor.authorBenner, Christopher
dc.contributor.authorHope, Thomas J
dc.contributor.authorFrieman, Matthew B
dc.contributor.authorGarcía-Sastre, Adolfo
dc.contributor.authorIdeker, Trey
dc.contributor.authorHultquist, Judd F
dc.contributor.authorGuatelli, John
dc.contributor.authorChanda, Sumit K
dc.date.accessioned2021-05-05T19:43:01Z
dc.date.available2021-05-05T19:43:01Z
dc.date.issued2021-04-13
dc.identifier.urihttp://hdl.handle.net/10713/15589
dc.description.abstractA 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.urihttps://doi.org/10.1016/j.molcel.2021.04.008en_US
dc.language.isoenen_US
dc.publisherCell Pressen_US
dc.relation.ispartofMolecular Cellen_US
dc.rightsCopyright © 2021 Elsevier Inc. All rights reserved.en_US
dc.subjectBST2en_US
dc.subjectISGen_US
dc.subjectOrf7aen_US
dc.subjectSARS-CoV-2en_US
dc.subjectinnate immunityen_US
dc.subjectinterferonen_US
dc.subjectviral evasionen_US
dc.titleFunctional landscape of SARS-CoV-2 cellular restrictionen_US
dc.typeArticleen_US
dc.identifier.doi10.1016/j.molcel.2021.04.008
dc.identifier.pmid33930332
dc.source.countryUnited States


Files in this item

Thumbnail
Name:
Publisher version

This item appears in the following Collection(s)

Show simple item record