Obesity is an established independent risk factor for SARS-CoV-2 infection as well as for the patients’ progression, once infected, to severe disease and death. Possible reasons range from impaired breathing resulting from the pressure of extra weight to altered immune responsiveness in obese people.
But a new Stanford School of Medicine study provides a more straightforward reason: SARS-CoV-2 can directly infect fat tissue. That, in turn, cooks up a cycle of viral replication within resident fat cells and causes pronounced inflammation in immune cells that hang out in fat tissue. The inflammation converts even uninfected “bystander” cells within the tissue into an inflammatory state.
The researchers observed this in fat tissue excised from patients undergoing stomach and heart surgeries and later infected in a laboratory dish with SARS-CoV-2. They confirmed their findings in autopsy samples from deceased COVID-19 patients.
Fat tissue surrounds our hearts, guts, kidneys and pancreases, which can be adversely affected by tissue inflammation. Ominously, the scientists found infection capable of driving inflammation in virtually every SARS-CoV-2-infected fat-tissue sample they collected and analyzed.
“It’s reasonable to infer that having a lot of infected fat could contribute to the overall inflammatory profile of severely ill COVID-19 patients,” said Catherine Blish, MD, PhD, professor of infectious diseases, co-senior author of the Science Translational Medicine study published in September 2022.
It could also contribute to the enduring post-infection symptoms collectively called long COVID, a hypothesis Blish and the study’s other co-senior author, Tracey McLaughlin, MD, professor of endocrinology and of infectious diseases, are exploring.
“With more than 4 in 10 American adults overweight, this is a potential cause for concern,” McLaughlin said.
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