L'Honneur Anne-Sophie, Rozenberg Flore
Hôpital Cochin, Pôle biologie pharmacie pathologie, Université Paris Descartes et APHP, Service de virologie bâtiment Jean-Dausset, 27, rue du Faubourg-saint-Jacques, 75679 Paris cedex 14, France.
Virologie (Montrouge). 2016 Jun 1;20(3):174-187. doi: 10.1684/vir.2016.0653.
JC virus (JCV) is an ubiquitous human polyomavirus which causes persistent infections. The biological cycle of JCV in its host is incompletely known. Most infected individuals remain asymptomatic lifelong despite occasional viral urinary shedding. In some cases of immune depression, JCV may reactivate, gain access to the central nervous system, infect and harm glial cells involved in myelin production, leading to a fatal demyelinating disease called progressive multifocal leukoencephalopathy (PML). PML cases have recently increased in patients receiving monoclonal antibody therapies - in particular multiple sclerosis patients treated with natalizumab - raising a new interest in the pathophysiology of JCV infection. The tropism of JCV for glial cells has been associated with various mutations and rearrangements in the non-coding control region (NCCR) of JCV genome, a regulator of viral expression. Several hypotheses have taken into account this hypervariability to explain the pathogenesis of JCV infection.
JC病毒(JCV)是一种普遍存在的人类多瘤病毒,可引起持续性感染。JCV在其宿主中的生物循环尚不完全清楚。尽管偶尔会有病毒从尿液中排出,但大多数受感染个体终身无症状。在某些免疫抑制的情况下,JCV可能会重新激活,进入中枢神经系统,感染并损害参与髓鞘生成的神经胶质细胞,导致一种致命的脱髓鞘疾病,称为进行性多灶性白质脑病(PML)。最近,接受单克隆抗体治疗的患者,尤其是接受那他珠单抗治疗的多发性硬化症患者中,PML病例有所增加,这引发了人们对JCV感染病理生理学的新兴趣。JCV对神经胶质细胞的嗜性与JCV基因组非编码控制区(NCCR)的各种突变和重排有关,NCCR是病毒表达的调节因子。有几种假说考虑到了这种高度变异性来解释JCV感染的发病机制。