• Katie C Coate, Jeeyeon Cha, Shristi Shrestha, Wenliang Wang, Luciana Mateus Gonçalves, Joana Almaça, Meghan E Kapp, Maria Fasolino, Ashleigh Morgan, Chunhua Dai, Diane C Saunders, Rita Bottino, Radhika Aramandla, Regina Jenkins, Roland Stein, Klaus H Kaestner, Golnaz Vahedi, HPAP Consortium, Marcela Brissova, and Alvin C Powers.
• Division of Diabetes, Endocrinology and Metabolism, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN 37232, USA.
• Cell Metab. 2020 Dec 1; 32 (6): 1028-1040.e4.

AbstractIsolated reports of new-onset diabetes in individuals with COVID-19 have led to the hypothesis that SARS-CoV-2 is directly cytotoxic to pancreatic islet β cells. This would require binding and entry of SARS-CoV-2 into β cells via co-expression of its canonical cell entry factors, angiotensin-converting enzyme 2 (ACE2) and transmembrane serine protease 2 (TMPRSS2); however, their expression in human pancreas has not been clearly defined. We analyzed six transcriptional datasets of primary human islet cells and found that ACE2 and TMPRSS2 were not co-expressed in single β cells. In pancreatic sections, ACE2 and TMPRSS2 protein was not detected in β cells from donors with and without diabetes. Instead, ACE2 protein was expressed in islet and exocrine tissue microvasculature and in a subset of pancreatic ducts, whereas TMPRSS2 protein was restricted to ductal cells. These findings reduce the likelihood that SARS-CoV-2 directly infects β cells in vivo through ACE2 and TMPRSS2.Copyright © 2020 Elsevier Inc. All rights reserved.

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