Liang Chengyu, Lee Jong-Soo, Jung Jae U
Department of Molecular Microbiology and Immunology, University of Southern California, Los Angeles, CA 90033, USA.
Semin Cancer Biol. 2008 Dec;18(6):423-36. doi: 10.1016/j.semcancer.2008.09.003. Epub 2008 Oct 2.
A hallmark of herpesviruses is a lifelong persistent infection, which often leads to diseases upon immune suppression of infected host. Kaposi's sarcoma-associated herpesvirus (KSHV), also known as human herpesvirus 8 (HHV8), is etiologically linked to the development of Kaposi's sarcoma (KS), primary effusion lymphoma (PEL), and Multicentric Castleman's disease (MCD). In order to establish a persistent infection, KSHV dedicates a large portion of its genomic information to sabotage almost every aspect of host immune system. Thus, understanding the interplay between KSHV and the host immune system is important in not only unraveling the complexities of viral persistence and pathogenesis, but also discovering novel therapeutic targets. This review summarizes current knowledge of host immune evasion strategies of KSHV and their contributions to KSHV-associated diseases.
疱疹病毒的一个标志是终身持续感染,这在受感染宿主免疫抑制时常常引发疾病。卡波西肉瘤相关疱疹病毒(KSHV),也称为人类疱疹病毒8型(HHV8),在病因上与卡波西肉瘤(KS)、原发性渗出性淋巴瘤(PEL)和多中心Castleman病(MCD)的发生有关。为了建立持续感染,KSHV将其大部分基因组信息用于破坏宿主免疫系统的几乎各个方面。因此,了解KSHV与宿主免疫系统之间的相互作用不仅对于揭示病毒持续存在和发病机制的复杂性很重要,而且对于发现新的治疗靶点也很重要。本综述总结了目前关于KSHV宿主免疫逃逸策略及其对KSHV相关疾病贡献的知识。