The coronavirus can infect body fat, new research suggests — a clue about obesity's link to severe COVID-19

• The coronavirus can directly infect fat cells, a recent study awaiting peer review found.
• The finding may help explain why obese or overweight people are more vulnerable to severe COVID-19.

More than two-thirds of American adults are obese or overweight, putting them at elevated risk of severe COVID-19 illness and death. Obesity in particular may triple the risk of hospitalization from the disease.

But for most of the pandemic, scientists haven't understood why.

While obesity-related conditions such as diabetes and heart disease can independently raise the risk of severe COVID-19, scientists now have evidence that body fat may be a contributing factor.

An October study from Stanford University that has not yet been peer-reviewed found that the coronavirus can directly infect fat cells. That process, in turn, may activate a harmful cascade of inflammation that damages other organs, such as the heart or lungs.

"It's an aspect of COVID that hasn't received a whole lot of attention," Dr. William Schaffner, a professor of infectious diseases at the Vanderbilt University School of Medicine, told Insider. "The fat itself may actually become a reservoir for the virus and somehow be involved in its inflammatory response."

Researchers have come to understand body fat as an active tissue rather than an inert mass. But scientists need further data to determine if extra body fat actually predisposes people with COVID-19 to hospitalization or death.

Researchers studied fat tissue in people who died of COVID-19

The Stanford researchers conducted two experiments to see how the coronavirus interacted with body fat.

In the first experiment, they collected samples of fat tissue from people about to undergo surgery, then exposed that tissue to the coronavirus. Not only did those fat cells become infected with the coronavirus, but the virus also infected certain macrophages — immune cells that can trigger inflammation — in and around the fat tissue.

The researchers noticed a dramatic inflammatory response shortly after the infection took hold, including an increase in several inflammatory molecules associated with severe COVID-19.

A second experiment reinforced those results: The researchers studied tissue samples from people in Europe who had died of COVID-19 and found the coronavirus had made its way into patients' fat tissue. Strikingly, virus concentrations in fat tissue samples were relatively on par with concentrations in heart and kidney samples, though lower than concentrations in lung samples.

The results were consistent with other studies showing that viruses like HIV and influenza can infect fat cells, the researchers wrote.

Since obese and overweight people tend to have more body fat than lower-weight people, their fat cells could give the coronavirus more opportunities to replicate or promote inflammation.

"If you really are very obese, fat is the biggest single organ in your body," David Kass, a professor of cardiology at Johns Hopkins, told The New York Times.

The researchers also theorized that obesity could contribute to long COVID, a condition characterized by persistent symptoms, such as fatigue, body aches, chest pain, or shortness of breath, that last weeks or months after a coronavirus infection.

Schaffner said the study could even offer clues about why obese people are more likely to have complications from other viral infections, such as the flu.

"Clearly, more studies are needed," he said. "But it's a very interesting line of investigation."