Pandori M W, Fitch N J, Craig H M, Richman D D, Spina C A, Guatelli J C
Department of Medicine, University of California San Diego School of Medicine, California 92093-0619, USA.
J Virol. 1996 Jul;70(7):4283-90. doi: 10.1128/JVI.70.7.4283-4290.1996.
Type 1 human immunodeficiency viruses encoding mutated nef reading frames are 10- to 30-fold less infectious than are isogenic viruses in which the nef gene is intact. This defect in infectivity causes nef-negative viruses to grow at an attenuated rate in vitro. To investigate the mechanism of Nef-mediated enhancement of viral growth rate and infectivity, a complementation analysis of nef mutant viruses was performed. To provide Nef in trans upon viral infection, a CEM derivative cell line (designated CLN) that expresses Nef under the control of the viral long terminal repeat was constructed. When nef-negative virus was grown in CLN cells, its growth rate was restored to wild-type levels. However, the output of nef-negative virus during the first 72 h after infection of CLN cells was not restored, suggesting that provision of Nef within the newly infected cell does not enhance the productivity of a nef-negative provirus. The genetically nef-negative virions produced by the CLN cells, however, were restored to wild-type levels of infectivity as measured in a syncytium formation assay in which CD4-expressing HeLa cells were targets. These trans-complemented, genetically nef-negative virions yielded wild-type levels of viral output following a single cycle of replication in primary CD4 T cells as well as in parental CEM cells. To define the determinants for producer cell modification of virions by Nef, the role of myristoylation was investigated. Virus that encodes a myristoylation-negative nef was as impaired in infectivity as was virus encoding a deleted nef gene. Because myristoylation is required for both membrane association of Nef and optimal viral infectivity, the possibility that Nef protein is included in the virion was investigated. Wild-type virions were purified by filtration and exclusion chromatography. A Western blot (immunoblot) of the eluate fractions revealed a correlation between peak Nef signal and peak levels of p24 antigen. Although virion-associated Nef was detected in part as the 27-kDa full-length protein, the majority of immunoreactive protein was detected as a 20-kDa isoform. nef-negative virus lacked both 27- and 20-kDa immunoreactive species. Production of wild-type virions in the presence of a specific inhibitor of the human immunodeficiency virus type 1 protease resulted in virions which contained only 27-kDa full-length Nef protein. These data indicate that Nef is a virion protein which is processed by the viral protease into a 20-kDa isoform within the virion particle.
编码突变型nef读码框的1型人类免疫缺陷病毒的感染性比nef基因完整的同基因病毒低10至30倍。这种感染性缺陷导致nef阴性病毒在体外以减弱的速率生长。为了研究Nef介导的病毒生长速率和感染性增强的机制,对nef突变病毒进行了互补分析。为了在病毒感染时反式提供Nef,构建了一种CEM衍生细胞系(命名为CLN),该细胞系在病毒长末端重复序列的控制下表达Nef。当nef阴性病毒在CLN细胞中生长时,其生长速率恢复到野生型水平。然而,在感染CLN细胞后的最初72小时内,nef阴性病毒的产量并未恢复,这表明在新感染的细胞中提供Nef并不能提高nef阴性前病毒的产生效率。然而,用表达CD4的HeLa细胞作为靶细胞进行的合胞体形成试验检测显示,CLN细胞产生的基因上nef阴性的病毒粒子的感染性恢复到了野生型水平。这些反式互补的、基因上nef阴性的病毒粒子在原代CD4 T细胞以及亲代CEM细胞中进行单个复制周期后,产生的病毒产量达到野生型水平。为了确定Nef对病毒粒子进行生产者细胞修饰的决定因素,研究了豆蔻酰化的作用。编码无豆蔻酰化nef的病毒与编码缺失nef基因的病毒一样,感染性受损。由于豆蔻酰化对于Nef的膜结合和最佳病毒感染性都是必需的,因此研究了Nef蛋白是否包含在病毒粒子中的可能性。通过过滤和排阻色谱法纯化野生型病毒粒子。对洗脱级分进行的蛋白质免疫印迹(免疫印迹)显示,Nef信号峰值与p24抗原峰值水平之间存在相关性。虽然在病毒粒子相关的Nef中部分检测为27 kDa的全长蛋白,但大多数免疫反应性蛋白检测为20 kDa的异构体。nef阴性病毒缺乏27 kDa和20 kDa的免疫反应性物种。在存在1型人类免疫缺陷病毒蛋白酶的特异性抑制剂的情况下产生野生型病毒粒子,结果产生的病毒粒子仅含有27 kDa的全长Nef蛋白。这些数据表明,Nef是一种病毒粒子蛋白,在病毒粒子内被病毒蛋白酶加工成20 kDa的异构体。