Department of Microbiology and Immunology, Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill Chapel Hill, NC, USA.
Front Immunol. 2011 Jun 17;2:19. doi: 10.3389/fimmu.2011.00019. eCollection 2011.
Kaposi's sarcoma-associated herpesvirus (KSHV) is a large double-stranded DNA gammaherpesvirus, and the etiological agent for three human malignancies: Kaposi's sarcoma, primary effusion lymphoma, and multicentric Castleman's disease. To establish and maintain infection, KSHV has evolved unique mechanisms to evade the host immune response. Cellular interferon regulatory factors (IRFs) are a critical part of the host anti-viral immune response. KSHV encodes four homologs of IRFs, vIRF1-4, which inhibit the activity of their cellular counterparts. vIRF1, 2, and 3 have been shown to interact directly with cellular IRFs. Additionally, the vIRFs have other functions such as modulation of Myc, p53, Notch, transforming growth factor-β, and NF-κB signaling. These activities of vIRFs may contribute to KSHV tumorigenesis. KSHV vIRF1 and vIRF3 have been implicated as oncogenes, making the understanding of KSHV vIRF function vital to understanding KSHV pathogenesis.
卡波济肉瘤相关疱疹病毒（KSHV）是一种大型双链 DNA γ疱疹病毒，也是三种人类恶性肿瘤的病原体：卡波济肉瘤、原发性渗出性淋巴瘤和多中心卡斯特曼病。为了建立和维持感染，KSHV 已经进化出独特的机制来逃避宿主的免疫反应。细胞干扰素调节因子（IRFs）是宿主抗病毒免疫反应的重要组成部分。KSHV 编码四个 IRF 同源物，vIRF1-4，它们抑制其细胞对应物的活性。已经表明 vIRF1、2 和 3 可以直接与细胞 IRFs 相互作用。此外，vIRFs 还有其他功能，如调节 Myc、p53、Notch、转化生长因子-β和 NF-κB 信号转导。这些 vIRFs 的活性可能有助于 KSHV 的肿瘤发生。KSHV vIRF1 和 vIRF3 已被认为是致癌基因，因此了解 KSHV vIRF 的功能对于理解 KSHV 的发病机制至关重要。
