Moore Patrick S, Chang Yuan
Molecular Virology Program, Hillman Cancer Research Center, University of Pittsburgh, Pittsburgh, Pennsylvania 15213-1863, USA.
Annu Rev Microbiol. 2003;57:609-39. doi: 10.1146/annurev.micro.57.030502.090824.
Kaposi's sarcoma-associated herpesvirus (KSHV) [or human herpesvirus 8 (HHV-8)] is the most frequent cause of malignancy among AIDS patients. KSHV and related herpesviruses have extensively pirated cellular cDNAs from the host genome, providing a unique opportunity to examine the range of viral mechanisms for controlling cell proliferation. Many of the viral regulatory homologs encode proteins that directly inhibit host adaptive and innate immunity. Other viral proteins target retinoblastoma protein and p53 control of tumor suppressor pathways, which also play key effector roles in intracellular immune responses. The immune evasion strategies employed by KSHV, by targeting tumor suppressor pathways activated during immune system signaling, may lead to inadvertent cell proliferation and tumorigenesis in susceptible hosts.
卡波西肉瘤相关疱疹病毒（KSHV）[即人类疱疹病毒8型（HHV - 8）]是艾滋病患者中最常见的恶性肿瘤病因。KSHV及相关疱疹病毒广泛盗用了宿主基因组中的细胞cDNA，这为研究控制细胞增殖的病毒机制范围提供了独特的机会。许多病毒调节同源物编码的蛋白质可直接抑制宿主的适应性免疫和先天性免疫。其他病毒蛋白靶向视网膜母细胞瘤蛋白和肿瘤抑制途径的p53控制，这些在细胞内免疫反应中也起关键效应作用。KSHV采用的免疫逃避策略通过靶向免疫系统信号传导过程中激活的肿瘤抑制途径，可能会在易感宿主中导致意外的细胞增殖和肿瘤发生。
