Laboratory of Molecular Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA.
Inflammation, Repair and Development Section, National Heart and Lung Institute, Faculty of Medicine, Imperial College London, London, United
J Innate Immun. 2018;10(5-6):465-478. doi: 10.1159/000492161. Epub 2018 Aug 30.
Viruses use diverse molecular mechanisms to exploit and evade the immune response. Herpesviruses, in particular, encode functional chemokine and chemokine receptor homologs pirated from the host, as well as secreted chemokine-binding proteins with unique structures. Multiple functions have been described for herpesvirus chemokine components, including attraction of target cells, blockade of leukocyte migration, and modulation of gene expression and cell entry by the virus. Here we review current concepts about how human herpesvirus chemokines, chemokine receptors, and chemokine-binding proteins may be used to shape a proviral state in the host.
病毒利用多种分子机制来利用和逃避免疫反应。疱疹病毒，特别是，编码从宿主中窃取的功能性趋化因子和趋化因子受体同源物，以及具有独特结构的分泌趋化因子结合蛋白。已经描述了疱疹病毒趋化因子成分的多种功能，包括吸引靶细胞、阻断白细胞迁移以及病毒对基因表达和细胞进入的调节。在这里，我们回顾了关于人类疱疹病毒趋化因子、趋化因子受体和趋化因子结合蛋白如何在宿主中形成前病毒状态的现有概念。
