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 in the peer-reviewed journal.
The SARS-CoV-2 coronavirus directly infects fat cells and specific immune cells found in fat tissue, triggering inflammation that can then spread to nearby uninfected “bystander” cells.
In a study published September 22 in the journal Science Translational Medicine (opens in a new tab)scientists have experimented big tissue obtained from patients undergoing bariatric, cardiac and thoracic surgeries, to see if the tissue could be infected with the coronavirus. They discovered that the virus could infect and replicate in mature fat cells, called adipocytes, and these infected cells became inflamed. They also discovered that specific subsets of immune cells housed in fatty tissue, called macrophages, were also infected and triggered a much more intense inflammatory response.
Notably, the virus couldn’t make new copies of itself inside macrophages – the pathogen could enter immune cells, but the blame stops there. However, even this short-lived invasion triggered a significant change in macrophages, causing them to spew inflammatory substances into surrounding tissues. There, immature fat cells, called pre-adipocytes, reacted to the onslaught of chemical signals by igniting themselves.
These pre-adipocytes cannot be directly infected with SARS-CoV-2, the team found, but through this chain reaction they were indirectly affected by the virus.
Related: COVID-19 can infiltrate insulin-producing cells in the pancreas, study finds
In addition to these experiments, the team examined fatty tissue from patients who died from COVID-19 infections and found coronavirus genetic material in the fat that surrounded various organs. viruses like HIV and flu can skim into 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 persistent symptoms seen in people with long COVID, the team wrote in their report. .
Additionally, in two patients who died of COVID-19, the team found that inflammatory immune cells had gathered around infected adipocytes in the fatty tissue surrounding the heart. “We were very concerned about this because epicardial fat sits right next to heart muscle, with no physical barrier separating them,” said co-lead author Dr. Tracey McLaughlin, professor of endocrinology at Stanford University School of Medicine. Medical. statement (opens in a new tab). “So any inflammation can directly affect the heart muscle or the coronary arteries.”
Since the early days of the pandemic, obese people have faced a higher risk of developing severe symptoms, requiring hospitalization and dying from COVID-19, Previously reported Live Science. A number of theories have arisen as to why fat increases the risk of poor COVID-19 outcomes.
For starters, excess fat in the abdomen can push on the diaphragm and thus restrict airflow into the lungs; if people already struggle to get enough oxygen to their lungs on a good day, they may fare worse against COVID-19, Scientific report (opens in a new tab). In addition, the blood of obese people tends to clot more easily than that of people with low fat levels – another major problem in the context of COVID-19, which can trigger significant 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 both the number and efficiency of immune cells produced. Excess fat can also cause chronic, low-grade inflammation throughout the body, as fat cells release inflammatory substances called cytokines and macrophages do the same, in an effort to slough off dead fat cells from the body, Science reported.
While all of these factors can worsen COVID-19 outcomes for obese people, there is now evidence that the virus directly infects fat cells.
“Infected fatty tissue pumps out precisely the inflammatory chemicals you see in the blood of severe COVID patients,” said co-lead author Dr. Catherine Blish, professor of infectious diseases at Stanford University School of Medicine, in the press release. “It is reasonable to infer that having a lot of infected fat could contribute to the overall inflammatory profile of critically ill COVID-19 patients.”
It is still unclear how the virus infiltrates fat and adipose tissue-borne immune cells. That’s because the study authors found negligible amounts of ACE2 – the main “doorway” 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 posted on Live Science.
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