Coutelier Jean-Paul
Université catholique de Louvain, Christian de Duve Institute, unité de médecine expérimentale, 1200 Bruxelles, Belgique.
Virologie (Montrouge). 2014 Feb 1;18(1):17-24. doi: 10.1684/vir.2014.0545.
Lactate dehydrogenase-elevating virus (LDV), a mouse arterivirus, is characterized by a lifelong viremia, despite antiviral innate and adaptative immune response. It induces strong modifications of the host immune microenvironment, including macrophage and natural killer cell activation, secretion of pro-inflammatory cytokines, modulation of T helper cell differentiation and polyclonal activation of B-lymphocytes. This modification of the immune microenvironment results in the protection against some diseases such as allergies, graft-versus-host reaction, experimental autoimmune encephalitis, and growth of some tumors. In contrast, it exacerbates other pathologies such as endotoxin shock and autoantibody-mediated autoimmune diseases. Thus, LDV infection provides an interesting model to understand the consequences of viral infections on pathogenic mechanisms and to define new therapeutic approaches.
乳酸脱氢酶升高病毒（LDV）是一种小鼠动脉炎病毒，其特征是尽管存在抗病毒固有免疫和适应性免疫反应，但仍会出现终身病毒血症。它会引起宿主免疫微环境的强烈改变，包括巨噬细胞和自然杀伤细胞的激活、促炎细胞因子的分泌、辅助性T细胞分化的调节以及B淋巴细胞的多克隆激活。免疫微环境的这种改变可导致对某些疾病的保护作用，如过敏、移植物抗宿主反应、实验性自身免疫性脑脊髓炎以及某些肿瘤的生长。相反，它会加剧其他病理状况，如内毒素休克和自身抗体介导的自身免疫性疾病。因此，LDV感染为理解病毒感染对致病机制的影响以及确定新的治疗方法提供了一个有趣的模型。
