SARS-CoV-2 may hijack body’s cholesterol system to help the spread

The SARS-CoV-2 virus, which causes COVID-19, may hijack our host cell’s internal cholesterol processing system to help it spread through the body, according to a study which hints at new targets for a potential therapy against the disease.

The cell culture study, published in the journal Nature Metabolism, intended to find a potential molecular connection between cholesterol metabolism and COVID-19.


The researchers from the Academy of Military Medical Sciences (AMMS) in China found that the SARS-CoV-2 clings on to a receptor on the human cells that usually binds to HDL cholesterol, also known as ‘good’ cholesterol.

When the researchers blocked the cholesterol receptor in the cells, the virus could no longer cling on to them. According to the researchers, this could help in the development of potential treatment of COVID-19.

SARS-CoV-2 uses the cell’s internal cholesterol mechanisms to enhance infection, as per the study. During SARS-CoV-2 infection, the spike protein on the virus binds a host-cell receptor called angiotensin-converting enzyme 2 (ACE2).

The researchers also stressed the role of another receptor, called HDL scavenger receptor B type 1 (SR-B1), which is present in several tissues of lung cells.

The researchers noted in their study that 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.

They conclude that the study highlights a potential molecular connection between COVID-19 and cholesterol, and they suggest that drugs targeting SR-B1 could inhibit COVID-19 infection.