Department of Medicine, The University of North Carolina, Chapel Hill, NC 27599-7292, USA.
Curr Top Microbiol Immunol. 2013;369:263-88. doi: 10.1007/978-3-642-27340-7_11.
Chronic hepatitis C virus (HCV) infection is a leading cause of liver-specific morbidity and mortality in humans, including progressive liver fibrosis, cirrhosis, and hepatocellular carcinoma. It has also been associated with altered function in other organs, including those of the endocrine, hematopoietic, and nervous systems. Disease results from both direct regulation of cellular metabolism and signaling pathways by viral proteins as well as indirect consequences of the host response to HCV infection, including inflammatory responses stemming from immune recognition of the virus. Recent in vitro studies have begun to reveal molecular mechanisms responsible for virus-induced changes in cell metabolism and cellular kinase cascades that culminate in pathologic consequences in the liver, such as steatosis, insulin resistance, and carcinogenesis. Here we discuss how these findings may be relevant to disease pathogenesis in patients, and suggest future directions in the field.
慢性丙型肝炎病毒(HCV)感染是人类肝脏特异性发病率和死亡率的主要原因,包括进行性肝纤维化、肝硬化和肝细胞癌。它还与其他器官的功能改变有关,包括内分泌、造血和神经系统。疾病的发生不仅源于病毒蛋白对细胞代谢和信号通路的直接调控,还源于宿主对 HCV 感染的反应的间接后果,包括来自病毒免疫识别的炎症反应。最近的体外研究开始揭示导致病毒诱导的细胞代谢和细胞激酶级联改变的分子机制,这些改变最终导致肝脏的病理后果,如脂肪变性、胰岛素抵抗和癌变。在这里,我们讨论这些发现如何与患者的疾病发病机制相关,并为该领域提出未来的研究方向。