The coronavirus infects fat cells, study shows

Editor’s Note: This article was first run on December 9, 2021 after a previous version of the study was posted to the preprint database. Bio Rxiv (opens in new tab)This article was updated on September 23, 2022 to reflect new information contained in peer-reviewed journals.

The coronavirus SARS-CoV-2 can directly infect certain immune cells found in fat cells and adipose tissue, causing inflammation and spreading to nearby uninfected “bystander” cells.

In a study published September 22 in the journal Science Translational Medicine (opens in new tab)scientists have experimented thick Tissue taken from patients who have undergone bariatric surgery, heart surgery, or thoracic surgery to see if the tissue may be infected. coronavirusThey found that the virus can infect and replicate in mature fat cells, known as adipocytes, and these infected cells become inflamed. They also found that a specific subset of immune cells housed within adipose tissue called macrophages also become infected and initiate a much stronger inflammatory response.

Notably, the virus failed to create new copies of itself within macrophages. Pathogens can invade immune cells, but the expense stopped there. But even this brief invasion caused profound changes in macrophages, causing them to spit out inflammatory substances into the surrounding tissue. It reacted with inflammation.

The team found that these preadipocytes are not directly infected with SARS-CoV-2, but are indirectly affected by the virus through this chain reaction.

In addition to these experiments, the team examined adipose tissue from patients who died of COVID-19 infection and found coronavirus genetic material in the fat surrounding various organs.viruses like HIV When influenza You can hide in fatty tissue as a way to hide from. immune systemSimilarly, “adipose tissue may serve as a potential reservoir for SARS-CoV-2,” and it is theoretically possible that this hidden reservoir contributes to the persistent symptoms seen in long-term patients with COVID. The team wrote in its report that it could.

Additionally, in two patients who died of COVID-19, the team found that inflammatory immune cells clustered around infected fat cells in the adipose tissue surrounding the heart. “This was a big concern for us because the epicardial fat is right next to the myocardium and there is no physical barrier separating them,” says Tracy, co-lead author and professor of endocrinology at Stanford University School of Medicine. Dr. McLaughlin says statement (opens in new tab)“So inflammation can directly affect the heart muscle and coronary arteries.”

Since the early days of the pandemic, obese people have developed severe symptoms, required hospitalization, and were at increased risk of dying from COVID-19. Previously reported live scienceA number of theories have emerged to explain why fat increases the risk of adverse COVID-19 outcomes.

First of all, excess fat in the abdomen can push against the diaphragm, restricting airflow in the lungs. People who already struggle to get enough oxygen into their lungs on sunny days may be even worse off against COVID-19. science reported (opens in new tab)Additionally, the blood of obese people tends to clot more easily than those with low fat levels. This is another big problem in his COVID-19 situation which can cause extensive blood clots.

Furthermore, when fat accumulates in the body, adipocytes infiltrate the spleen, bone marrow, and thymus, producing many immune cells. This can weaken the immune system as it reduces the number of immune cells produced and compromises their effectiveness. Excess fat can also cause chronic low-grade inflammation throughout the body as fat cells release inflammatory substances called pro-inflammatory substances. cytokine Macrophages also do the same to rid the body of dead fat cells, Science reports.

All of these factors could exacerbate COVID-19 outcomes for obese people, but there is now evidence that the virus directly infects fat cells.

“Infected adipose tissue excretes precisely the inflammatory chemicals found in the blood of severe COVID patients,” said co-lead author Katherine Blish, Ph.D., professor of infectious diseases at Stanford University School of Medicine, in a statement. “It is reasonable to speculate that high levels of infected fat may contribute to the overall inflammatory profile in patients with severe COVID-19.”

It is not yet clear how the virus enters immune cells derived from fat and adipose tissue. This is because we discovered the main “doorway” to use for “Since we were unable to detect any functional protein in adipose tissue, it is highly unlikely that the virus entered through ACE2,” Blish said.

Originally published in Live Science.

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