Editor’s note: This article was first published on December 9, 2021, after an earlier version of the study was published in the preprint database. bioRxiv (opens in a new tab). The article was updated on September 23, 2022 to reflect new information contained in the peer-reviewed journal.
The SARS-CoV-2 coronavirus directly infects fat cells and specific immune cells found in fat tissue, causing inflammation that can then spread to nearby uninfected “bystander” cells.
In a study published Sept. 22 in the journal Science Translational Medicine (opens in a new tab)scientists experimented with fat tissue obtained from patients undergoing bariatric, cardiac, and thoracic surgery, to see if the tissue might be infected by the coronavirus. They found that the virus could infect and replicate within mature fat cells, known as adipocytes, and these infected cells became inflamed. They also found that specific subsets of immune cells housed within the fatty tissue, called macrophages, also became infected and triggered a much more intense inflammatory response.
In particular, the virus was unable to make new copies of itself inside macrophages: the pathogen could penetrate immune cells, but the ball stopped there. However, even this short-lived invasion triggered a significant change in the macrophages, causing them to shed inflammatory substances into the surrounding tissue. There, immature fat cells, called preadipocytes, reacted to the onslaught of chemical signals by swelling.
These preadipocytes cannot be directly infected with SARS-CoV-2, the team found, but through this chain reaction, the virus affected them indirectly.
Related: COVID-19 can infiltrate insulin-producing cells in the pancreas, study suggests
In addition to these experiments, the team examined fat tissue from patients who died from COVID-19 infections and found genetic material from the coronavirus in fat surrounding various organs. viruses like HIV Y influenza they can hide in fatty tissue, as a way to hide from the immune system. Similarly, “adipose tissue could serve as a potential reservoir for SARS-CoV-2” and, in theory, this hidden reservoir could contribute to the long-lasting symptoms seen in people with prolonged COVID, the team wrote in your report.
Furthermore, in two patients who died of COVID-19, the team found that inflammatory immune cells had assembled around infected adipocytes in the fatty tissue surrounding the heart. “This was of great concern to us, as epicardial fat sits right next to the heart muscle, with no physical barrier separating them,” co-senior author Dr. Tracey McLaughlin, a professor of endocrinology in the School of Medicine, said in a statement. Stanford University Medicine. statement (opens in a new tab). “So any inflammation there can directly affect the heart muscle or the coronary arteries.”
Since the early days of the pandemic, people with obesity have faced a higher risk of developing severe symptoms, requiring hospitalization, and dying from COVID-19. Live Science previously reported. Several theories emerged to explain why fat increased the risk of poor outcomes from COVID-19.
To begin with, excess fat in the abdomen can put pressure on the diaphragm and therefore restrict airflow in the lungs; if people are already struggling to get enough oxygen into their lungs on a good day, they may fare worse against COVID-19, reported science (opens in a new tab). Also, the blood of obese people tends to clot more easily than those with lower levels of fat, another major issue in the context of COVID-19, which can trigger extensive blood clotting.
Also, as fat accumulates in the body, the fat cells infiltrate the spleen, bone marrow, and thymus, where many immune cells are produced. This can weaken the immune system by reducing the number and undermining the effectiveness of the immune cells produced. Excess fat can also lead to chronic low-grade inflammation throughout the body, as fat cells release inflammatory substances called cytokines and macrophages do the same, in an effort to remove dead fat cells from the body, reported Science.
While all of these factors may worsen COVID-19 outcomes for people with obesity, there is now this evidence that the virus infects fat cells directly.
“Infected fat tissue pumps out precisely the inflammatory chemicals seen in the blood of severe COVID patients,” co-senior author Dr. Catherine Blish, a professor of infectious diseases in the UCLA School of Medicine, said in the statement. Stanford University. “It is reasonable to infer that having a lot of infected fat might contribute to the overall inflammatory profile of severely ill COVID-19 patients.”
It is not yet clear how the virus infiltrates fat and adipose tissue-borne immune cells. That’s because the study authors found negligible amounts of ACE2, the main “gateway” the virus uses to enter cells, in their tissue samples. “It’s very unlikely that the virus enters through ACE2, because we couldn’t detect the functional protein in adipose tissue,” Blish said.
Originally published on Live Science.