Elgretli Wesal, Chen Tianyan, Kronfli Nadine, Sebastiani Giada
Division of Experimental Medicine, McGill University, Montreal, QC H4A 3J1, Canada.
Division of Gastroenterology and Hepatology, Department of Medicine, McGill University Health Centre, Montreal, QC H4A 3J1, Canada.
Biomedicines. 2023 Jan 19;11(2):271. doi: 10.3390/biomedicines11020271.
Hepatitis C virus (HCV) infection represents the major cause of chronic liver disease, leading to a wide range of hepatic diseases, including cirrhosis and hepatocellular carcinoma. It is the leading indication for liver transplantation worldwide. In addition, there is a growing body of evidence concerning the role of HCV in extrahepatic manifestations, including immune-related disorders and metabolic abnormalities, such as insulin resistance and steatosis. HCV depends on its host cells to propagate successfully, and every aspect of the HCV life cycle is closely related to human lipid metabolism. The virus circulates as a lipid-rich particle, entering the hepatocyte via lipoprotein cell receptors. It has also been shown to upregulate lipid biosynthesis and impair lipid degradation, resulting in significant intracellular lipid accumulation (steatosis) and circulating hypocholesterolemia. Patients with chronic HCV are at increased risk for hepatic steatosis, dyslipidemia, and cardiovascular disease, including accelerated atherosclerosis. This review aims to describe different aspects of the HCV viral life cycle as it impacts host lipoproteins and lipid metabolism. It then discusses the mechanisms of HCV-related hepatic steatosis, hypocholesterolemia, and accelerated atherosclerosis.
丙型肝炎病毒（HCV）感染是慢性肝病的主要病因，可导致多种肝脏疾病，包括肝硬化和肝细胞癌。它是全球肝移植的主要指征。此外，越来越多的证据表明HCV在肝外表现中发挥作用，包括免疫相关疾病和代谢异常，如胰岛素抵抗和脂肪变性。HCV依赖其宿主细胞成功繁殖，并且HCV生命周期的各个方面都与人类脂质代谢密切相关。该病毒以富含脂质的颗粒形式循环，通过脂蛋白细胞受体进入肝细胞。研究还表明，它可上调脂质生物合成并损害脂质降解，导致细胞内大量脂质积累（脂肪变性）和循环性低胆固醇血症。慢性HCV患者发生肝脂肪变性、血脂异常和心血管疾病（包括动脉粥样硬化加速）的风险增加。本综述旨在描述HCV病毒生命周期影响宿主脂蛋白和脂质代谢的不同方面。然后讨论HCV相关肝脂肪变性、低胆固醇血症和动脉粥样硬化加速的机制。
