疱疹病毒对趋化因子受体的分子劫持。

Infectious agents and disease Pub Date : 1994-04-01
P M Murphy
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引用次数: 0

摘要

病毒要成为一个成功的生物实体,必须利用正常的细胞功能,避开宿主的免疫系统;它们通常通过分子模仿来做到这一点。模仿可能发生的一种方式是病毒复制和修改宿主基因。这方面研究得最好的例子是RNA逆转录病毒的致癌基因,但越来越多的例子也被称为DNA病毒。到目前为止,它们都来自两组DNA病毒,疱疹病毒和痘病毒,大多数例子是基因的产物调节免疫反应,如细胞因子,细胞因子受体和补体控制蛋白。这篇综述将关注人类和疱疹病毒趋化因子受体,趋化因子是白细胞趋化因子和激活因子家族,被认为是重要的炎症介质。虽然病毒趋化因子受体同源物的生物学作用目前尚不清楚,但它们与特定的趋化因子集的联系提示了许多可能的功能。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Molecular piracy of chemokine receptors by herpesviruses.

To succeed as a biological entity, viruses must exploit normal cellular functions and elude the host immune system; they often do so by molecular mimicry. One way that mimicry may occur is when viruses copy and modify host genes. The best studied examples of this are the oncogenes of RNA retroviruses, but a growing number of examples are also known for DNA viruses. So far they all come from just two groups of DNA viruses, the herpesviruses and poxviruses, and the majority of examples are for genes whose products regulate immune responses, such as cytokines, cytokine receptors, and complement control proteins. This review will focus on human and herpesvirus receptors for chemokines, a family of leukocyte chemoattractant and activating factors that are thought to be important mediators of inflammation. Although the biological roles of the viral chemokine receptor homologues are currently unknown, their connection to specific sets of chemokines has suggested a number of possible functions.

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