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Towards predicting the therapeutic response in patients with hepatitis C.

机译:预测丙型肝炎患者的治疗反应。

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The study by Angelico et al, recently published in Alimentary Pharmacology ft Therapeutics1 confirms the strong positive correlation between the level of HDL cholesterol at baseline and the virological response to the combined therapy using interferon-alfa and ribavirin. The direct relationship between HCV entiy into cells is a multi-step and slow process. It is believed that the initial capture of HCV particles by glycosaminoglycans and/or lipoprotein receptors is followed by coordinated interactions with the scavenger receptor class B type I (SR-BI), a major receptor of high-density lipoprotein (HDL), the CD81 tetraspanin, and the tight junction protein Claudin-1, ultimately leading to uptake and cellular penetration of HCV via low-pH endosomes. Competitive inhibition of HCV binding to SR-BI by HDL has been shown in vitro and is a better candidate than LDL receptor. If similar inhibition occurs in vivo, an elevated concentration of HDL may reduce the efficiency of infecting hepatocytes with HCV by competitively inhibiting HCV viral SR-BI receptor binding. This effect could be important during the initiation of therapy.
机译:Angelico等人的研究最近发表在《 Alimentary Pharmacology》(《治疗学》)1上,证实了基线时HDL胆固醇水平与联合使用干扰素-α和利巴韦林的联合疗法的病毒学应答之间呈强正相关。 HCV全部进入细胞之间的直接关系是一个多步骤且缓慢的过程。据信,糖胺聚糖和/或脂蛋白受体最初捕获HCV颗粒后,是与清除剂受体I类B(SR-BI)(高密度脂蛋白(HDL)的主要受体CD81)协同相互作用。四跨膜蛋白和紧密连接蛋白Claudin-1,最终通过低pH值内体导致HCV的吸收和细胞渗透。业已显示,HDL具有竞争性抑制HCV与SR-BI结合的作用,并且比LDL受体更好。如果体内发生类似的抑制作用,则高浓度的HDL可能会通过竞争性抑制HCV病毒SR-BI受体的结合而降低用HCV感染肝细胞的效率。在治疗开始期间,这种作用可能很重要。

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