The role of the interaction of the CMV m11 immune evasion molecule with CD44 in viral pathogenesis

疱疹病毒可引起持续宿主一生的感染。它们已经进化出许多机制来躲避宿主的免疫反应，否则这些免疫反应会消灭它们。巨细胞病毒是疱疹病毒家族中一个特别擅长逃避宿主免疫的成员。这种病毒虽然不会在健康个体中引起症状，但在免疫系统受到抑制的个体（如移植和艾滋病患者）和免疫系统发育不良的胎儿中，是疾病和死亡的重要原因。在目前的项目中，我们将在分子水平上探索一种名为m11的病毒编码分子如何干扰一种名为CD44的细胞受体的功能，该受体具有一系列细胞功能，包括细胞迁移，活化和增殖以及信号转导。m11与CD44的相互作用改变细胞迁移，并可能影响细胞活化。明确m11是如何介导其影响的，将使我们能够确定开发潜在抗病毒疗法的策略。由于CD44也参与促进一系列疾病，其中不适当的炎症发展，可能是m11或其衍生物，可以用来改善这些炎症性疾病。

Herpesviruses can cause infections that persist for the lifetime of the host. They have evolved many mechanisms to elude the host's immune response that would otherwise eliminate them. One memberof the herpesvirus family that is particularly adept at avoiding host immunity is cytomegalovirus. This virus, while not causing symptoms in healthy individuals, is a significant cause of disease and mortality in individuals with suppressed immune systems such as transplant and AIDS patients, and in the fetus which has a poorly developed immune system. In the current project we will explore at a molecular level how a virus-encoded molecule called m11 interferes with the functions of a cellular receptor called CD44 that has a range of cell functions including cell migration, activation and proliferation and signal transduction. The interaction of m11 with CD44 modifies cell migration and is likely to affect cell activation. Defining how m11 mediates its affects will allow us to define strategies to develop potential antiviral therapies. As CD44 is also involed in contributing to a range of diseases where inappropriate inflammation develops it may be that m11, or derivatives of it, could be harnessed to ameliorate these inflammatory diseases.