Interplay between host cell and hepatitis C virus in regulating viral replication

Interplay between host cell and hepatitis C virus in regulating viral replication
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DOI:
10.1515/bc.2009.118
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发表时间:
2009-10-01
影响因子:
3.7
通讯作者:
Haeussinger, Dieter
Haeussinger, Dieter
中科院分区:
生物学2区
文献类型:
--
作者:
Bode, Johannes G.;Brenndorfer, Erwin D.;Haeussinger, Dieter

文献摘要

被引文献

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丙型肝炎病毒(HCV)的病毒生命周期完全依赖于宿主细胞的基础结构,前提是病毒已经进化出利用和控制病毒生命周期所需的所有细胞分子或途径的机制。因此,HCV必须获得进入控制过程的关键途径的能力,例如细胞生长,凋亡和蛋白质合成,这些都被认为对肝再生也至关重要。这以一种平衡的方式发生,允许病毒基因组的持续复制和感染性颗粒的产生,而不危及宿主细胞的活力和存活。特别是在过去十年中,越来越多的证据表明,丙型肝炎病毒利用宿主的信号传导途径,对细胞生长、活力、细胞周期或细胞代谢产生重大影响,例如表皮生长因子受体介导的信号、PI 3 K/Akt级联反应或Src家族激酶。此外,HCV特异性地与参与蛋白质翻译、加工、成熟和转运的细胞机制的部分相互作用,例如翻译复合物的组分、热休克蛋白家族、亲免疫素或囊泡相关膜蛋白相关蛋白A和B。本综述着重于病毒蛋白和宿主细胞的这些因子之间的相互作用,使病毒能够利用宿主细胞的基础设施。
Viral life cycle as that of the hepatitis C virus ( HCV) completely relies on host cell infrastructure, presupposing that the virus has evolved mechanisms to utilize and control all cellular molecules or pathways required for viral life cycle. Hence, HCV must have acquired the ability to gain access to key pathways controlling processes, such as cell growth, apoptosis and protein synthesis, which are all considered to also be crucial for liver regeneration. This occurs in a balanced way permitting persistent replication of viral genomes and production of infectious particles without endangering host cell viability and survival. In particular during the last decade, accumulating evidence indicates that HCV utilizes signaling pathways of the host with major impact on cellular growth, viability, cell cycle or cellular metabolism, such as epidermal growth factor-receptor mediated signals, the PI3K/Akt cascade or the family of Src kinases. Furthermore, HCV specifically interacts with parts of the cellular machinery involved in protein translation, processing, maturation and transport, such as components of the translation complex, the heat shock protein family, the immunophilins or the vesicle-associated membrane protein-associated proteins A and B. The present review focuses on the interplay between viral proteins and these factors of the host cell enabling the virus to utilize host cell infrastructure.