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Müller, J.A.* ; Groß, R.* ; Conzelmann, C.* ; Krüger, J.* ; Merle, U.* ; Steinhart, J.* ; Weil, T.* ; Koepke, L.* ; Bozzo, C.P.* ; Read, C.* ; Fois, G.* ; Eiseler, T.* ; Gehrmann, J.* ; van Vuuren, J. ; Wessbecher, I.M.* ; Frick, M.* ; Costa, I.G.* ; Breunig, M.* ; Grüner, B.* ; Peters, L.* ; Schuster, M.* ; Liebau, S.* ; Seufferlein, T.* ; Stenger, S.* ; Stenzinger, A.* ; MacDonald, P.E.* ; Kirchhoff, F.* ; Sparrer, K.M.J.* ; Walther, P.* ; Lickert, H. ; Barth, T.F.E.* ; Wagner, M.* ; Münch, J.* ; Heller, S.* ; Kleger, A.*

SARS-CoV-2 infects and replicates in cells of the human endocrine and exocrine pancreas.

Nat. Metab. 3, 149-165 (2021)
Postprint DOI PMC
Open Access Green
Infection-related diabetes can arise as a result of virus-associated β-cell destruction. Clinical data suggest that the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), causing the coronavirus disease 2019 (COVID-19), impairs glucose homoeostasis, but experimental evidence that SARS-CoV-2 can infect pancreatic tissue has been lacking. In the present study, we show that SARS-CoV-2 infects cells of the human exocrine and endocrine pancreas ex vivo and in vivo. We demonstrate that human β-cells express viral entry proteins, and SARS-CoV-2 infects and replicates in cultured human islets. Infection is associated with morphological, transcriptional and functional changes, including reduced numbers of insulin-secretory granules in β-cells and impaired glucose-stimulated insulin secretion. In COVID-19 full-body postmortem examinations, we detected SARS-CoV-2 nucleocapsid protein in pancreatic exocrine cells, and in cells that stain positive for the β-cell marker NKX6.1 and are in close proximity to the islets of Langerhans in all four patients investigated. Our data identify the human pancreas as a target of SARS-CoV-2 infection and suggest that β-cell infection could contribute to the metabolic dysregulation observed in patients with COVID-19.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Korrespondenzautor
ISSN (print) / ISBN 2522-5812
e-ISSN 2522-5812
Zeitschrift Nature metabolism
Quellenangaben Band: 3, Heft: 2, Seiten: 149-165 Artikelnummer: , Supplement: ,
Verlag Springer
Verlagsort London
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Diabetes and Regeneration Research (IDR)
Förderungen Baden-Württemberg Stiftung (Baden-Württemberg Foundation)
Deutsche Forschungsgemeinschaft (German Research Foundation)