Ambystoma tigrinum virus (ATV) (family Iridoviridae, genus Ranavirus) was isolated from diseased tiger salamanders (Ambystoma tigrinum stebbinsi) from the San Rafael Valley in southern Arizona, USA in 1996. Genomic sequencing of ATV, as well as other members of the genus, identified an open reading frame that has homology to the eukaryotic translation initiation factor, eIF2α (ATV eIF2α homologue, vIF2αH). Therefore, we asked if the ATV vIF2αH could also inhibit PKR. To test this hypothesis, the ATV vIF2αH was cloned into vaccinia virus (VACV) in place of the well-characterized VACV PKR inhibitor, E3L. Recombinant VACV expressing ATV vIF2αH partially rescued deletion of the VACV E3L gene. Rescue coincided with rapid degradation of PKR in infected cells. These data suggest that the salamander virus, ATV, contains a novel gene that may counteract host defenses, and this gene product may be involved in the presentation of disease caused by this environmentally important pathogen.

Ambystoma螈病毒（ATV）（家庭虹彩病毒科，属株蛙虹彩病毒）的患病虎纹钝口螈隔离（Ambystoma螈stebbinsi）于1996年从美国亚利桑那州南部的圣拉斐尔山谷（San Rafael Valley）进行。ATV以及该属的其他成员的基因组测序确定了一个与真核翻译起始因子eIF2α（ATVeIF2α同源物，vIF2αH同源）的开放阅读框。 ）。因此，我们询问ATVvIF2αH是否也可以抑制PKR。为了验证该假设，将ATVvIF2αH克隆到牛痘病毒（VACV）中，以替代特征明确的VACV PKR抑制剂E3L。表达ATVvIF2αH的重组VACV部分挽救了VACV E3L基因的缺失。抢救与感染细胞中PKR的快速降解相吻合。这些数据表明，sal病毒ATV包含可能抵消宿主防御的新基因，并且该基因产物可能参与了这种由环境重要的病原体引起的疾病。