The AMMS (Academy of Military Medical Sciences) researchers in their study found that the SARS-CoV-2 virus sticks to a receptor on the human cells that usually binds to HDL cholesterol, also known as 'good' cholesterol. When the scientists blocked the cholesterol receptor in the cells, the virus was no longer able to stick to them.
The study further points out that SARS-CoV-2 virus, which causes COVID-19, may hijack our cells' internal cholesterol processing system to help it spread through the body. The cell culture study, published in the journal Nature Metabolism, identifies a potential molecular connection between cholesterol metabolism and COVID-19.
They say this hints at new targets for treatment, although this is very early-stage research. The study suggests that SARS-CoV-2 may use the cell's internal cholesterol mechanisms to enhance infection. During SARS-CoV-2 infection, the spike protein on the virus binds a host-cell receptor called angiotensin-converting enzyme 2 (ACE2). The researchers highlight the role of another receptor, called HDL scavenger receptor B type 1 (SR-B1), which is expressed in several tissues, including human lung cells.
This receptor usually binds high-density lipoprotein. However, in this study, the viral spike protein-bound cholesterol, and expression of SR-B1 and the presence of HDL together helped the virus bind and enter ACE2-expressing cells.