The virus that causes COVID-19 takes over the body's fat-processing system, creating cellular storehouses of fat that empower 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.

The authors of the recent paper in Nature Communications caution that the results are in cell culture, not in people; much more research needs to be done to see if such compounds hold promise for people diagnosed with COVID-19. But the scientists, from Oregon Health & Science University (OHSU) and the Department of Energy's Pacific Northwest National Laboratory (PNNL), call the work a significant step toward understanding the virus.

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"This is exciting work, but it's the start of a very long journey," said Fikadu Tafesse, the corresponding author of the study and assistant professor of molecular microbiology and immunology at OHSU. "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 (BMI) and conditions like cardiovascular disease and diabetes are more sensitive to the disease.

'An attractive target for a virus'

The team 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 percent of fats were altered by the virus; in the other, levels of slightly more than half were changed.

The lipids affected most were triglycerides, those little packets of fat that most patients try to keep to a minimum. Triglycerides are crucial for our health, allowing us to store energy and to maintain healthy membranes in our cells.

"Lipids are an important part of every cell. They literally hold us together by keeping our cells intact, and they're a major source of energy storage for our bodies," said Jennifer Kyle, a biomedical scientist at PNNL who specializes in the measurement of lipids. "They are an attractive target for a virus."

The team found that SARS-CoV2 does not simply boost the number of triglycerides in our cells. The virus also changes much of our fat-processing system, changing the body's ability to use fat as fuel.