{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,16]],"date-time":"2026-10-16T06:40:14Z","timestamp":1792132814634,"version":"4.4.0"},"reference-count":43,"publisher":"American Association for the Advancement of Science (AAAS)","issue":"6513","license":[{"start":{"date-parts":[[2020,10,9]],"date-time":"2020-10-09T00:00:00Z","timestamp":1602201600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/100000060","name":"National Institute of Allergy and Infectious Diseases","doi-asserted-by":"publisher","award":["R33AI102266"],"award-info":[{"award-number":["R33AI102266"]}],"id":[{"id":"10.13039\/100000060","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000060","name":"National Institute of Allergy and Infectious Diseases","doi-asserted-by":"publisher","award":["U01AI070330"],"award-info":[{"award-number":["U01AI070330"]}],"id":[{"id":"10.13039\/100000060","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000060","name":"National Institute of Allergy and Infectious Diseases","doi-asserted-by":"publisher","award":["R33AI119341"],"award-info":[{"award-number":["R33AI119341"]}],"id":[{"id":"10.13039\/100000060","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000060","name":"National Institute of Allergy and Infectious Diseases","doi-asserted-by":"publisher","award":["3U19AI125378 - 04W1"],"award-info":[{"award-number":["3U19AI125378 - 04W1"]}],"id":[{"id":"10.13039\/100000060","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Science"],"published-print":{"date-parts":[[2020,10,9]]},"abstract":"<jats:title>The CIITAdel keeps viruses at bay<\/jats:title>\n                  <jats:p>\n                    A better understanding of cellular mechanisms involved in viral resistance is needed for the next generation of antiviral therapies. Bruchez\n                    <jats:italic>et al.<\/jats:italic>\n                    used a transposon-mediated gene-activation screen to search for previously unreported host restriction factors for Ebola virus (see the Perspective by Wells and Coyne). The authors found that a transcription factor, major histocompatibility complex class II transactivator (CIITA), induces resistance in human cell lines by directing the expression of the p41 isoform of the invariant chain (CD74). CD74 p41 then disrupts cathepsin-mediated Ebola glycoprotein processing, which prevents viral fusion and entry. CD74 p41 can also stymie the endosomal entry of coronaviruses, including severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). This work should inform future treatments against cathepsin-dependent viruses such as filoviruses and coronaviruses. Additionally, the screening strategy used may serve as a blueprint for uncovering resistance mechanisms against other dangerous pathogens.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:italic>Science<\/jats:italic>\n                    , this issue p.\n                    <jats:related-article xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" ext-link-type=\"doi\" issue=\"6513\" page=\"241\" related-article-type=\"in-this-issue\" vol=\"370\" xlink:href=\"10.1126\/science.abb3753\">241<\/jats:related-article>\n                    see also p.\n                    <jats:related-article xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" ext-link-type=\"doi\" issue=\"6513\" page=\"167\" related-article-type=\"in-this-issue\" vol=\"370\" xlink:href=\"10.1126\/science.abe2977\">167<\/jats:related-article>\n                  <\/jats:p>","DOI":"10.1126\/science.abb3753","type":"journal-article","created":{"date-parts":[[2020,8,27]],"date-time":"2020-08-27T19:19:19Z","timestamp":1598555959000},"page":"241-247","source":"Crossref","is-referenced-by-count":109,"title":["MHC class II transactivator CIITA induces cell resistance to Ebola virus and SARS-like coronaviruses"],"prefix":"10.1126","volume":"370","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1695-5349","authenticated-orcid":true,"given":"Anna","family":"Bruchez","sequence":"first","affiliation":[{"name":"Benaroya Research Institute, Seattle, WA 98101, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8802-4186","authenticated-orcid":true,"given":"Ky","family":"Sha","sequence":"additional","affiliation":[{"name":"Benaroya Research Institute, Seattle, WA 98101, 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USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hannah","family":"McConnell","sequence":"additional","affiliation":[{"name":"Benaroya Research Institute, Seattle, WA 98101, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lea","family":"Gaucherand","sequence":"additional","affiliation":[{"name":"Benaroya Research Institute, Seattle, WA 98101, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3973-9406","authenticated-orcid":true,"given":"Rachel","family":"Prins","sequence":"additional","affiliation":[{"name":"Benaroya Research Institute, Seattle, WA 98101, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9149-551X","authenticated-orcid":true,"given":"Kenneth A.","family":"Matreyek","sequence":"additional","affiliation":[{"name":"Department of Genome Sciences, University of Washington, Seattle, WA 98109, 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