疱疹单一的病毒(HSV-1 和 HSV-2 ) 引起全球病态并且 synergistically 与 HIV 感染相关。HSV 存在在在有断断续续的复活的感觉神经原的一种潜伏的形式终生,在里面尽管有主人免疫监视。当时为防碍天生的有免疫力的回答以便赞成病毒的复制和繁殖的 HSV 的丰富的证据,证据的几根线声明 HSV 由各种各样的机制稀释适应豁免,包括然而并非限于抗原表示的脱离,细胞死感应,并且细胞的发信号的打断。在这评论,我们将在 T 房间发信号集中于 HSV 的 perturbative 角色。
Herpes simplex viruses (HSV-1 and HSV-2) cause global morbidity and synergistically correlate with HIV infection. HSV exists life-long in a latent form in sensory neurons with intermittent reactivation, in despite of host immune surveillatlce. While abundant evidence for HSV interfering with innate immune responses so as to favor the replication and propagation of the virus, several lines of evidence declare that HSV attenuates adaptive immunity by various mechanisms, including but not limited to the ablation of antigen presentation, induction of apoptosis, and interruption of cellular signaling. In this review, we will focus on the perturbative role of HSV in T cells signaling.