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首页> 外文期刊>Viral immunology >Immune mechanisms in murine gammaherpesvirus-68 infection.
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Immune mechanisms in murine gammaherpesvirus-68 infection.

机译:鼠γ疱疹病毒68感染的免疫机制。

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The murine gamma-herpesvirus-68 (MHV-68) is a relative of the Kaposi's sarcoma-associated herpesvirus (KSHV) and Epstein-Barr virus (EBV) that infects mice. All these gamma-herpesviruses are subject to immune control, but limit the impact of this control through immune evasion. Molecular evasion mechanisms have been described in abundance. However, we can only speculate what EBV and KSHV immune evasion contributes to the viral lifecycle. With MHV-68, we can analyze in vivo the contribution of immunological and virological gene expression to pathogenesis. While the physiology of infection seems quite well conserved between these viruses, the pathologies associated with immune suppression are obviously very different. MHV-68 is therefore more suited to uncovering the basic biology of gamma-herpesvirus infection than to testing disease interventions. Nevertheless, it may make some useful predictions about effective strategies of vaccination and infection control. This review aims to outline our current state of knowledge and to highlight some limitations of the MHV-68 model as it stands, in the hope of stimulating constructive progress.
机译:鼠γ-疱疹病毒68(MHV-68)是感染小鼠的卡波西氏肉瘤相关疱疹病毒(KSHV)和爱泼斯坦-巴尔病毒(EBV)的亲戚。所有这些伽玛疱疹病毒都受到免疫控制,但是通过逃避免疫来限制这种控制的影响。已经大量描述了分子逃逸机制。但是,我们只能推测EBV和KSHV免疫逃逸对病毒生命周期的贡献。借助MHV-68,我们可以在体内分析免疫学和病毒学基因表达在发病机理中的作用。尽管这些病毒之间的感染生理学非常保守,但与免疫抑制相关的病理学却明显不同。因此,MHV-68比测试疾病干预措施更适合揭示γ-疱疹病毒感染的基本生物学。但是,它可以对疫苗接种和感染控制的有效策略做出一些有用的预测。这篇综述旨在概述我们目前的知识水平,并强调MHV-68模型目前的局限性,以期刺激建设性进展。

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