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Loss of insulin\u2010producing pancreatic islet \u03b2 cells is one of the many causes of T1D. Viral infections have long been associated with new\u2010onset T1D and the balance between virulence and host immunity determines whether the viral infection would lead to T1D. Herein, we detail the dynamic interaction of\u00a0pancreatic \u03b2 cells with severe acute respiratory syndrome coronavirus 2 (SARS\u2010CoV\u20102) and the host immune system with respect to new\u2010onset T1D. Importantly, \u03b2 cells express the crucial entry receptors and multiple studies confirmed that \u03b2 cells are infected by SARS\u2010CoV\u20102. Innate immune system effectors, such as natural killer cells, can eliminate such infected \u03b2 cells. Although CD4<jats:sup>+<\/jats:sup>CD25<jats:sup>+<\/jats:sup>FoxP3<jats:sup>+<\/jats:sup> regulatory T (T<jats:sub>REG<\/jats:sub>) cells provide immune tolerance to prevent the destruction of the islet \u03b2\u2010cell population by autoantigen\u2010specific CD8<jats:sup>+<\/jats:sup> T cells, it can be speculated that SARS\u2010CoV\u20102 infection may compromise self\u2010tolerance by depleting T<jats:sub>REG<\/jats:sub>\u2010cell numbers or diminishing T<jats:sub>REG<\/jats:sub>\u2010cell functions by repressing Forkhead box P3 (FoxP3) expression. However, the expansion of \u03b2 cells by self\u2010duplication, and regeneration from progenitor cells, could effectively replace lost \u03b2 cells. Appearance of islet autoantibodies following SARS\u2010CoV\u20102 infection was reported in a few cases, which could imply a breakdown of immune tolerance in the pancreatic islets. However, many of the cases with newly diagnosed autoimmune response following SARS\u2010CoV\u20102 infection also presented with significantly high HbA<jats:sub>1c<\/jats:sub> (glycated hemoglobin) levels that indicated progression of an already set diabetes, rather than new\u2010onset T1D. Here we review the potential underlying mechanisms behind loss of functional \u03b2\u2010cell mass as a result of SARS\u2010CoV\u20102 infection that can trigger new\u2010onset T1D.<\/jats:p>","DOI":"10.1111\/imcb.12615","type":"journal-article","created":{"date-parts":[[2022,12,19]],"date-time":"2022-12-19T06:29:55Z","timestamp":1671431395000},"page":"191-203","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":19,"title":["New\u2010onset type 1 diabetes and severe acute respiratory syndrome coronavirus 2 infection"],"prefix":"10.1111","volume":"101","author":[{"given":"Roy","family":"Anindya","sequence":"first","affiliation":[{"name":"Department of Biotechnology Indian Institute of Technology Hyderabad  Sangareddy Telangana India"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Guy A","family":"Rutter","sequence":"additional","affiliation":[{"name":"Section\u00a0of Cell Biology and Functional Genomics, Division 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