Dr. Dirk Homann

The relationship between SARS-CoV-2 infection and diabetes has been proposed to exhibit a “bidirectional dynamic”, where pre-existing diabetes may exacerbate the course of COVID-19, and SARS-CoV-2 infection, in turn, may precipitate diabetes. Thus far, both type 1 and type 2 diabetes have been firmly established as independent risk factors of COVID-19 morbidity and mortality. In contrast, support for SARS-CoV-2 infection as a trigger for diabetes is based on more limited albeit tantalizing observations.


In this webinar, Dr. Dirk Homann of Icahn School of Medicine at Mount Sinai, will describe a series of ongoing studies: expression patterns of viral entry factors in pancreatic tissue; permissiveness of pancreatic tissue to in vitro SARS-CoV-2 infection; histopathological alterations in pancreatic COVID-19 autopsy samples; humanized mouse models to test the diabetogenicity of SARS-CoV-2 infection in vivo. Together with epidemiological data, these studies challenge the concept of a “bidirectional dynamic” in that they do not support a direct diabetogenic potential of SARS-CoV-2 infection. It remains to be assessed if a prior history of COVID-19 correlates with enhanced diabetes incidence at later stages.


What you will learn:

  • The critical importance of leveraging complementary strains of evidence to demonstrate a hypothesized SARS-CoV-2 infection etiology of diabetes.
  • The balanced assessment of experimental and epidemiological evidence currently does not support the notion of SARS-CoV-2 infection as a trigger for acute diabetes onset.

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