Editor’s note: This article was originally published on December 9, 2021, after an earlier version of the study was posted to the preprint database. bioRxiv (Opens in a new tab). The article was updated on September 23, 2022 to reflect new information in the peer-reviewed journal.
The coronavirus SARS-CoV-2 directly affects fat cells and certain immune cells in adipose tissue, triggering inflammation, which can then spread to nearby uninfected “bystander” cells.
The study was published in the journal on September 22 Science Translational Medicine (Opens in a new tab)Scientists have experimented Fat The tissue is Corona virus. They found that the virus could infect and replicate in mature fat cells known as adipocytes, and these infected cells became inflamed. They also found that immune cells in the fat tissue, called macrophages, were infected and started a very aggressive inflammatory response.
In particular, the virus could not make new copies in the macrophages – the pathogen could be broken into immune cells, but the buck stopped there. However, even this short-term invasion caused a significant change in the macrophages, which caused them to secrete inflammatory substances in the surrounding tissues. There, immature fat cells called preadipocytes respond to the onslaught of chemical signals by burning themselves up.
These pre-adipocytes cannot be directly infected by SARS-CoV-2, the team found, but through this chain reaction, they are indirectly affected by the virus.
In addition to these experiments, the team examined the fat tissue of patients who died of Covid-19 infections and found the genetic material of the coronavirus in the fat surrounding various organs. Like viruses HIV And Influenza They can hide themselves in the fat tissue, as a way of hiding Immune system. Likewise, “adipose tissue may serve as a potential reservoir for SARS-CoV-2,” and in theory, this latent reservoir could contribute to persistent symptoms in people with prolonged COVID, the team wrote in their report.
Moreover, in two patients who died of Covid-19, the team found that inflammatory immune cells clustered around the infected adipocytes in the fatty tissue surrounding the heart. “This was very concerning to us, because epicardial fat is located next to the heart muscle, without any physical barrier,” said co-senior author Dr. Tracy McLaughlin, professor of endocrinology at Stanford University School of Medicine. press release (Opens in a new tab). “So any inflammation can directly affect the heart muscle or the heart arteries.”
Since the early days of the epidemic, obese people are more likely to be hospitalized and die from COVID-19. Live Science has previously reported. Several theories have been advanced to explain why fat may increase the risk of adverse covid-19 outcomes.
For starters, excess fat in the abdomen can push against the diaphragm, restricting airflow in the lungs; If people are struggling to get enough oxygen into their lungs on a good day, they may be getting worse with Covid-19. Science reports (Opens in a new tab). In addition, the blood of obese people tends to clot more easily than that of people with low levels of fat – another major problem in the context of Covid-19, which can cause widespread blood clots.
Also, when fat accumulates in the body, fat cells infiltrate the spleen, bone marrow, and thymus, where more immune cells are formed. This can weaken the immune system by reducing the number and effectiveness of the immune cells produced. Excess fat can trigger chronic, low-grade inflammation in the body, as fat cells release inflammatory substances. Cytokines And macrophages do the same in an effort to clear dead fat cells from the body, Science reports.
While all of these factors could worsen the effects of Covid-19 on obese people, there is now evidence that the virus directly affects fat cells.
“The infected fat tissue produces exactly the same inflammatory chemicals that you see in the blood of severe COVID patients,” said Dr. Catherine Blish, professor of infectious diseases at Stanford University School of Medicine. “It is reasonable to assume that high levels of saturated fat may contribute to the overall inflammatory profile of critically ill COVID-19 patients.”
It is still not clear how the virus enters fat and fat tissue-borne immune cells. This is because the study authors found small amounts of ACE2, the main “gateway” the virus uses to enter cells, in their tissue samples. “It is more likely that the virus enters through ACE2, because we have not been able to identify the protein that works in adipose tissue.” Blish said.
Originally published on Live Science.