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在γ疱疹病毒裂解感染过程中直接操纵宿主 mRNA 积累的信息。

Getting the message direct manipulation of host mRNA accumulation during gammaherpesvirus lytic infection.

机构信息

Department of Plant and Microbial Biology, University of California, Berkeley, USA.

出版信息

Adv Virus Res. 2010;78:1-42. doi: 10.1016/B978-0-12-385032-4.00001-X.

DOI:10.1016/B978-0-12-385032-4.00001-X
PMID:21040830
Abstract

The Gammaherpesvirinae subfamily of herpesviruses comprises lymphotropic viruses, including the oncogenic human pathogens Epstein-Barr virus and Kaposi's sarcoma-associated herpesvirus. During lytic infection, gammaherpesviruses manipulate host gene expression to optimize the cellular environment for viral replication and to evade the immune response. Additionally, although a lytically infected cell will itself be killed in the process of viral replication, lytic infection can contribute to pathogenesis by inducing the secretion of paracrine factors with functions in cell survival and proliferation, and angiogenesis. The mechanisms by which these viruses manipulate host gene expression are varied and target the accumulation of cellular mRNAs and their translation, signaling pathways, and protein stability. Here, we discuss how gammaherpesviral proteins directly influence host mRNA biogenesis and stability, either selectively or globally, in order to fine-tune the cellular environment to the advantage of the virus. Appreciation of the mechanisms by which these viruses interface with and adapt normal cellular processes continues to inform our understanding of gammaherpesviral biology and the regulation of mRNA accumulation and turnover in our own cells.

摘要

γ疱疹病毒亚科的疱疹病毒包括淋巴嗜性病毒,包括致癌的人类病原体 EBV(Epstein-Barr 病毒)和卡波济肉瘤相关疱疹病毒。在裂解性感染期间,γ疱疹病毒操纵宿主基因表达,以优化细胞环境促进病毒复制并逃避免疫反应。此外,虽然裂解感染的细胞本身将在病毒复制过程中被杀死,但裂解感染可以通过诱导具有细胞存活和增殖以及血管生成功能的旁分泌因子的分泌来促进发病机制。这些病毒操纵宿主基因表达的机制多种多样,靶向细胞 mRNA 的积累及其翻译、信号通路和蛋白质稳定性。在这里,我们讨论了γ疱疹病毒蛋白如何直接影响宿主 mRNA 的生物发生和稳定性,无论是选择性地还是全局性地,以便微调细胞环境以有利于病毒。对这些病毒与正常细胞过程相互作用和适应的机制的认识不断推动我们对γ疱疹病毒生物学以及我们自身细胞中 mRNA 积累和周转的调节的理解。

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