Herpes simplex virus hepatitis in macrophage-depleted mice: the role of massive, apoptotic cell death in pathogenesis
Herpes simplex virus hepatitis in macrophage-depleted mice: the role of massive, apoptotic cell death in pathogenesis
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DOI：
10.1099/0022-1317-79-5-1225
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发表时间：
1998-05-01
影响因子：
3.8
通讯作者：
Hill, T
中科院分区：
文献类型：
--
作者：
Irie, H;Koyama, H;Hill, T
单纯疱疹病毒或肝炎病毒感染可导致暴发性肝炎，但对这种疾病所需的基础条件存在争议。为了研究如何损害宿主防御可能涉及，巨噬细胞被耗尽的二氧化硅给小鼠静脉注射单纯疱疹病毒1型（HSV-1）之前。这些小鼠迅速死亡，肝脏呈黄色并萎缩（急性黄色萎缩），偶尔出现严重出血。肝小叶中出现凋亡细胞的小病灶;随着时间的推移，这些细胞迅速融合并呈带状。总体病变模式类似于大面积肝坏死，并且在肝脏病变中存在广泛的HSV复制。在肝脏中，细胞凋亡的DNA片段化特征遵循HSV-1传播的时间过程。这些发现表明，暴发性病毒性肝炎的潜在条件之一可能是巨噬细胞反应不足，而通常被定义为细胞坏死的大规模肝损伤实际上可能是病毒感染后肝细胞的凋亡。
Infection with herpes simplex virus or hepatitis viruses can lead to fulminant hepatitis, but there is controversy about the underlying conditions needed for such disease. To investigate how the impairment of host defences might be involved, macrophages were depleted by administration of silica to mice before intravenous injection with herpes simplex virus type 1 (HSV-1). Such mice died rapidly and their livers were yellowish and shrunken (acute yellow atrophy), and occasionally grossly haemorrhagic. Small foci of apoptotic cells developed in the liver lobules; these rapidly became confluent and zonal over time. The overall lesion pattern was similar to massive hepatic necrosis, and there was extensive HSV replication in the liver lesions. In the liver, DNA fragmentation characteristic of apoptosis followed the time course of HSV-1 propagation. These findings suggest that one of the underlying conditions for fulminant viral hepatitis may be inadequate macrophage response, and that the massive hepatic damage, often defined as cell necrosis, may actually be apoptosis of liver cells subsequent to virus infection.