Galindo Inmaculada, Hernaez Bruno, Díaz-Gil Gema, Escribano Jose M, Alonso Covadonga
Departamento de Biotecnología, Instituto Nacional de Investigación y Tecnología Agraria y Alimentaria (INIA), Madrid, Spain.
Virology. 2008 Jun 5;375(2):561-72. doi: 10.1016/j.virol.2008.01.050. Epub 2008 Mar 10.
Several large DNA viruses encode Bcl-2 protein homologues involved in the regulation of the cellular apoptosis cascade. This regulation often involves the interaction of these viral proteins with diverse cellular Bcl-2 family members. We have identified the specific interactions of A179L, an African swine fever virus (ASFV) Bcl-2 homologue, with the active forms of the porcine BH3-only Bid protein (truncated Bid p13 and p15). Transient expression of ASFV A179L gene in Vero cells prevented apoptosis induced by these active forms of Bid protein. Interestingly, A179L protein was able to interact, also with the main core Bcl-2 proapoptotic proteins Bax and Bak, and with several BH3-only proteins with selective binding restrictions for full length Bid and Noxa. These results suggest a fine regulation for A179L action in the suppression of apoptosis in infected cells which is essential for efficient virus replication.
几种大型DNA病毒编码参与细胞凋亡级联反应调控的Bcl-2蛋白同源物。这种调控通常涉及这些病毒蛋白与多种细胞Bcl-2家族成员的相互作用。我们已经确定了非洲猪瘟病毒（ASFV）的Bcl-2同源物A179L与猪仅含BH3结构域的Bid蛋白（截短的Bid p13和p15）的活性形式之间的特异性相互作用。ASFV A179L基因在Vero细胞中的瞬时表达可防止由这些活性形式的Bid蛋白诱导的细胞凋亡。有趣的是，A179L蛋白还能够与主要的核心促凋亡Bcl-2蛋白Bax和Bak相互作用，并且能够与几种仅含BH3结构域的蛋白相互作用，这些蛋白对全长Bid和Noxa具有选择性结合限制。这些结果表明，A179L在抑制感染细胞凋亡中的作用存在精细调控，这对于有效的病毒复制至关重要。
