Journal
JCI INSIGHT
Volume 6, Issue 16, Pages -Publisher
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/jci.insight.151551
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Funding
- Tulane University Histology core
- University Medical Center - New Orleans Histology Laboratory
- NIH [DK074970, DK107444, P510D011104]
- Department of Veterans Affairs Merit Review Award [BX003725]
- American Diabetes Association COVID-19 Diabetes Research Award [7-20-COVID-051]
- Tulane Center of Excellence in Sex-Based Biolo-gy Medicine
- Tulane University Fast Grant [COVID-19]
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Evidence suggests that SARS-CoV-2 infection may lead to pancreatic inflammation and fibrosis, potentially resulting in new-onset diabetes. Signs of SARS-CoV-2 infection were found in the pancreas of both monkeys and humans.
Evidence suggests an association between severe acute respiratory syndrome-cornavirus-2 (SARSCoV-2) infection and the occurrence of new-onset diabetes. We examined pancreatic expression of angiotensin-converting enzyme 2 (ACE2) and transmembrane serine protease 2 (TMPRSS2), the cell entry factors for SARS-CoV-2, using publicly available single-cell RNA sequencing data sets, and pancreatic tissue from control male and female nonhuman primates (NHPs) and humans. We also examined SARS-CoV-2 immunolocalization in pancreatic cells of SARS-CoV-2-infected NHPs and patients who had died from coronavirus disease 2019 (COVID-19). We report expression of ACE2 in pancreatic islet, ductal, and endothelial cells in NHPs and humans. In pancreata from SARSCoV-2-infected NHPs and COVID-19 patients, SARS-CoV-2 infected ductal, endothelial, and islet cells. These pancreata also exhibited generalized fibrosis associated with multiple vascular thrombi. Two out of 8 NHPs developed new-onset diabetes following SARS-CoV-2 infection. Two out of 5 COVID-19 patients exhibited new-onset diabetes at admission. These results suggest that SARSCoV-2 infection of the pancreas may promote acute and especially chronic pancreatic dysfunction that could potentially lead to new-onset diabetes.
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