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Viral infiltration of pancreatic islets in patients with COVID-19 #MMPMID34112801
Steenblock C; Richter S; Berger I; Barovic M; Schmid J; Schubert U; Jarzebska N; von Massenhausen A; Linkermann A; Schurmann A; Pablik J; Dienemann T; Evert K; Rodionov RN; Semenova NY; Zinserling VA; Gainetdinov RR; Baretton G; Lindemann D; Solimena M; Ludwig B; Bornstein SR
Nat Commun 2021[Jun]; 12 (1): 3534 PMID34112801show ga
Metabolic diseases are associated with an increased risk of severe COVID-19 and conversely, new-onset hyperglycemia and complications of preexisting diabetes have been observed in COVID-19 patients. Here, we performed a comprehensive analysis of pancreatic autopsy tissue from COVID-19 patients using immunofluorescence, immunohistochemistry, RNA scope and electron microscopy and detected SARS-CoV-2 viral infiltration of beta-cells in all patients. Using SARS-CoV-2 pseudoviruses, we confirmed that isolated human islet cells are permissive to infection. In eleven COVID-19 patients, we examined the expression of ACE2, TMPRSS and other receptors and factors, such as DPP4, HMBG1 and NRP1, that might facilitate virus entry. Whereas 70% of the COVID-19 patients expressed ACE2 in the vasculature, only 30% displayed ACE2-expression in beta-cells. Even in the absence of manifest new-onset diabetes, necroptotic cell death, immune cell infiltration and SARS-CoV-2 viral infection of pancreatic beta-cells may contribute to varying degrees of metabolic dysregulation in patients with COVID-19.