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风疹病毒是披膜病毒科风疹病毒属的唯一成员,能够诱导细胞发生细胞凋亡。Ras-Raf-MEK-ERK和PI3KAkt信号通路是病毒增殖与细胞生存的必要通路,在细胞凋亡过程中起着必不可少的作用。p53蛋白和TAp63蛋白能够进入细胞核与DNA特异结合,抑制Bcl-2的表达,促进Bax的表达,导致线粒体内外膜间的物质(细胞色素C等)释放,进而引起caspase级联反应,最终导致细胞凋亡。本文从风疹病毒感染的细胞系,病毒感染导致的细胞病理改变和病毒诱导的细胞凋亡信号通路及其相关因子等方面对风疹病毒诱导细胞凋亡的分子机制进行了综述。
Rubella virus is the only member of the genus Togaviridae that is capable of inducing apoptosis in cells. Ras-Raf-MEK-ERK and PI3KAkt signaling pathways are the necessary pathways for virus proliferation and cell survival, and play an essential role in the process of apoptosis. p53 protein and TAp63 protein can enter the nucleus and DNA specific binding, inhibit the expression of Bcl-2 and promote the expression of Bax, resulting in the release of mitochondrial substances between the outer membrane (cytochrome C, etc.), which in turn led to caspase cascade, eventually leading to cells Apoptosis. This review summarizes the molecular mechanisms of rubella virus-induced apoptosis in cell lines infected with rubella virus, cytopathological changes caused by virus infection, virus-induced apoptosis signaling pathways and their related factors.