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根據德國科學家研究發現,The novel coronavirus 2019 (2019-nCoV) uses the SARS-coronavirus receptor ACE2 and the cellular protease TMPRSS2 for entry into target cells(於January 31, 2020發表在bioRxiv上)。也就是說採用了跟SARS相同的路線感染細胞。當然不排除還有其他不同途徑。同時發現sars患者血清能夠中和2019-nCoV,也就是說sars抗體能夠治療2019-nCov。
那麼我們來看一下sars病毒進入細胞的一些途徑和阻斷靶點。

根據Proteolytic activation of the SARS-coronavirus spike protein: cutting enzymes at the cutting edge of antiviral research這篇文章的綜述,Routes employed by the SARS-coronavirus for entry into target cells. The SARS-coronavirus can employ two routes for host cell entry, which are determined by the localization of the proteases required for activation of the SARS-coronavirus spike protein. Binding of SARS-coronavirus to the cellular receptor, ACE2, can result in uptake of virions into endosomes, where the spike protein is activated by the pH dependent cysteine protease cathepsin L. Activation of the spike protein by cathepsin L can be blocked by lysosomotropic agents, like bafilomycin A1 and ammonium chloride, which indirectly inhibit cathepins L activity by interfering with endosomal acidification, or by compounds which directly block the proteolytic activity of cathepsin L, like MDL28170. Alternatively, the spike protein can be activated by TMPRSS2 at (or close to) the cell surface, resulting in fusion of the viral membrane with the plasma membrane. 也就是說至少有三個靶點(TMPRSS2,cathepsin L,溶酶體H+)是實驗證實可以通過相關藥物有效抑制sars病毒感染的。
這些靶點同樣適用於對2019-nCoV感染治療。臨床上對相關藥物可以展開積極的試驗。
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