COVID can infect fat cells. May explain why some get much sicker

The virus that causes COVID-19 can infect and replicate in fat cells, and cause inflammation in fat tissue, Stanford University researchers found in a new study that could help explain why obese people are at a higher risk for severe COVID.

Since the early days of the pandemic, doctors and researchers have observed that people who are obese, across many ethnic groups, experience disproportionately bad COVID outcomes, including hospitalization, ICU admission, mechanical ventilation and death. But it wasn’t clear how or why.

The study, published last week in the journal Science Translational Medicine, offers some potential clues, though its authors caution there’s still much to uncover about the link between obesity and severe COVID.

The analysis found that SARS-CoV-2 can infect two types of cells in fat tissue — the fat cells themselves, called adipocytes, as well as immune cells in fat tissue, called macrophages. When the virus infects macrophages, it results in a big inflammatory response, which potentially contributes to overall inflammation seen in severe COVID cases.

It may not be as simple as the more fat cells someone has, the more likely they are to develop severe COVID.

“It’s certainly possible, but we didn’t directly address that in our study because it’s a little challenging,” said study co-author Dr. Catherine Blish, a professor of medicine in the division of infectious diseases at Stanford. “That’s certainly our worry. If fat is a source (of infection) and you have more fat and inflammation, it could contribute to that disease. But that’s an important area of ​​future investigation.”

The analysis also uncovered another important and potentially concerning finding: the fat around vital organs, known as visceral fat, can also be infected with the virus. This type of fat makes up a smaller proportion of the body’s fat than subcutaneous fat, which is just under the skin and makes up the majority of the body’s fat.

Visceral fat “is adjacent to vital organs, and inflammation in the fat could have a damaging regional effect on the organs it surrounds, such as the heart and kidney,” said co-author Dr. Tracey McLaughlin, a Stanford endocrinologist who studies fat cells and fat tissue.

The study analyzed autopsy samples from people who died of COVID, as well as fat samples from people who did not have COVID. For the latter group, the samples were collected from people undergoing weight-loss surgery or cardiothoracic surgery, and the samples were later infected with the virus in a dish in a lab.

It’s not clear from the study how the virus, which initially enters the body through the upper respiratory tract, gets into fat tissue.

The findings open the door to other questions, such as whether treatments can be developed to halt viral replication or the inflammatory response in fat cells. This could be similar to how the antiviral remdesivir, which has been used to treat severe COVID patients since 2020, blocks viral replication of SARS-CoV-2, but in fat cells specifically.

The researchers are further exploring the link between obesity and long COVID syndrome in an ongoing large study funded by the National Institutes of Health, Blish said.

Catherine Ho (she/her) is a San Francisco Chronicle staff writer. Email: Twitter: @Cat_Ho

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