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首页> 外文期刊>Journal of Molecular Biology >Innate immunity to dengue virus infection and subversion of antiviral responses
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Innate immunity to dengue virus infection and subversion of antiviral responses

机译：对登革热病毒感染的先天免疫和抗病毒反应的颠覆

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摘要

Dengue is a major public health issue in tropical and subtropical regions worldwide. The four serotypes of dengue virus (DENV1-DENV4) are spread primarily by Aedes aegypti and Aedes albopictus mosquitoes, whose geographic range continues to expand. Humans are the only host for epidemic strains of DENV, and the virus has developed sophisticated mechanisms to evade human innate immune responses. The host cell's first line of defense begins with an intracellular signaling cascade resulting in production of interferon α/β (IFN-α/β), which promotes intracellular antiviral responses and helps initiates the adaptive response during the course of DENV infection. In response, DENV has developed numerous ways to subvert these intracellular antiviral responses and directly inhibit cellular signaling cascades. Specifically, DENV manipulates the unfolded protein response and autophagy to counter cellular stress and delay apoptosis. The DENV non-structural protein NS4B and subgenomic flavivirus RNA interfere with the RNA interference pathway by inhibiting the RNase Dicer. During heterotypic secondary DENV infection, subneutralizing antibodies can enable viral uptake through Fcγ receptors and down-regulate signaling cascades initiated via the pattern recognition receptors TLR-3 and MDA5/RIG-I, thus reducing the antiviral state of the cell. The DENV NS2B/3 protein cleaves human STING/MITA, interfering with induction of IFN-α/β. Finally, DENV NS2A, NS4A, and NS4B complex together to block STAT1 phosphorylation, while NS5 binds and promotes degradation of human STAT2, thus preventing formation of the STAT1/STAT2 heterodimer and its transcriptional induction of interferon stimulating genes. Here, we discuss the host innate immune response to DENV and the mechanisms of immune evasion that DENV has developed to manipulate cellular antiviral responses.
机译：登革热是全球热带和亚热带地区的主要公共卫生问题。登革热病毒的四种血清型（DENV1-DENV4）主要由埃及伊蚊和白纹伊蚊传播，它们的地理范围在不断扩大。人是DENV流行株的唯一宿主，并且该病毒已经开发出复杂的机制来逃避人的先天免疫应答。宿主细胞的第一道防线始于细胞内信号传导级联反应，从而导致产生干扰素α/β（IFN-α/β），从而促进细胞内抗病毒应答，并有助于在DENV感染过程中启动适应性应答。作为响应，DENV已开发出许多方法来破坏这些细胞内抗病毒反应并直接抑制细胞信号传导级联。具体而言，DENV操纵未折叠的蛋白质反应和自噬以抵抗细胞应激并延迟凋亡。 DENV非结构蛋白NS4B和亚基因组黄病毒RNA通过抑制RNase Dicer干扰RNA干扰途径。在异型继发性DENV感染期间，亚中和抗体可以使病毒通过Fcγ受体摄取，并下调通过模式识别受体TLR-3和MDA5 / RIG-1引发的信号级联，从而降低细胞的抗病毒状态。 DENV NS2B / 3蛋白切割人STING / MITA，从而干扰IFN-α/β的诱导。最后，DENV NS2A，NS4A和NS4B复合在一起以阻止STAT1磷酸化，而NS5结合并促进人STAT2的降解，从而阻止STAT1 / STAT2异二聚体的形成及其干扰素刺激基因的转录诱导。在这里，我们讨论了宿主对DENV的先天免疫反应以及DENV开发的操纵细胞抗病毒反应的免疫逃逸机制。

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