https://socictopen.socict.org/files/original/d3176e056dcf0c0dba4e48ed40d3d496.pdf 682056679ce59c59b0e125c85eeeded4 Dublin Core The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/. Title A name given to the resource Coronavirus Description An account of the resource Dominio científico: Coronavirus Text A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text. Dublin Core The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/. Title A name given to the resource Distinct patterns of IFITM-mediated restriction of filoviruses, SARS coronavirus, and influenza A virus. Creator An entity primarily responsible for making the resource I-Chueh Huang, Charles C Bailey, Jessica L Weyer, Sheli R. Radoshitzky, Michelle M Becker, Jessica J. Chiang, Abraham L. Brass, Asim A. Ahmed, Xiaoli Chi, Lian Dong, Lindsay E Longobardi, Dutch Boltz, Jens H. Kuhn, Stephen J. Elledge, Sina Bavari, Mark R. Denison, Hyeryun Choe, Michael Farzan Description An account of the resource Interferon-inducible transmembrane proteins 1, 2, and 3 (IFITM1, 2, and 3) are recently identified viral restriction factors that inhibit infection mediated by the influenza A virus (IAV) hemagglutinin (HA) protein. Here we show that IFITM proteins restricted infection mediated by the entry glycoproteins (GP(1,2)) of Marburg and Ebola filoviruses (MARV, EBOV). Consistent with these observations, interferon-β specifically restricted filovirus and IAV entry processes. IFITM proteins also inhibited replication of infectious MARV and EBOV. We observed distinct patterns of IFITM-mediated restriction: compared with IAV, the entry processes of MARV and EBOV were less restricted by IFITM3, but more restricted by IFITM1. Moreover, murine Ifitm5 and 6 did not restrict IAV, but efficiently inhibited filovirus entry. We further demonstrate that replication of infectious SARS coronavirus (SARS-CoV) and entry mediated by the SARS-CoV spike (S) protein are restricted by IFITM proteins. The profile of IFITM-mediated restriction of SARS-CoV was more similar to that of filoviruses than to IAV. Trypsin treatment of receptor-associated SARS-CoV pseudovirions, which bypasses their dependence on lysosomal cathepsin L, also bypassed IFITM-mediated restriction. However, IFITM proteins did not reduce cellular cathepsin activity or limit access of virions to acidic intracellular compartments. Our data indicate that IFITM-mediated restriction is localized to a late stage in the endocytic pathway. They further show that IFITM proteins differentially restrict the entry of a broad range of enveloped viruses, and modulate cellular tropism independently of viral receptor expression. Date A point or period of time associated with an event in the lifecycle of the resource 2011 Identifier An unambiguous reference to the resource within a given context DOI: 10.1371/journal.ppat.1001258 Source A related resource from which the described resource is derived PLoS Pathogens Publisher An entity responsible for making the resource available Public Library of Science (PLoS) Coverage The spatial or temporal topic of the resource, the spatial applicability of the resource, or the jurisdiction under which the resource is relevant Biology (General), Immunologic diseases. Allergy Language A language of the resource EN