Manipulation of the host cell membrane by humanγ-herpesviruses EBV and KSHV for pathogenesis  

作　　者：Fang Wei Qing Zhu Ling Ding Qing Liang Qiliang Cai 

机构地区：[1]Sheng Yushou Center of Cell Biology and Immunology,School of Life Sciences and Biotechnology Shanghai Jiao Tong University,Shanghai 200240,China [2]Key Laboratory of Medical Molecular Virology(Ministries of Education and Health),School of Basic Medical Sciences,Fudan University,Shanghai 200032,China

出　　处：《Virologica Sinica》2016年第5期395-405,共11页中国病毒学（英文版）

基　　金：supported by the National Natural Science Foundation of China(81471930,81402542);the National Basic Research Program of China(973 Program)(2012CB519001);the National Key Research and Development Program of China(2016YFC1200400)

摘　　要：The cell membrane regulates many physiological processes including cellular communication,homing and metabolism. It is therefore not surprising that the composition of the host cell membrane is manipulated by intracellular pathogens. Among these, the human oncogenic herpesviruses Epstein–Barr virus(EBV) and Kaposi's sarcoma-associated herpesvirus(KSHV)exploit the host cell membrane to avoid immune surveillance and promote viral replication.Accumulating evidence has shown that both EBV and KSHV directly encode several similar membrane-associated proteins, including receptors and receptor-specific ligands(cytokines and chemokines), to increase virus fitness in spite of host antiviral immune responses. These proteins are expressed individually at different phases of the EBV/KSHV life cycle and employ various mechanisms to manipulate the host cell membrane. In recent decades, much effort has been made to address how these membrane-based signals contribute to viral tumorigenesis. In this review, we summarize and highlight the recent understanding of how EBV and KSHV similarly manipulate host cell membrane signals, particularly how remodeling of the cell membrane allows EBV and KSHV to avoid host antiviral immune responses and favors their latent and lytic infection.The cell membrane regulates many physiological processes including cellular communication, homing and metabolism. It is therefore not surprising that the composition of the host cell membrane is manipulated by intracellular pathogens. Among these, the human oncogenic herpesviruses Epstein-Barr virus （EBV） and Kaposi＇s sarcoma-associated herpesvirus （KSHV） exploit the host cell membrane to avoid immune surveillance and promote viral replication. Accumulating evidence has shown that both EBV and KSHV directly encode several similar membrane-associated proteins, including receptors and receptor-specific ligands （cytokines and chemokines）, to increase virus fitness in spite of host antiviral immune responses. These proteins are expressed individually at different phases of the EBV/KSHV life cycle and employ various mechanisms to manipulate the host ceil membrane. In recent decades, much effort has been made to address how these membrane-based signals contribute to viral tumorigenesis. In this review, we summarize and highlight the recent understanding of how EBV and KSHV similarly manipulate host cell membrane signals, particularly how remodeling of the cell membrane allows EBV and KSHV to avoid host antiviral immune responses and favors their latent and lytic infection.

关 键 词：cell membrane remodeling Epstein-Barr virus(EBV) Kaposi’s sarcoma-associated herpesvirus(KSHV) 

分 类 号：R373.1[医药卫生—病原生物学]