Infection and direct injury in human hepatocyte explants and a hepatoblastoma cell line due to hepatiticomimetic (non‐hepatitis) viruses
Infection and direct injury in human hepatocyte explants and a hepatoblastoma cell line due to hepatiticomimetic (non‐hepatitis) viruses
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DOI：
10.1002/jmv.20783
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发表时间：
2007-04
影响因子：
12.7
通讯作者：
J. Phromjai;N. Aiba;Mikiko Suzuki;Hitoshi Sato;T. Takahara;Sachiko Kondo;K. Shiraki
中科院分区：
文献类型：
--
作者：
J. Phromjai;N. Aiba;Mikiko Suzuki;Hitoshi Sato;T. Takahara;Sachiko Kondo;K. Shiraki
肝炎是由肝炎病毒引起的，但肝炎或肝细胞酶异常有时与拟肝炎病毒感染有关。在两个人肝细胞系统中检测了拟肝炎病毒感染的直接和间接效应。脊髓灰质炎病毒、腺病毒和单纯疱疹病毒（HSV）在Hep G2细胞中诱导细胞病理学。麻疹病毒未引起肝细胞变化。脊髓灰质炎病毒感染不影响细胞蛋白质合成，肝细胞酶释放高峰与病毒释放高峰重合。腺病毒蛋白合成的增加与转铁蛋白合成的减少相关，并且酶释放不显著。HSV诱导病毒蛋白质合成，并增强加工和抑制α1-抗胰蛋白酶的合成。酶释放高峰晚于病毒释放高峰。在原代肝细胞中，脊髓灰质炎病毒、腺病毒和诱导广泛的细胞病理学和酶释放，VZV引起细胞病理学和显著但微小的酶释放。脊髓灰质炎病毒感染肝细胞乳酸脱氢酶与天冬氨酸氨基转移酶释放的比值均大于HSV或VZV感染。虽然脊髓灰质炎病毒和腺病毒通过细胞溶解释放，HSV和VZV通过胞质空泡的胞吐分泌，但酶释放与病毒释放的类型无关。腺病毒显示出很强的细胞毒性，但不改变膜，也不引起酶释放。酶释放与脊髓灰质炎病毒引起的细胞凋亡和HSV引起的细胞坏死引起的表面膜修饰有关。因此，病毒感染引起的肝细胞损伤并不能反映肝细胞酶释放的数量或模式。J. Med. Virol. 79：413-425，2007.© 2007 Wiley利斯公司
Hepatitis is caused by hepatitis viruses, but hepatitis or hepatocellular enzyme abnormalities is sometimes associated with infection by the hepatiticomimetic viruses. The direct and indirect effects of infection with hepatiticomimetic viruses were examined in two human hepatocyte systems. Poliovirus, adenovirus, and herpes simplex virus (HSV) induced cytopathology in Hep G2 cells. Measles virus caused no change in hepatocytes. Poliovirus infection did not affect cellular protein synthesis, and the peak of hepatocellular enzyme release coincided with the peak of virus release. The increase in adenovirus protein synthesis correlated with the decrease of transferrin synthesis, and enzyme release was not prominent. HSV induced viral protein synthesis with enhanced processing and inhibition of synthesis of α1‐antitrypsin. The peak of enzyme release was later than the peak of virus release. In primary hepatocytes, poliovirus, adenovirus, and induced extensive cytopathology and enzyme release, and VZV caused cytopathology and significant but minute enzyme release. The ratio of lactate dehydrogenase to aspartate aminotransferase release was larger in poliovirus infection in both hepatocytes than in HSV or VZV infection. Although poliovirus and adenovirus are released by cytolysis and HSV and VZV are secreted by exocytosis of cytoplasmic vacuoles, enzyme release was independent of the type of virus release. Adenovirus showed strong cytotoxicity but did not modify the membrane nor cause enzyme release. Enzyme release was associated with modification of the surface membrane due to apoptosis with poliovirus and necrosis with HSV. Consequently hepatocellular injury by viral infection did not reflect the amount or pattern of hepatocellular enzyme release. J. Med. Virol. 79:413–425, 2007. © 2007 Wiley‐Liss, Inc.