Polčic P, Mentel M, Gavurníková G, Bhatia-Kiššová I
Acta Virol. 2017;61(3):240-251. doi: 10.4149/av_2017_302.
Apoptosis, an intrinsic cellular pathway that eliminates unwanted cells from multicellular organisms, represents an important mechanism for protection against viral infections. When cells infected by viruses get recognized by immune cells, apoptosis is triggered in the infected cells. Among the many regulators of apoptosis involved in this process, a family of proteins homologous to oncogene Bcl-2 plays a central role. Their concerted activities converge to permeabilization of mitochondrial membranes and activation of apoptotic pathways in the presence of diverse apoptotic signals, including virus infection. In the genomes of many viruses, genes encoding for homologues of antiapoptotic proteins of Bcl-2 family can be found. These proteins, collectively referred to as vBcl-2 proteins, inhibit apoptosis in infected cells at the different stages of virus life cycle to enable the virus to complete its replication and to spread.
细胞凋亡是一种从多细胞生物中清除不需要细胞的内在细胞途径,是抵御病毒感染的重要机制。当被病毒感染的细胞被免疫细胞识别时,受感染细胞会触发细胞凋亡。在参与这一过程的众多细胞凋亡调节因子中,与癌基因Bcl-2同源的蛋白质家族发挥着核心作用。在存在包括病毒感染在内的多种凋亡信号的情况下,它们的协同活动共同导致线粒体膜通透性增加和凋亡途径激活。在许多病毒的基因组中,可以发现编码Bcl-2家族抗凋亡蛋白同源物的基因。这些蛋白质统称为vBcl-2蛋白,在病毒生命周期的不同阶段抑制受感染细胞中的细胞凋亡,以使病毒能够完成其复制并传播。