![]() ![]() ![]() SARS-CoV-2 infection of these macrophages is abortive: It produces no viable viral progeny.īut it does induce a major mood change in the macrophages. The researchers identified a subset of macrophages in fat tissue that become infected by SARS-CoV-2, although only fleetingly. These cells (whose name derives from two Greek words meaning “big eaters”) carry out a number of actions ranging from tissue repair and general garbage cleanup to fierce attacks on perceived pathogens - sometimes producing substantial collateral damage to normal tissue in the process. Rigorous experiments showed that the virus could infect and replicate in fat cells, exit the cells and cause new infections in other cells.įat tissue contains not only fat cells but also a wide variety of immune cells, including a type called macrophages. Then, in a secure facility, the researchers infected the samples with a solution containing SARS-CoV-2 or, as a control, a SARS-CoV-2-free solution. The scientists obtained samples of fat tissue from various locations in the bodies of 22 patients undergoing bariatric or cardiothoracic surgery at the Stanford Medicine Bariatric Surgery and Cardiothoracic Surgery clinic. 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.” “Infected fat tissue pumps out precisely the inflammatory chemicals you see in the blood of severe COVID patients. “Fat tissue’s susceptibility to SARS-CoV-2 infection may be playing a role in making obesity a COVID-19 risk factor,” said Blish, who is the George E. Obese individuals are up to 10 times as likely to die from COVID-19, McLaughlin said, but increased risk for poor outcomes of SARS-CoV-2 infection begins at BMIs as low as 24. Someone with a BMI of 25 or greater is defined as being overweight. Obesity is defined medically as having a body mass index (weight in kilograms divided by the square of height in meters) of 30 or greater. Lead authorship is shared by former postdoctoral scholar Giovanny Martínez-Colón, PhD, and graduate student Kalani Ratnasiri. McLaughlin and Catherine Blish, MD, PhD, professor of infectious diseases, are the study’s senior authors. The findings are described in a study published online Sept. “With 2 of every 3 American adults overweight and more than 4 in 10 of them obese, this is a potential cause for concern,” said Tracey McLaughlin, MD, professor of endocrinology. The inflammation converts even uninfected “bystander” cells within the tissue into an inflammatory state. That, in turn, cooks up a cycle of viral replication within resident fat cells, or adipocytes, and causes pronounced inflammation in immune cells that hang out in fat tissue. Reasons offered for this increased vulnerability range from impaired breathing resulting from the pressure of extra weight to altered immune responsiveness in obese people.īut the new study provides a more direct reason: SARS-CoV-2, the virus that causes COVID-19, can directly infect adipose tissue (which most of us refer to as just plain “fat”). ![]()
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