Mechanisms of Hepatocellular Injury in Hepatitis A.
Mechanisms of Hepatocellular Injury in Hepatitis A.
复制标题
甲型肝炎肝细胞损伤的机制
DOI：
10.3390/v13050861
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发表时间：
2021-05-08
期刊：
影响因子：
--
通讯作者：
Feng Z
中科院分区：
文献类型：
--
作者：
Wang M;Feng Z
甲型肝炎病毒(HAV)感染是全世界急性病毒性肝炎的常见原因。尽管经过几十年的研究，甲型肝炎的致病机制仍不完全清楚。由于甲型肝炎病毒的复制在体外是非细胞病变的，一个被广泛接受的概念是病毒特异性的细胞毒性T细胞负责肝脏损伤。然而，越来越多的证据表明，自然杀伤(NK)细胞、NKT细胞，甚至非甲型肝炎病毒特异性CD8+T细胞在甲型肝炎病毒感染过程中导致肝脏损伤。此外，在甲型肝炎的小鼠模型中，病毒感染的肝细胞的内源性死亡被认为是造成肝损伤的原因之一。此外，宿主因子如T细胞免疫球蛋白-1(TIM1)和IL-18结合蛋白(IL-18BP)的基因变异与甲型肝炎的严重程度有关。本文综述了甲型肝炎肝细胞损伤机制的研究现状，在不同的条件下可能涉及不同的机制，它们不一定是相互排斥的。更好地了解这些机制将有助于诊断和治疗与甲型肝炎病毒感染相关的疾病。
Hepatitis A virus (HAV) infection is a common cause of acute viral hepatitis worldwide. Despite decades of research, the pathogenic mechanisms of hepatitis A remain incompletely understood. As the replication of HAV is noncytopathic in vitro, a widely accepted concept has been that virus-specific cytotoxic T cells are responsible for liver injury. However, accumulating evidence suggests that natural killer (NK) cells, NKT cells, and even non-HAV-specific CD8+ T cells contribute to liver damage during HAV infection. In addition, intrinsic death of virus-infected hepatocytes has been implicated as a cause of liver injury in a murine model of hepatitis A. Furthermore, genetic variations in host factors such as T cell immunoglobulin-1 (TIM1) and IL-18 binding protein (IL-18BP) have been linked to hepatitis A severity. This review summarizes the current knowledge of the mechanisms of hepatocellular injury in hepatitis A. Different mechanisms may be involved under different conditions and they are not necessarily mutually exclusive. A better understanding of these mechanisms would aid in diagnosis and treatment of diseases associated with HAV infection.
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