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甲型肝炎病毒接种狨猴感染急性期肝细胞损伤机制的形态学研究

Morphological studies on the mechanism of hepatocellular injury during acute phase of infection in marmosets inoculated with hepatitis A virus.

作者信息

Inoue O

出版信息

Acta Pathol Jpn. 1985 Nov;35(6):1319-31. doi: 10.1111/j.1440-1827.1985.tb01431.x.

Abstract

The histological changes during the acute phase of infection in the livers of marmosets inoculated with hepatitis A virus were examined. The acute phase was divided into four stages according to the liver enzyme changes and serological markers for the viral infection (Stage I, II, III, IV). Round cell infiltration in the portal tracts was first recognized in Stage I. Localization of parenchymal changes was predominantly periportal in Stage I, II, and IV, whereas the lesion was diffuse in Stage III. Hepatitis A virus antigen (HAVA) was widely distributed but spotty and the largest amount of HAVA was found in Stage II by immunofluorescent and immunoperoxidase study. By electron microscopy the endoplasmic reticulum was altered in the liver cells and in some area there was interaction between the hepatocytes and lymphocytes. These findings suggest that hepatocellular damages seen in this model are the result of immune response rather than cytotoxic effect.

摘要

对接种甲型肝炎病毒的狨猴肝脏感染急性期的组织学变化进行了检查。根据肝酶变化和病毒感染的血清学标志物,急性期分为四个阶段(阶段I、II、III、IV)。在阶段I首次发现门管区有圆形细胞浸润。在阶段I、II和IV,实质改变主要位于门周,而在阶段III病变为弥漫性。通过免疫荧光和免疫过氧化物酶研究发现,甲型肝炎病毒抗原(HAVA)分布广泛但呈斑点状,且在阶段II中发现的HAVA量最多。通过电子显微镜观察,肝细胞内的内质网发生改变,在某些区域肝细胞与淋巴细胞之间存在相互作用。这些发现表明,该模型中所见的肝细胞损伤是免疫反应而非细胞毒性作用的结果。

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