Reporter : Feng Lifei / Publisher : China Science News / http://news.sciencenet.cn/htmlnews/2020/11/449245.shtm / Translation, editing : Gan Yung Chyan, KUCINTA SETIA
Zhong Hui of the Institute of Bioengineering of the Chinese Academy of Military Medical Sciences (Beijing) and his colleagues found that SARS-CoV-2 (covi, CCP virus, novel coronavirus) may use the intrinsic cholesterol metabolism of cells to enhance infection. Related research results were published online in "Nature-Metabolism" on November 26. This discovery may help explain why patients with covid and metabolic diseases (such as diabetes) or cardiovascular diseases have higher morbidity and mortality, and suggest new targets for potential therapeutic interventions.
When a covi infection occurs, the spike protein of the novel coronavirus binds to the host cell receptor angiotensin converting enzyme 2 (ACE2). In a cell culture study, the role of another receptor, HDL Class B scavenger receptor type 1 (SR-B1), was emphasized. SR-B1 is expressed in several tissues, including human lung cells. This receptor usually binds to high-density lipoprotein (HDL, also known as good cholesterol), but in this study, cholesterol bound to the viral spike protein, SR-B1 expression and high-density lipoprotein together helped the new coronavirus to bind And enter ACE2 expressing cells.
Covi seems to hijack the cholesterol uptake machinery of the cell to help the virus enter the host cell, but when the author uses monoclonal antibodies or a specific pharmacological antagonist of SR-B1 to block this pathway, HDL-mediated enhancement of viral infection does not exist. The authors concluded that this study highlights the potential molecular link between new coronary pneumonia and cholesterol, and suggests that drugs targeting SR-B1 may help curb the covi infection.
Related paper information: https://doi.org/10.1038/s42255-020-00324-0
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