Ghosh Sourish, Basu Anirban
National Brain Research Centre, Manesar 122051, Haryana, India.
Natl Med J India. 2017 Jan-Feb;30(1):21-25.
Chandipura virus (CHPV) has been contributing to the rising number of premature deaths due to acute encephalitis syndrome for over a decade in India. CHPV belongs to the family Rhabdoviridae. Neuropathogenesis of CHPV has been well established but the exact route of entry into the central nervous system (CNS) and the triggering factor for neuronal death are still unknown. Rabies virus and vesicular stomatitis virus, which are related closely to CHPV, enter the CNS retrogradely from peripheral or olfactory neurons. Disruption of the blood-brain barrier has also been connoted in the entry of CHPV into the CNS. CHPV upon entering the neurons triggers cellular stress factors and release of reactive oxygen species (ROS). The stress granules produced in response to cellular stress have been implicated in viral replication and ROS generation, which stimulates neuronal death. Both these phenomena cohesively explain the neuropathogenesis and neurodegeneration following CHPV infection.
在印度，十多年来，钱迪普拉病毒（CHPV）一直导致因急性脑炎综合征而早亡的人数不断上升。CHPV属于弹状病毒科。CHPV的神经发病机制已得到充分证实，但进入中枢神经系统（CNS）的确切途径以及神经元死亡的触发因素仍然未知。与CHPV密切相关的狂犬病病毒和水疱性口炎病毒从外周或嗅觉神经元逆行进入中枢神经系统。血脑屏障的破坏也与CHPV进入中枢神经系统有关。CHPV进入神经元后会触发细胞应激因子并释放活性氧（ROS）。细胞应激产生的应激颗粒与病毒复制和ROS生成有关，后者会刺激神经元死亡。这两种现象共同解释了CHPV感染后的神经发病机制和神经变性。
