Simon J H, Southerling T E, Peterson J C, Meyer B E, Malim M H
Howard Hughes Medical Institute, University of Pennsylvania School of Medicine, Philadelphia 19104-6148, USA.
J Virol. 1995 Jul;69(7):4166-72. doi: 10.1128/JVI.69.7.4166-4172.1995.
The productive infection of many susceptible human cells, including lymphocytes and macrophages derived from peripheral blood, by the pathogenic lentivirus human immunodeficiency virus type 1 requires expression of the virally encoded vif (for virion infectivity factor) gene. Interestingly, this gene appears to have been conserved among all of the lentiviruses of primates and almost all of the lentiviruses of nonprimates. Using T cells constitutively expressing vif genes derived from diverse sources and virus replication assays, we show that the vif gene of a second primate lentivirus, simian immunodeficiency virus from macaques, complements vif-defective human immunodeficiency virus type 1 but that those of three distinct nonprimate lentiviruses do not. Although the molecular basis for Vif function has yet to be defined, the potential implications of this noted restriction of vif complementarity are discussed.
致病性慢病毒1型人类免疫缺陷病毒对包括源自外周血的淋巴细胞和巨噬细胞在内的许多易感人类细胞进行有效感染,需要表达病毒编码的vif(病毒体感染因子)基因。有趣的是,该基因似乎在所有灵长类慢病毒以及几乎所有非灵长类慢病毒中都得以保留。我们使用组成性表达源自不同来源的vif基因的T细胞和病毒复制试验,结果表明,第二种灵长类慢病毒——猕猴猿猴免疫缺陷病毒的vif基因可补充有vif缺陷的1型人类免疫缺陷病毒,但三种不同的非灵长类慢病毒的vif基因则不能。尽管Vif功能的分子基础尚未明确,但我们讨论了这种vif互补性明显受限的潜在影响。