Sarikonda Ghanashyam, von Herrath Matthias G
Department of Developmental Immunology-3, Diabetes Center of San Diego, La Jolla Institute for Allergy and Immunology, La Jolla, CA, USA.
Methods Mol Biol. 2011;677:431-47. doi: 10.1007/978-1-60761-869-0_27.
For a virus to establish persistence in the host, it has to exploit the host immune system such that the active T-cell responses against the virus are curbed. On the other hand, the goal of the immune system is to clear the virus, following which the immune responses need to be downregulated, by a process known as immunoregulation. There are multiple known immunoregulatory mechanisms that appear to play a role in persistent viral infections. In the recent past, IL-10 and PD-1 have been identified to be playing a significant role in the regulation of antiviral immune responses. The evidence that viruses can escape immunologic attack by taking advantage of the host's immune system is found in LCMV infection of mice and in humans persistently infected with HIV and HCV. The recent observation that the functionally inactive T-cells during chronic viral infections can be made to regain their cytokine secretion and cytolytic abilities is very encouraging. Thus, it would be likely that neutralization negative immune regulation during persistent viral infection would result in the preservation of effector T-cell responses against the virus, thereby resulting in the elimination of the persistent infection.
病毒若要在宿主体内建立持续性感染,就必须利用宿主免疫系统,抑制针对该病毒的活跃T细胞反应。另一方面,免疫系统的目标是清除病毒,之后通过一种称为免疫调节的过程下调免疫反应。有多种已知的免疫调节机制似乎在持续性病毒感染中发挥作用。最近,已确定白细胞介素-10(IL-10)和程序性死亡受体-1(PD-1)在抗病毒免疫反应调节中发挥重要作用。在小鼠的淋巴细胞脉络丛脑膜炎病毒(LCMV)感染以及人类持续感染艾滋病毒(HIV)和丙型肝炎病毒(HCV)的情况中,发现了病毒可通过利用宿主免疫系统逃避免疫攻击的证据。最近观察到,慢性病毒感染期间功能失活的T细胞能够恢复其细胞因子分泌和细胞溶解能力,这非常令人鼓舞。因此,持续性病毒感染期间中和负性免疫调节可能会保留针对病毒的效应T细胞反应,从而消除持续性感染。