Department of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, California 90033, USA.
J Interferon Cytokine Res. 2009 Sep;29(9):621-7. doi: 10.1089/jir.2009.0067.
Upon viral infection, the major defensive strategy employed by the host immune system is the activation of the interferon (IFN)-mediated antiviral pathway, which is overseen by IFN regulatory factors (IRFs). In order to complete their life cycles, viruses must find a way to modulate the host IFN-mediated immune response. Kaposi's sarcoma-associated herpesvirus (KSHV), a human tumor-inducing herpesvirus, has developed a unique mechanism for antagonizing cellular IFN-mediated antiviral activity by incorporating viral homolog of the cellular IRFs, called vIRFs, into its genome. Here, we summarize the novel evasion mechanisms by which KSHV, through its vIRFs, circumvents IFN-mediated innate immune responses and deregulates the cell growth control mechanism.
病毒感染后,宿主免疫系统采用的主要防御策略是激活干扰素(IFN)介导的抗病毒途径,该途径由干扰素调节因子(IRFs)监管。为了完成其生命周期,病毒必须找到一种方法来调节宿主 IFN 介导的免疫反应。卡波济肉瘤相关疱疹病毒(KSHV)是一种人类肿瘤诱导疱疹病毒,它通过将细胞 IRF 的病毒同源物,称为 vIRF,整合到其基因组中,开发了一种独特的拮抗细胞 IFN 介导的抗病毒活性的机制。在这里,我们总结了 KSHV 通过其 vIRFs 规避 IFN 介导的先天免疫反应并使细胞生长控制机制失调的新型逃逸机制。