In people with COVID-19, the SARS-CoV-2 virus can also infect the pancreatic islet cells and replicate there. This is the result of a recent study in which DZD researchers also participated. The study has now been published in Nature Communications.
Metabolic disorders increase the risk of severe courses of COVID-19 disease. On the other hand, new-onset hyperglycemia (elevated blood glucose levels), metabolic derailments (ketoacidosis), diabetes, and severe metabolic complications of pre-existing diabetes, among others, are also observed in COVID-19 patients. But what is the cause of this? Does the virus also infect the insulin-producing beta cells? Initial studies on stem cells indicated that the SARS-CoV-2 virus can infiltrate and infect human alpha cells and the insulin-producing beta cells of the pancreas and can replicate there. Now, a team of researchers has analyzed pancreatic autopsy tissue from COVID-19 patients. Here, too, they found viral SARS-CoV-2 inﬁltration of beta cells. Using SARS-CoV-2 pseudoviruses, the team also demonstrated that isolated human islet cells are susceptible (permissive) to infection.
In eleven COVID-19 patients, the team of scientists examined the expression of various receptors and factors that can facilitate viral entry, including ACE2. They found that while 70% of COVID-19 patients expressed ACE2 in the circulatory system, only 30% displayed ACE2 expression in beta cells.
"In summary, using human islet cells and autopsy tissue from patients who died of COVID-19, we have provided unequivocal evidence that beta cells are permissive for infection with SARS-CoV-2," said last author Stefan Bornstein of the DZD-Paul Langerhans Institute Dresden of Helmholtz Zentrum München at the University Hospital and Medical Faculty Carl Gustav Carus of TU Dresden. "However, the exact mechanisms of viral entry are not fully understood at this point, as ACE2 is expressed in beta cells only in a subset of patients."
Steenblock et al.: Viral infiltration of pancreatic islets in patients with COVID-19. Nature Communications (2021) 12:3534, DOI: doi.org/10.1038/s41467-021-23886-3