Novel immune evasion strategy of CMV: targeting of an adhesion molecule involved in leukocyte recruitment/activation.

疱疹病毒引起持续的终身感染。为了实现这一目标，它们进化出了各种机制来逃避免疫反应，以对抗它们。它们还将其基因产物的表达最小化为最小的一组潜伏相关蛋白质。疱疹病毒家族的一个成员是巨细胞病毒。虽然在健康个体中，它会引起免疫系统感染，但在免疫系统受到抑制的个体（如移植和AIDS患者）以及免疫系统发育不良的胎儿中，它会引起严重的疾病和死亡。巨细胞病毒引起持续性和潜伏性终身感染。在目前的建议中，我们将评估存在于小鼠巨细胞病毒中的病毒基因，该基因编码与细胞粘附分子结合的蛋白质。这种称为CD 44的粘附分子参与免疫效应细胞向感染部位的迁移及其活化。因此，病毒基因代表了一种潜在的免疫逃避分子，其具有通过减少清除病毒感染的细胞的浸润和/或活化来破坏宿主免疫应答的能力。这些研究的结果可以帮助我们设计抗病毒药物，干扰这种病毒蛋白的作用，从而提供一种新的抗病毒治疗策略。

Herpesviruses cause persistent lifelong infection. To achieve this they have evolved a variety of mechanisms to evade the immune response mounted to combat them. They also minimise the expression of their gene products to a minimal suite of latency associated proteins. One member of the herpesvirus family is cytomegalovirus. While in healthy individuals it causes aymptomatic infection, it causes significant disease and mortality in individuals whose immune systems are suppressed such as transplant and AIDS patients, and also in the fetus which has a poorly developed immune system. Cytomegaloviruses set up persistent and latent lifelong infections. In the current proposal we will be assessing a viral gene present in mouse cytomegalovirus that codes for a protein that binds to a cellular adhesion molecule. This adhesion molecule called CD44 is involved in the migration of immune effector cell to sites of infection and in their activation. The viral gene thus represents a potential immune evasion molecule with the ability to subvert the host's immune response by reducing the infiltration and-or activation of cells that clear virus infection. The results from these studies could help us design anti-viral drugs that interfere with the effect of this viral protein, thus providing a novel anti-viral treatment strategy.