The ability of the virus to infect adipose tissue may explain why obesity increases the risk of serious disease.
Obesity is a proven independent risk factor for SARS-CoV-2 infection as well as disease progression from infection to death. Stanford writes that possible causes range from respiratory impairment as a result of weight pressure to altered immune responses in obese people.
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A new study from the Stanford School of Medicine offers a simpler reason: SARS-CoV-2 can infect fat tissue directly. This triggers the virus reproduction cycle in fat cells and causes significant inflammation in immune cells in adipose tissue. Inflammation affects even uninfected cells.
The researchers observed this in adipose tissue from patients who had undergone gastric and heart surgery and subsequently became infected with SARS-CoV-2 in the laboratory. They confirmed their findings in autopsy samples from deceased COVID-19 patients.
Adipose tissue surrounds our heart, intestines, kidneys, and pancreas, which can be adversely affected by inflammation. Surprisingly, the scientists found an infection that could cause inflammation in nearly every SARS-CoV-2-infected adipose tissue sample they collected and analyzed.
“It is reasonable to speculate that having large amounts of infected fat may contribute to the overall inflammatory profile of critically ill COVID-19 patients,” said Katherine Blish, Professor of Infectious Diseases and co-author of Translational Medicine Science.
It may also contribute to persistent post-infection symptoms, collectively termed prolonged COVID. This hypothesis is being explored by Blish and another co-author of the study, Tracey McLaughlin, professor of endocrinology and infectious diseases.
Previously Focus He wrote that COVID has taken over the entire human body. In the largest post-mortem tissue study to date, scientists are finding traces of the SARS-CoV-2 virus throughout the body, from the brain and heart to the eyes.
Source: Focus
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