Murphy P M
Laboratory of Host Defenses, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892.
Infect Agents Dis. 1994 Apr-Jun;3(2-3):137-54.
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.
作为生物实体要成功存活,病毒必须利用正常的细胞功能并躲避宿主免疫系统;它们常常通过分子模拟来做到这一点。模拟可能发生的一种方式是病毒复制并修饰宿主基因。对此研究得最透彻的例子是RNA逆转录病毒的癌基因,但DNA病毒的此类例子也越来越多。到目前为止,它们都仅来自两组DNA病毒,即疱疹病毒和痘病毒,并且大多数例子是关于其产物调节免疫反应的基因,如细胞因子、细胞因子受体和补体控制蛋白。本综述将聚焦于人类疱疹病毒的趋化因子受体,趋化因子是一类白细胞趋化和激活因子,被认为是炎症的重要介质。尽管目前尚不清楚病毒趋化因子受体同源物的生物学作用,但它们与特定趋化因子组的联系提示了一些可能的功能。