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丙型肝炎病毒与其他肝炎病毒合并感染的病毒相互作用及临床意义。

Viral interaction and clinical implications of coinfection of hepatitis C virus with other hepatitis viruses.

作者信息

Lin Lan, Verslype Chris, van Pelt Jos F, van Ranst Marc, Fevery Johan

机构信息

Department of Hepatology, University Hospital Gasthuisberg, Leuven, Belgium.

出版信息

Eur J Gastroenterol Hepatol. 2006 Dec;18(12):1311-9. doi: 10.1097/01.meg.0000243881.09820.09.

DOI:10.1097/01.meg.0000243881.09820.09
PMID:17099381
Abstract

Coinfection with other hepatitis viruses modifies the viral profile in serum and leads to more liver damage and more rapid progression during the course of hepatitis C virus infection. The viral interference is not only carried out by virus-virus or by virus-cell interactions but also by an enhanced immune response. A superinfecting viral infection does not crossactivate protective immune responses to the pre-existing virus albeit the latter can become undetectable. The induced cytokine stimulation might enhance the hepatic inflammation. Moreover, hepatitis B virus coinfection increases the risk of development of hepatocellular carcinoma in hepatitis C virus patients through common necro-inflammatory pathways or by direct oncogenic activity of hepatitis B virus. Viral interaction also complicates the management of the coinfection because hepatitis C virus impairs the humoral response to hepatitis A virus and hepatitis B virus vaccines, and because pharmacological suppression of hepatitis C virus endangers dually infected patients with reactivation of coinfected hepatitis B virus. Optimized strategies and follow-up are thus necessary in the treatment of infection with multiple viruses. It seems thus necessary to look for markers of hepatitis B virus and/or hepatitis D virus infection in chronic hepatitis patients positive for hepatitis C virus antibodies but negative for hepatitis C virus RNA, and equally well to search for hepatitis C virus RNA in HBsAg-negative/anti-HBc-positive patients with a low level of serum hepatitis B virus DNA.

摘要

与其他肝炎病毒合并感染会改变血清中的病毒谱,并导致在丙型肝炎病毒感染过程中出现更多肝脏损伤和更快进展。病毒干扰不仅通过病毒-病毒或病毒-细胞相互作用进行,还通过增强的免疫反应进行。尽管先前存在的病毒可能变得无法检测到,但重叠感染的病毒感染不会交叉激活对其的保护性免疫反应。诱导的细胞因子刺激可能会加剧肝脏炎症。此外,乙型肝炎病毒合并感染通过共同的坏死性炎症途径或乙型肝炎病毒的直接致癌活性增加了丙型肝炎病毒患者发生肝细胞癌的风险。病毒相互作用也使合并感染的管理变得复杂,因为丙型肝炎病毒会损害对甲型肝炎病毒和乙型肝炎病毒疫苗的体液反应,并且因为对丙型肝炎病毒的药物抑制会使双重感染患者面临合并感染的乙型肝炎病毒重新激活的风险。因此,在治疗多种病毒感染时,优化策略和随访是必要的。因此,似乎有必要在丙型肝炎病毒抗体阳性但丙型肝炎病毒RNA阴性的慢性肝炎患者中寻找乙型肝炎病毒和/或丁型肝炎病毒感染的标志物,同样也有必要在血清乙型肝炎病毒DNA水平较低的HBsAg阴性/抗-HBc阳性患者中寻找丙型肝炎病毒RNA。

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