Enjoji M, Nakamuta M, Kinukawa N, Sugimoto R, Noguchi K, Tsuruta S, Iwao M, Kotoh K, Iwamoto H, Nawata H
Department of Medicine and Bioreguratory Science, Graduate School of Medical Sciences, Kyushu University, 3-1-1 Maidashi, Higashiku, Fukuoka 812-8582, Japan.
Med Sci Monit. 2000 Sep-Oct;6(5):841-4.
Low density lipoprotein receptor (LDLR) has been proposed as a candidate receptor for hepatitis C virus (HCV). According to previous reports, free beta-lipoproteins in a human serum may regulate the rate of hepatocyte infection by competing with the virus. Therefore, serum HCV levels should be regulated by the rise and fall of serum beta-lipoproteins since the infection rate of virions influences HCV replication in hepatocytes and release of virions by hepatocytes. In this study, we examined the relationship between serum beta-lipoproteins and HCV-antigen (Ag) levels in patients with chronic type C hepatitis. Patients were selected based on strict criteria to eliminate other factors that might influence serum HCV levels. Serum concentrations of beta-lipoproteins and HCV-Ag were measured two or more times within 3 months for each patient. The result showed that HCV-Ag levels were negatively correlated with the increased beta-lipoproteins. The results support the concept that LDLR is a HCV receptor and that beta-lipoproteins competitively inhibit the infection of hepatocytes with HCV through the LDLR.
低密度脂蛋白受体（LDLR）已被提出作为丙型肝炎病毒（HCV）的候选受体。根据先前的报道，人血清中的游离β-脂蛋白可能通过与病毒竞争来调节肝细胞感染率。因此，由于病毒粒子的感染率影响HCV在肝细胞中的复制以及肝细胞释放病毒粒子，血清HCV水平应受血清β-脂蛋白升降的调节。在本研究中，我们检测了慢性丙型肝炎患者血清β-脂蛋白与HCV抗原（Ag）水平之间的关系。根据严格标准选择患者以排除可能影响血清HCV水平的其他因素。每位患者在3个月内测量血清β-脂蛋白和HCV-Ag浓度两次或更多次。结果显示，HCV-Ag水平与β-脂蛋白升高呈负相关。这些结果支持了LDLR是HCV受体以及β-脂蛋白通过LDLR竞争性抑制HCV感染肝细胞这一概念。
