Yoo Seung-Min, Lee Myung-Shin
Department of Microbiology and Immunology, Eulji University School of Medicine, Daejeon 34824, Korea.
Pathogens. 2020 Apr 3;9(4):260. doi: 10.3390/pathogens9040260.
Kaposi's sarcoma-associated herpesvirus (KSHV) modulates the immune response to allow the virus to establish persistent infection in the host and facilitate the development of KSHV-associated cancer. The complement system has a central role in the defense against pathogens. Hence, KSHV has adopted an evasion strategy for complement attack using the viral protein encoded by KSHV open reading frame 4. However, despite this defense mechanism, the complement system appears to become activated in KSHV-infected cells as well as in the region surrounding Kaposi's sarcoma tumors. Given that the complement system can affect cell fate as well as the inflammatory microenvironment, complement activation is likely associated with KSHV pathogenesis. A better understanding of the interplay between KSHV and the complement system may, therefore, translate into the development of novel therapeutic interventions for KSHV-associated tumors. In this review, the mechanisms and functions of complement activation in KSHV-infected cells are discussed.
卡波西肉瘤相关疱疹病毒（KSHV）调节免疫反应，以使病毒在宿主中建立持续感染，并促进与KSHV相关癌症的发展。补体系统在抵御病原体方面发挥着核心作用。因此，KSHV采用了一种逃避补体攻击的策略，利用KSHV开放阅读框4编码的病毒蛋白。然而，尽管有这种防御机制，补体系统似乎在KSHV感染的细胞以及卡波西肉瘤肿瘤周围区域也会被激活。鉴于补体系统可以影响细胞命运以及炎症微环境，补体激活可能与KSHV发病机制有关。因此，更好地理解KSHV与补体系统之间的相互作用可能会转化为针对与KSHV相关肿瘤的新型治疗干预措施的开发。在这篇综述中，将讨论KSHV感染细胞中补体激活的机制和功能。
