Neuropathogenesis of Japanese encephalitis virus.
Neuropathogenesis of Japanese encephalitis virus.
复制标题
日本脑炎病毒的神经发病机制。
作者：
K. Yasui
在中枢神经系统中，日本脑炎病毒只能在神经元中复制。并对嗜神经性的机理进行了分析。大鼠脑对日本脑炎病毒感染的易感性与神经元的不成熟密切相关。病毒与细胞的初始特异性结合是日本脑炎病毒嗜神经性的原因之一。用抗E蛋白的中和性单克隆抗体治疗日本脑炎病毒感染，不能抑制病毒与细胞表面的结合，但强烈抑制日本脑炎病毒诱导的细胞融合和病毒内化到宿主细胞中。其中一个基因组区域负责的神经发病机制的日本脑炎病毒位于E蛋白编码区。E蛋白第138位氨基酸对乙脑病毒的神经致病性表达具有重要意义。E蛋白的细胞融合活性与病毒的神经致病性密切相关。
In the central nervous system, the Japanese encephalitis virus can replicate only in neurons. The mechanism of the type of neurotropism was analyzed. The susceptibility to Japanese encephalitis virus infection in the rat brain was closely associated with neuronal immaturity. The initial specific binding of the virus to cells is one of the reasons for neurotropism of the Japanese encephalitis virus. The treatment of Japanese encephalitis virus infection with the neutralizing monoclonal antibody against the E protein did not inhibit the virus from binding to the cell surfaces, but strongly inhibited Japanese encephalitis virus-induced cell fusion and internalization of the virus into the host cells. One of the genome regions responsible for neuropathogenesis of the Japanese encephalitis virus was located on the E protein-coding region. The 138th amino acid of the E protein was important for neuropathogenesis expression of the Japanese encephalitis virus. The cell fusion activity of the E protein was closely correlated with neuropathogenesis of the virus.