丙型肝炎病毒劫持宿主脂质代谢。
Hepatitis C virus hijacks host lipid metabolism.
机构信息
Department of Medicine, Moores Cancer Center, University of California, San Diego, CA 92093, USA.
出版信息
Trends Endocrinol Metab. 2010 Jan;21(1):33-40. doi: 10.1016/j.tem.2009.07.005. Epub 2009 Oct 23.
Abstract
Hepatitis C virus (HCV) enhances its replication by modulating host cell lipid metabolism. HCV circulates in the blood in association with lipoproteins. HCV infection is associated with enhanced lipogenesis, reduced secretion, and beta-oxidation of lipids. HCV-induced imbalance in lipid homeostasis leads to steatosis. Many lipids are crucial for the virus life cycle, and inhibitors of cholesterol/fatty acid biosynthetic pathways inhibit virus replication, maturation and secretion. HCV negatively modulates the synthesis and secretion of very low-density lipoproteins (VLDL). Components involved in VLDL assembly are also required for HCV morphogenesis/secretion, suggesting that HCV co-opts the VLDL secretory pathway for its own secretion. This review highlights HCV-altered lipid metabolic events that aid the virus life cycle and ultimately promote liver disease.
摘要
丙型肝炎病毒（HCV）通过调节宿主细胞脂质代谢来增强其复制。HCV 与脂蛋白一起在血液中循环。HCV 感染与脂肪生成增加、脂质分泌减少和β氧化减少有关。HCV 诱导的脂质动态平衡失衡导致脂肪变性。许多脂质对病毒生命周期至关重要，胆固醇/脂肪酸生物合成途径的抑制剂抑制病毒复制、成熟和分泌。HCV 负调节极低密度脂蛋白（VLDL）的合成和分泌。VLDL 组装涉及的成分也需要用于 HCV 形态发生/分泌，这表明 HCV 为自身分泌而篡夺 VLDL 分泌途径。这篇综述强调了 HCV 改变的脂质代谢事件，这些事件有助于病毒生命周期，并最终促进肝病。
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