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). Article updated 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 cells.
In a study published September 22 in the journal Translational Medicine Sciences (Opens in a new tab)Try the scientists Fat Tissue taken from patients undergoing bariatric, heart and chest surgeries, to see if the tissue can become infected Corona Virus. They found that the virus can infect and replicate inside mature fat cells, known as adipocytes, and these infected cells become inflamed. They also found that certain subsets of immune cells found within fat tissue, called macrophages, also became infected and triggered a more intense inflammatory response.
Notably, the virus could not make new copies of itself inside macrophages – the pathogen could break into immune cells, but the responsibility stopped there. However, even this short-lived invasion caused a significant change in the macrophages, causing the release of inflammatory substances into the surrounding tissues. There, immature fat cells, called former fat cells, responded to the onslaught of chemical signals by inflaming themselves.
The team found that these adipocytes could not be directly infected with SARS-CoV-2, but through this chain reaction, they were indirectly affected by the virus.
In addition to these experiments, the team examined the fatty tissue of patients who had died of COVID-19 infection and found genetic material for the coronavirus in the fat that surrounds various organs. Viruses like human immunodeficiency virus And the flu It can shed itself in fatty tissue, as a way to hide from immune system. Likewise, the team wrote in its report that “adipose tissue could serve as a potential reservoir for SARS-CoV-2,” and in theory, this hidden reservoir could contribute to the long-term persistence of symptoms in people infected with the COVID virus.
Moreover, in two patients who died of COVID-19, the team found that inflammatory immune cells had congregated around the affected adipocytes in the fatty tissue surrounding the heart. “This was a major concern for us, as the epicardial fat is located right next to the heart muscle, and there is no physical barrier separating it,” said lead researcher Dr. Tracy McLaughlin, professor of endocrinology at Stanford University School of Medicine. statement (Opens in a new tab). Therefore, any inflammation there may directly affect the heart muscle or the coronary arteries.
Since the early days of the epidemic, obese people have faced a higher risk of developing severe symptoms requiring hospitalization and dying from COVID-19, Live Science previously reported. A number of theories have emerged to explain why excess fat increases the risk of poor COVID-19 outcomes.
For starters, excess belly fat can put pressure on the diaphragm and thus 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, I mentioned science (Opens in a new tab). In addition, the blood of obese people tends to clot more easily than those with lower lipid levels – another major problem in the context of COVID-19, which can lead to widespread coagulation.
In addition, as fat accumulates in the body, 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 immune-producing cells. Excess fat can also lead to chronic low-grade inflammation throughout the body, as fat cells release inflammatory substances called cytokines Science reports that macrophages do the same, trying to remove dead fat cells from the body.
While all of these factors may worsen the outcome of COVID-19 for people with obesity, there is now evidence that the virus directly infects fat cells.
“Infected adipose tissue delicately pumps out the inflammatory chemicals you see in the blood of severe Covid patients,” Dr. Catherine Bleich, professor of infectious diseases at Stanford University School of Medicine, said in the statement. “It is reasonable to conclude that having a lot of affected fat could contribute to the overall inflammatory profile of critically ill COVID-19 patients.”
It is still not clear how the virus infiltrates fat-borne immune cells and adipose tissue. That’s because the study’s authors found trace amounts of ACE2 – the main “portal” the virus uses to enter cells – in their tissue samples. “It is highly unlikely that the virus entered through ACE2, because we were unable to detect the functional protein in adipose tissue,” Bleach said.
Originally published on Live Science.