Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill Chapel Hill, NC, USA ; Department of Microbiology and Immunology, University of North Carolina at Chapel Hill Chapel Hill, NC, USA.
Front Immunol. 2013 Jan 7;3:401. doi: 10.3389/fimmu.2012.00401. eCollection 2012.
As an obligate intracellular parasite, Kaposi sarcoma-associated herpesvirus (KSHV) relies on the host cell machinery to meet its needs for survival, viral replication, production, and dissemination of progeny virions. KSHV is a gammaherpesvirus that is associated with three different malignancies: Kaposi sarcoma (KS), and two B cell lymphoproliferative disorders, primary effusion lymphoma (PEL) and multicentric Castleman's disease. KSHV viral proteins modulate the cellular phosphatidylinositol-3-kinase (PI3K)/AKT/mammalian target of rapamycin (mTOR) signaling pathway, which is a ubiquitous pathway that also controls B lymphocyte proliferation and development. We review the mechanisms by which KSHV manipulates the PI3K/AKT/mTOR pathway, with a specific focus on B cells.
作为一种专性细胞内寄生虫，卡波西肉瘤相关疱疹病毒（KSHV）依赖宿主细胞机制来满足其生存、病毒复制、产生和传播子代病毒颗粒的需求。KSHV 是一种γ疱疹病毒，与三种不同的恶性肿瘤有关：卡波济肉瘤（KS），以及两种 B 细胞淋巴瘤增生性疾病，原发性渗出性淋巴瘤（PEL）和多中心卡斯特曼病。KSHV 病毒蛋白调节细胞磷脂酰肌醇-3-激酶（PI3K）/AKT/雷帕霉素靶蛋白（mTOR）信号通路，该通路是一种普遍存在的通路，也控制 B 淋巴细胞的增殖和发育。我们回顾了 KSHV 操纵 PI3K/AKT/mTOR 通路的机制，特别关注 B 细胞。
