{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,5]],"date-time":"2026-09-05T03:47:02Z","timestamp":1788580022763,"version":"build-2803163510"},"reference-count":36,"publisher":"American Society for Microbiology","issue":"19","license":[{"start":{"date-parts":[[2019,10,1]],"date-time":"2019-10-01T00:00:00Z","timestamp":1569888000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"funder":[{"DOI":"10.13039\/100000002","name":"HHS | National Institutes of Health","doi-asserted-by":"publisher","award":["AR070918"],"award-info":[{"award-number":["AR070918"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"HHS | National Institutes of Health","doi-asserted-by":"publisher","award":["AI143982"],"award-info":[{"award-number":["AI143982"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"HHS | National Institutes of Health","doi-asserted-by":"publisher","award":["AI141716"],"award-info":[{"award-number":["AI141716"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"HHS | National Institutes of Health","doi-asserted-by":"publisher","award":["AI139314"],"award-info":[{"award-number":["AI139314"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["J Virol"],"published-print":{"date-parts":[[2019,10]]},"abstract":"<jats:p>\n            Mechanisms of immunodeficiency related to STAT1 gain of function have not been previously studied in an animal model of viral pathogenesis. Using virological and immunological techniques, we examined the immune response to \u03b3HV68 in heterozygous mice that have an autosomal dominant mutation in the STAT1 coiled-coil domain (STAT1 R274W). We observed impaired control of infection, which was associated with diminished production of gamma interferon (IFN-\u03b3), fewer effector CD4\n            <jats:sup>+<\/jats:sup>\n            and CD8\n            <jats:sup>+<\/jats:sup>\n            T cells, and a reduction in the number of antigen-specific CD8\n            <jats:sup>+<\/jats:sup>\n            T cells. These findings indicate that a STAT1 gain-of-function mutation limits production of antiviral T cells, likely contributing to immunodeficiency against herpesviruses.\n          <\/jats:p>","DOI":"10.1128\/jvi.00307-19","type":"journal-article","created":{"date-parts":[[2019,7,16]],"date-time":"2019-07-16T13:06:21Z","timestamp":1563282381000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":13,"title":["A Human STAT1 Gain-of-Function Mutation Impairs CD8\n            <sup>+<\/sup>\n            T Cell Responses against Gammaherpesvirus 68"],"prefix":"10.1128","volume":"93","author":[{"given":"Wei","family":"Qian","sequence":"first","affiliation":[{"name":"Departments of Medicine, Washington University School of Medicine, Saint Louis, Missouri, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Cathrine A.","family":"Miner","sequence":"additional","affiliation":[{"name":"Departments of Medicine, 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