The virus that causes COVID-19 performs a takeover of the body’s fat-processing system, creating cellular storehouses of fat empowering the virus to hijack the body’s molecular machinery and cause disease.

After scientists discovered the important role of fat for SARS-CoV-2, they used weight-loss drugs and other fat-targeting compounds to try to stop the virus in cell culture.
Cut off from its fatty fuel, the virus stopped replicating within 48 hours. But the authors caution that the results are in cell culture, not in people.
Much more research is needed to see if such compounds hold promise for people diagnosed with COVID.
Fikadu Tafesse, the corresponding author of the study and an Assistant Professor of Molecular Microbiology, said: “This is exciting work, but it’s the start of a very long journey. We have an interesting observation, but we have a lot more to learn about the mechanisms of this disease.”
The team embarked on the study based on observations that people with a high body-mass index and conditions such as cardiovascular disease are more sensitive to the disease.
They studied the effect of SARS-CoV-2 on more than 400 lipids in two different human cell lines. Scientists found a massive shift in lipid levels, with some fats increasing as much as 64-fold. In one cell line, nearly 80% of fats were altered by the virus; in the other, levels of slightly more than half were changed.
The lipids affected most were triglycerides, which are crucial for our health, allowing us to store energy and to maintain healthy membranes in our cells.
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