登革热病毒和西尼罗河病毒的天然免疫逃逸
Innate immune escape by Dengue and West Nile viruses.
作者信息
Gack Michaela U, Diamond Michael S
机构信息
Department of Microbiology, The University of Chicago, Chicago, IL, 60637, USA.
Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA; Department of Pathology & Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA; Department of Molecular Microbiology, Washington University School of Medicine, St. Louis, MO 63110, USA; Center for Human Immunology and Immunotherapy Programs, Washington University School of Medicine, St. Louis, MO 63110, USA.
出版信息
Curr Opin Virol. 2016 Oct;20:119-128. doi: 10.1016/j.coviro.2016.09.013. Epub 2016 Oct 25.
Dengue (DENV) and West Nile (WNV) viruses are mosquito-transmitted flaviviruses that cause significant morbidity and mortality worldwide. Disease severity and pathogenesis of DENV and WNV infections in humans depend on many factors, including pre-existing immunity, strain virulence, host genetics and virus-host interactions. Among the flavivirus-host interactions, viral evasion of type I interferon (IFN)-mediated innate immunity has a critical role in modulating pathogenesis. DENV and WNV have evolved effective strategies to evade immune surveillance pathways that lead to IFN induction and to block signaling downstream of the IFN-α/β receptor. Here, we discuss recent advances in our understanding of the molecular mechanisms by which DENV and WNV antagonize the type I IFN response in human cells.
登革病毒（DENV）和西尼罗河病毒（WNV）是通过蚊子传播的黄病毒，在全球范围内导致了严重的发病和死亡。人类感染DENV和WNV后的疾病严重程度和发病机制取决于许多因素，包括既往免疫力、毒株毒力、宿主遗传学以及病毒与宿主的相互作用。在黄病毒与宿主的相互作用中，病毒对I型干扰素（IFN）介导的固有免疫的逃避在调节发病机制中起着关键作用。DENV和WNV已经进化出有效的策略来逃避导致IFN诱导的免疫监视途径，并阻断IFN-α/β受体下游的信号传导。在此，我们讨论了我们对DENV和WNV在人类细胞中拮抗I型IFN反应的分子机制的最新认识进展。
Zotero 插件