当前位置: X-MOL 学术Annu. Rev. Microbiol. › 论文详情
Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)
Kaposi's sarcoma-associated herpesvirus immunoevasion and tumorigenesis: two sides of the same coin?
Annual Review of Microbiology ( IF 8.5 ) Pub Date : 2003-01-01 , DOI: 10.1146/annurev.micro.57.030502.090824
Patrick S Moore 1 , Yuan Chang
Affiliation  

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.

中文翻译:


卡波西肉瘤相关疱疹病毒免疫逃避和肿瘤发生:同一枚硬币的两面?



卡波西肉瘤相关疱疹病毒 (KSHV) [或人类疱疹病毒 8 (HHV-8)] 是艾滋病患者中最常见的恶性肿瘤原因。 KSHV 和相关疱疹病毒广泛盗用了宿主基因组的细胞 cDNA,为检查控制细胞增殖的病毒机制提供了独特的机会。许多病毒调节同源物编码直接抑制宿主适应性和先天免疫的蛋白质。其他病毒蛋白以视网膜母细胞瘤蛋白和肿瘤抑制途径的 p53 控制为目标,这些蛋白在细胞内免疫反应中也发挥着关键的效应作用。 KSHV 采用的免疫逃避策略,通过针对免疫系统信号传导过程中激活的肿瘤抑制途径,可能会导致易感宿主无意中的细胞增殖和肿瘤发生。
更新日期:2019-11-01
down
wechat
bug