Human fat cells can be directly infected with the CCP (Chinese Communist Party) virus, providing an additional site for the virus to replicate, according to a group of Stanford researchers who set out to determine the COVID-19 risk posed directly by obesity.
According to the researchers mainly based at Stanford’s School of Medicine, studies have shown that fat cells can act as a reservoir for RNA viruses like influenza A and HIV. Their new research, which was released in an October preprint and is awaiting peer-review, suggests that the same is occurring with the CCP virus, which causes the disease COVID-19.
Overweight and obese individuals are known to be at higher risk of COVID-19 infection, severe illness, and death. However, the direct contribution of fatty tissue, also known as adipose tissue, to severe disease is still not well understood given the long list of comorbidities associated with obesity and COVID-19, like hypertension and metabolic disease.
According to the study, researchers confirmed they found SARS-CoV-2, another name for the virus, directly infecting fatty tissue surrounding various organs in autopsies of European COVID-19 patients who had recently died.
The findings also describe, for the first time, experiments observing a “dramatic inflammatory response” in components of the fatty tissue consistent with that reported in patients with severe COVID-19 symptoms.
For the experiment, adipose tissue was taken from bariatric and cardiothoracic surgery patients and immediately exposed to SARS-CoV-2. Researchers observed different responses between components of the adipose tissue, which is made up of mature fat cells (also called adipocytes), pre-adipocytes (which turn into adipocytes), and various types of immune cells.
In these lab exposures, SARS-CoV-2 was also found to replicate in adipocytes, and although not much inflammation was observed directly in these cells, their infection drove a strong inflammatory response in a subset of infected macrophage immune cells as well as, to a lesser extent, pre-adipocytes, which did not become infected.
The findings, if approved by peer-review despite a lack of samples from lean control subjects and related issues, would provide some evidence that infected fatty tissue likely contribute to the secretion of substances that boost the inflammatory reactions contributing to severe COVID-19.
“Whatever happens in fat doesn’t stay in fat,” Philipp Scherer, who studies fat cells at UT Southwestern Medical Center in Dallas but was not involved in the research, told The New York Times of the implications of the findings. “It affects the neighboring tissues as well.”
Scherer added that the indications from the lab research still need to be compared with the responses occurring directly in fatty tissue as arranged in the human body (in vivo studies).
Study co-author Dr. Catherine Blish from the Stanford University School of Medicine told the New York Times that the results show that processes in human fatty tissue “could well be contributing to severe disease.”
“We’re seeing the same inflammatory cytokines that I see in the blood of the really sick patients being produced in response to infection of those tissues,” she said.
Scientists had hope with this research that they might be able to find better ways to help treat overweight COVID-19 patients.
Authors say the observations suggest that lysozyme therapy could help reduce SARS-CoV-2 levels in adipose tissue, a step towards reducing severe disease. Lysozyme is a natural enzyme found in secretions such as tears, saliva, and milk that weakens cell-walls.
“Collectively, our data implies that infection in adipose tissue may partially explain the link between obesity and severe COVID-19,” the authors wrote. “More efforts to understand the complexity and contributions of this tissue to COVID-19 pathogenesis are warranted.”