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We demonstrated that mice harboring \u03b2-cells that do not respond to IFN because of the expression of the suppressor of cytokine signaling-1 (SOCS-1) succumb to an acute form of type 1 diabetes after infection with CVB3. Interestingly, the tropism of the virus was altered in SOCS-1 transgenic (Tg) mice, and CVB3 was detected in islet cells of SOCS-1\u2013Tg mice before \u03b2-cell loss and the onset of diabetes. Furthermore, insulitis was increased in SOCS-1\u2013Tg mice after infection with murine CMV, and a minority of the mice developed overt diabetes. However, infection with LCMV failed to cause \u03b2-cell destruction in SOCS-1 Tg mice. These findings suggest that CVB3 can cause diabetes in a host lacking adequate \u03b2-cell antiviral defense, and that incomplete target cell antiviral defense may enhance susceptibility to diabetes triggered by CMV. In conclusion, suppressed \u03b2-cell antiviral defense reveals the diabetogenic potential of two pathogens previously linked to the onset of type 1 diabetes in humans.<\/jats:p>","DOI":"10.2337\/diabetes.52.8.2025","type":"journal-article","created":{"date-parts":[[2007,3,6]],"date-time":"2007-03-06T19:04:22Z","timestamp":1173207862000},"page":"2025-2034","update-policy":"https:\/\/doi.org\/10.2337\/ada-journal-policies","source":"Crossref","is-referenced-by-count":37,"title":["Diabetogenic Potential of Human Pathogens Uncovered in Experimentally Permissive \u03b2-Cells"],"prefix":"10.2337","volume":"52","author":[{"given":"Malin","family":"Flodstro\u0308m","sequence":"first","affiliation":[{"name":"From the Department of Immunology, the Scripps Research Institute, La Jolla, California"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Devin","family":"Tsai","sequence":"additional","affiliation":[{"name":"From the Department of Immunology, the Scripps Research Institute, La Jolla, California"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Cody","family":"Fine","sequence":"additional","affiliation":[{"name":"From the Department of Immunology, the Scripps Research Institute, La Jolla, California"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Amy","family":"Maday","sequence":"additional","affiliation":[{"name":"From the Department of Immunology, the Scripps Research Institute, La Jolla, California"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nora","family":"Sarvetnick","sequence":"additional","affiliation":[{"name":"From the Department of Immunology, the Scripps Research Institute, La Jolla, California"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1167","reference":[{"key":"2022031209072325400_R1","doi-asserted-by":"crossref","unstructured":"Atkinson MA, Eisenbarth GS: Type 1 diabetes: new perspectives on disease pathogenesis and treatment. 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