Wagener S, Dittmar M T, Beer B, König R, Plesker R, Norley S, Kurth R, Cichutek K
Department of Medical Biotechnology, Paul-Ehrlich-Institut, Langen, Germany.
J Virol. 1998 Apr;72(4):3446-50. doi: 10.1128/JVI.72.4.3446-3450.1998.
Two chimeric proviruses comprising the U3 promoter and the nef gene of simian immunodeficiency virus (SIV) smmPBj1.9 in addition to other genomic regions of SIVagm3mc from African green monkeys (Cercopithecus aethiops) were constructed. The derived chimeric viruses (SIVagm3mc/SIVsmmPBj1.9) were both able to replicate in nonstimulated peripheral blood leukocytes from pig-tailed macaques (Macaca nemestrina), a biological property often correlated with acute pathogenicity. However, only one of the chimeric viruses was acutely pathogenic, inducing a rapid depletion of the peripheral CD4+ T cells in two infected pig-tailed macaques within 10 days after infection in a manner similar to infection with SIVsmmPBj1.9 itself. The other chimeric virus actively replicated during the first 8 weeks after experimental infection of two pig-tailed macaques but induced neither acute disease nor CD4+ T-cell depletion for 113 weeks after infection. Thus, the U3 promoter and the nef gene of SIVsmmPBj1.9 alone appear to be insufficient to confer acute pathogenicity to SIVagm3mc.
构建了两种嵌合前病毒，除了来自非洲绿猴（猕猴属埃塞俄比亚种）的SIVagm3mc的其他基因组区域外，还包含猿猴免疫缺陷病毒（SIV）smmPBj1.9的U3启动子和nef基因。衍生的嵌合病毒（SIVagm3mc/SIVsmmPBj1.9）都能够在来自猪尾猕猴（食蟹猕猴）的未刺激外周血白细胞中复制，这种生物学特性通常与急性致病性相关。然而，只有一种嵌合病毒具有急性致病性，在感染后的10天内，以类似于SIVsmmPBj1.9自身感染的方式，导致两只感染猪尾猕猴的外周CD4+T细胞迅速耗竭。另一种嵌合病毒在实验感染两只猪尾猕猴后的前8周内活跃复制，但在感染后的113周内既未引发急性疾病，也未导致CD4+T细胞耗竭。因此，单独的SIVsmmPBj1.9的U3启动子和nef基因似乎不足以赋予SIVagm3mc急性致病性。
