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

疱疹病毒可以引起感染，并持续宿主的一生。它们进化出许多机制来逃避宿主的免疫反应，否则这些免疫反应就会消灭它们。疱疹病毒家族中特别擅长避免宿主免疫的成员之一是巨细胞病毒。这种病毒虽然不会对健康的人造成症状，但在免疫系统受到抑制的人，如移植和艾滋病患者，以及免疫系统发育不良的胎儿中，它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名为CD44的细胞受体的功能，CD44具有一系列细胞功能，包括细胞迁移、激活和增殖以及信号转导。M11与CD44的相互作用改变了细胞的迁移，并可能影响细胞的激活。确定M11如何调节其影响将使我们能够定义开发潜在抗病毒疗法的策略。由于CD44也参与了一系列不适当炎症发展的疾病，因此M11或其衍生物可能被利用来缓解这些炎症性疾病。

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.