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Keeping your armour intact: How HIV-1 evades detection by the innate immune system HIV-1 capsid controls detection of reverse transcription products by the cytosolic DNA sensor cGAS

机译:保持铠甲​​完整:HIV-1如何逃避先天免疫系统的检测HIV-1衣壳控制细胞质DNA传感器cGAS检测逆转录产物

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HIV-1 infects dendritic cells (DCs) without triggering an effective innate antiviral immune response. As a consequence, the induction of adaptive immune responses controlling virus spread is limited. In a recent issue of Immunity, Lahaye and colleagues show that intricate interactions of HIV capsid with the cellular cofactor cyclophilin A (CypA) control infection and innate immune activation in DCs. Manipulation of HIV-1 capsid to increase its affinity for CypA results in reduced virus infectivity and facilitates access of the cytosolic DNA sensor cGAS to reverse transcribed DNA. This in turn induces a strong host response. Here, we discuss these findings in the context of recent developments in innate immunity and consider the implications for disease control and vaccine design
机译:HIV-1感染树突状细胞(DC),而不会触发有效的先天抗病毒免疫应答。结果,控制病毒传播的适应性免疫应答的诱导受到限制。在最近一期的《免疫》中,Lahaye及其同事表明,HIV衣壳与细胞辅因子亲环蛋白A(CypA)的复杂相互作用控制了DC中的感染和先天性免疫激活。操纵HIV-1衣壳以增加其对CypA的亲和力会导致病毒感染力降低,并有助于胞质DNA传感器cGAS逆转转录的DNA。反过来,这会引起强烈的宿主反应。在这里,我们在先天免疫的最新发展背景下讨论这些发现,并考虑对疾病控制和疫苗设计的影响

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