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    Home > Active Ingredient News > Immunology News > Wang Hongyan/Wei Bin collaboration reveals a new mechanism for cholesterol metabolism regulation of innate immune resistance to infection, cellPress dialogue scientists.

    Wang Hongyan/Wei Bin collaboration reveals a new mechanism for cholesterol metabolism regulation of innate immune resistance to infection, cellPress dialogue scientists.

    • Last Update: 2020-07-23
    • Source: Internet
    • Author: User
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    Viral infection can induce host cells to change the expression of cholesterol metabolizing enzymes and metabolites, and cholesterol metabolism can also regulate the antiviral response of host cells.recent international frontier work indicates that targeting individual key cholesterol metabolic enzymes and metabolites can improve the function of antiviral infection [1] [2] [3].recently, the Wang Hongyan research group of the center for excellence and innovation of molecular cell science of Chinese Academy of Sciences (Institute of Biochemistry and cell biology, hereinafter referred to as "molecular cell center") cooperated with Wei bin Laboratory of Shanghai University (formerly Wuhan virus Institute of Chinese Academy of Sciences) to screen and find that 7-dehydrocholesterol reductase (DHCR7) is knocked out or inhibited or 7-dehydrogenation of natural cholesterol metabolite is added Cholesterol (7-DHC) can promote the activation of transcription factor IRF3 and enhance the production of ifn-1 (such as IFN β), and then enhance macrophages or mice to eliminate various virus infections, including zikv, H1N1 and HSV.this study provides a new drug target for resistance to new or highly pathogenic virus infection.the results were published online on the journal immunity of cell press on December 24, and has applied for relevant patents.(
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