“…In contrast, the proposition of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection as a trigger for new-onset diabetes has to contend with seemingly conflicting evidence regarding increased diabetes incidence rates during the COVID-19 pandemic as well as the considerable difficulties to distinguish an infectious diabetes origin from a multiplicity of pandemicrelated but indirect potential causalities (Barrett et al, 2022;Drucker, 2021;Ibrahim et al, 2021;Kamrath et al, 2022;Khunti et al, 2021;Sathish et al, 2021). Although the aggregate epidemiological evidence ostensibly argues against a direct diabetogenic potential of SARS-CoV-2 infection, this assessment is certainly provisional in consideration of the manifold ramifications of pandemic containment measures, the evolving landscape of clinical studies, various diagnostic challenges (e.g., a precise clinical definition of diabetes, previously undiagnosed type 1 or 2 diabetes [T1D or T2D, respectively]), the different pathophysiological mechanisms promoting acute and/ or prolonged glycometabolic perturbations (including hyperglycemia and insulin resistance typically associated with critical illness), and the possibility that a history of SARS-CoV-2 infection may alter diabetes incidence rates in the future (Al-Aly et al, 2021;Clarke et al, 2021;Drucker, 2021;Ibrahim et al, 2021;Jivanji et al, 2017;Kamrath et al, 2022;Li et al, 2020a;Misra et al, 2021;Montefusco et al, 2021;Reiterer et al, 2021). However, in the current context, a balanced evaluation of the available evidence also has to inform and delimit any speculation about the precise relevance of ex vivo and in vitro studies seeking to elucidate the potential for b cell infection, incapacitation, and/or destruction by SARS-CoV-2 (Accili, 2021;Atkinson and Powers, 2021).…”