Lafon M
Neuroimmunologie Virale, Département de Virologie, Institut Pasteur, Paris, France.
Dev Biol (Basel). 2008;131:413-9.
It is intriguing to note that RABV progression is interrupted neither by destruction of the infected neuron nor by the immune response. Thus, it is likely that RABV has developed a subversive strategy to avoid functional neuron impairment, which compromises the infectious cycle. Rabies virus neuroinvasiveness results from two factors: not only does neurotropic rabies virus avoid inducing neuronal cell death, but also 'protective' T cells that migrate into the infected nervous system are killed by apoptosis or inactivated, as a result of the overexpression of immunosubversive molecules such as FasL, HLA-G or B7-H1 in the infected nervous system. This suggests that the preservation of the neuronal network and the destruction of T cells that invade the nervous system in response to the infection are crucial events for rabies virus neuroinvasion and for transmission of rabies virus to another animal. Implications of these findings for rabies treatment are discussed.
值得注意的是，狂犬病毒（RABV）的进展既不会被受感染神经元的破坏所阻断，也不会被免疫反应所阻断。因此，狂犬病毒很可能已经形成了一种颠覆性策略来避免功能性神经元损伤，而这种损伤会损害感染周期。狂犬病毒的神经侵袭性源于两个因素：嗜神经性狂犬病毒不仅能避免诱导神经元细胞死亡，而且由于感染的神经系统中免疫颠覆性分子如FasL、HLA - G或B7 - H1的过度表达，迁移到受感染神经系统的“保护性”T细胞会通过凋亡被杀死或失活。这表明，神经网络的保存以及对感染做出反应而侵入神经系统的T细胞的破坏，是狂犬病毒神经侵袭以及狂犬病毒传播给另一只动物的关键事件。文中讨论了这些发现对狂犬病治疗的意义。
