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, revealed the team from Oregon Health & Science University (OHSU) and the US Department of Energy (DoE).
However, in the paper published in Nature Communications journal, the team cautioned that the results are in cell culture, not in people, and much more research remains to see if such compounds hold promise for people diagnosed with Covid.
“As the virus replicates, it needs a continuous supply of energy,” said Fikadu Tafesse, Assistant Professor of molecular microbiology and immunology at OHSU.
“More triglycerides could provide that energy in the form of fatty acids. But we don’t know exactly how the virus uses these lipids to its advantage,” Tafesse added.
In the study, 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 per cent 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.
It turns out that those oily blobs of fat are also critical for the Covid virus.
The team found that SARS-CoV2 doesn’t 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.
At the same time, an approved weight-loss medication, Orlistat, a lipase inhibitor, and an experimental compound known as GSK2194069 stopped the virus. These and other compounds worked against all the SARS-CoV2 variants tested: Alpha, Beta, Gamma and Delta.
