Phillips T R, Talbott R L, Lamont C, Muir S, Lovelace K, Elder J H
Department of Molecular Biology, Scripps Clinic and Research Foundation, La Jolla, California 92037.
J Virol. 1990 Oct;64(10):4605-13. doi: 10.1128/JVI.64.10.4605-4613.1990.
Two molecular clones of feline immunodeficiency virus were compared. The first clone, 34TF10, was from a Petaluma, Calif., isolate; the second, PPR, was isolated from a cat in the San Diego, Calif., area. The cats from which the isolates were obtained suffered from chronic debilitating illnesses. The two molecular clones differed in their in vitro host cell range. The 34TF10 clone infected the Crandall feline kidney and G355-5 cell lines, but replicated less efficiently on feline peripheral blood leukocytes. In contrast, the PPR clone productively infected the primary feline peripheral blood leukocytes but not Crandall feline kidney or G355-5 cells. The 34TF10 and PPR clones had an overall sequence identity of 91%. The env gene was the least conserved (85% at the amino acid level). Additionally, the potential open reading frame for a Tat-like protein, ORF 2, contained a stop codon in the 34TF10 isolate which was not found in the PPR clone. This truncation did not prevent in vitro or in vivo replication of 34TF10. Two splice acceptor sites were identified in the 34TF10 clone. One was 5' to the beginning of the putative tat open reading frame, and the other was 5' to the putative vif product. Both of these acceptor sites were conserved in the PPR clone. The long terminal repeats of the viruses were 7% divergent between the two clones, with a lack of conservation in putative NF-kappa B, LBP-1, and CCAAT enhancer-promoter sites.
对猫免疫缺陷病毒的两个分子克隆进行了比较。第一个克隆34TF10来自加利福尼亚州佩塔卢马的一个分离株；第二个克隆PPR是从加利福尼亚州圣地亚哥地区的一只猫身上分离得到的。分离出这些毒株的猫患有慢性衰弱性疾病。这两个分子克隆在体外宿主细胞范围上有所不同。34TF10克隆可感染克兰德尔猫肾细胞和G355-5细胞系，但在猫外周血白细胞上的复制效率较低。相比之下，PPR克隆能有效感染原代猫外周血白细胞，但不能感染克兰德尔猫肾细胞或G355-5细胞。34TF10和PPR克隆的总体序列同一性为91%。env基因的保守性最低（氨基酸水平为85%）。此外，一个类似Tat蛋白的潜在开放阅读框ORF 2在34TF10分离株中含有一个终止密码子，而在PPR克隆中未发现。这种截短并不妨碍34TF10在体外或体内的复制。在34TF10克隆中鉴定出两个剪接受体位点。一个位于假定的tat开放阅读框起始处的5'端，另一个位于假定的vif产物的5'端。这两个剪接受体位点在PPR克隆中是保守的。两个克隆的病毒长末端重复序列有7%的差异，在假定的NF-κB、LBP-1和CCAAT增强子-启动子位点缺乏保守性。
