To keep the host alive - the role of viral Bcl-2 proteins

被引:10
作者
Polcic, P. [1 ]
Mentel, M. [1 ]
Gavurnikova, G. [1 ]
Bhatia-Kissova, I. [1 ]
机构
[1] Comenius Univ, Fac Nat Sci, Dept Biochem, Mlynska Dolina CH-1,Ilkovicova 6, Bratislava 84215, Slovakia
关键词
apoptosis; vBcl-2; Bcl-2; family; autophagy; virus; EPSTEIN-BARR-VIRUS; SARCOMA-ASSOCIATED HERPESVIRUS; PROGRAMMED CELL-DEATH; BECLIN 1-DEPENDENT AUTOPHAGY; MYXOMA-VIRUS; MURINE GAMMAHERPESVIRUS-68; INHIBITS APOPTOSIS; BH3-ONLY PROTEINS; BLOCKS APOPTOSIS; INFECTED-CELLS;
D O I
10.4149/av_2017_302
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
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.
引用
收藏
页码:240 / 251
页数:12
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