Nucleotide sequences of a feline leukemia virus subgroup A envelope gene and long terminal repeat and evidence for the recombinational origin of subgroup B viruses
Nucleotide sequences of a feline leukemia virus subgroup A envelope gene and long terminal repeat and evidence for the recombinational origin of subgroup B viruses
复制标题
猫白血病病毒A亚型包膜基因的核苷酸序列和长末端重复以及B亚型病毒重组起源的证据
作者：
M. Stewart;M. Warnock;A. Wheeler;N. Wilkie;J. Mullins;D. Onions;J. Neil
已获得A亚型猫白血病病毒FeLV-A/Glasgow-1的分子克隆。对原病毒基因组 3' 端的核苷酸序列分析以及与已发表的 FeLV-B/Gardner-Arnstein 序列的比较表明，最广泛的差异位于 env 基因的 5' 结构域内。在该结构域内，env 的几个不同区域被更保守的片段分隔开。 env 的 3' 末端高度保守，与 p15env 仅有一个氨基酸编码差异。原病毒长末端重复序列也高度保守，仅存在八个碱基取代和一个碱基插入。使用由 FeLV-A 或 FeLV-B env 基因构建的特异性探针来比较各种外源 FeLV 分离株和正常猫 DNA 的内源 FeLV 相关原病毒的 env 基因。 FeLV-A 衍生的 env 探针未显示与正常猫 DNA 的杂交，但检测到所有测试的 FeLV-A 和 FeLV-C 分离株。相比之下，FeLV-B env 探针检测到独立的 FeLV-B 分离株和内源性 FeLV 相关原病毒家族。我们的观察结果提供了强有力的证据来支持这样的假设：FeLV-B 病毒是由 FeLV-A 与猫 DNA 中内源性前病毒元件重组而产生的。
Molecular clones of the subgroup A feline leukemia virus FeLV-A/Glasgow-1 have been obtained. Nucleotide sequence analysis of the 3' end of the proviral genome and comparison with the published sequence of FeLV-B/Gardner-Arnstein showed that the most extensive differences are located within the 5' domain of the env gene. Within this domain, several divergent regions of env are separated by more conserved segments. The 3' end of env is highly conserved, with only a single amino acid coding difference in p15env. The proviral long terminal repeats are also highly conserved, differing by only eight base substitutions and one base insertion. Specific probes constructed from the FeLV-A or FeLV-B env genes were used to compare the env genes of various exogenous FeLV isolates and the endogenous FeLV-related proviruses of normal cat DNA. An FeLV-A-derived env probe showed no hybridization to normal cat DNA but detected all FeLV-A and FeLV-C isolates tested. In contrast, an FeLV-B env probe detected independent FeLV-B isolates and a family of endogenous FeLV-related proviruses. Our observations provide strong evidence to support the hypothesis that FeLV-B viruses have arisen by recombination between FeLV-A and endogenous proviral elements in cat DNA.