التفاصيل البيبلوغرافية
| العنوان: |
Limited extent and consequences of pancreatic SARS-CoV-2 infection. |
| المؤلفون: |
van der Heide, Verena, Jangra, Sonia, Cohen, Phillip, Rathnasinghe, Raveen, Aslam, Sadaf, Aydillo, Teresa, Geanon, Daniel, Handler, Diana, Kelley, Geoffrey, Lee, Brian, Rahman, Adeeb, Dawson, Travis, Qi, Jingjing, D'Souza, Darwin, Kim-Schulze, Seunghee, Panzer, Julia K., Caicedo, Alejandro, Kusmartseva, Irina, Posgai, Amanda L., Atkinson, Mark A. |
| المصدر: |
Cell Reports; Mar2022, Vol. 38 Issue 11, pN.PAG-N.PAG, 1p |
| مستخلص: |
Concerns that infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the etiological agent of coronavirus disease 2019 (COVID-19), may cause new-onset diabetes persist in an evolving research landscape, and precise risk assessment is hampered by, at times, conflicting evidence. Here, leveraging comprehensive single-cell analyses of in vitro SARS-CoV-2-infected human pancreatic islets, we demonstrate that productive infection is strictly dependent on the SARS-CoV-2 entry receptor ACE2 and targets practically all pancreatic cell types. Importantly, the infection remains highly circumscribed and largely non-cytopathic and, despite a high viral burden in infected subsets, promotes only modest cellular perturbations and inflammatory responses. Similar experimental outcomes are also observed after islet infection with endemic coronaviruses. Thus, the limits of pancreatic SARS-CoV-2 infection, even under in vitro conditions of enhanced virus exposure, challenge the proposition that in vivo targeting of β cells by SARS-CoV-2 precipitates new-onset diabetes. Whether restricted pancreatic damage and immunological alterations accrued by COVID-19 increase cumulative diabetes risk, however, remains to be evaluated. [Display omitted] • SARS-CoV-2 infection targets practically all human pancreatic cell types in vitro • Productive SARS-CoV-2 infection of islet cells is strictly dependent on ACE2 • Extent and consequences of pancreatic SARS-CoV-2 infection are notably restrained • Islets are also permissive to in vitro infection with endemic human coronaviruses Assessing the risk of SARS-CoV-2-induced new-onset diabetes requires integration of multiple complementary lines of investigation. Here, van der Heide et al. demonstrate that the specific limits of in vitro pancreatic SARS-CoV-2 infection suggest at best a minor, if any, role of virus-induced β cell damage directly promoting new-onset diabetes. [ABSTRACT FROM AUTHOR] |
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| قاعدة البيانات: |
Complementary Index |
