Genetic characterization of vif, vpr, and vpu sequences from long-term survivors of human immunodeficiency virus type 1 infection.
Genetic characterization of vif, vpr, and vpu sequences from long-term survivors of human immunodeficiency virus type 1 infection.
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人类免疫缺陷病毒 1 型感染长期幸存者的 vif、vpr 和 vpu 序列的遗传特征。
DOI：
10.1006/viro.1996.8378
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发表时间：
1997
期刊：
影响因子：
--
通讯作者：
Ho,DD
中科院分区：
文献类型：
--
作者：
Zhang,L;Huang,Y;Yuan,H;Tuttleton,S;Ho,DD
识别hiv -1感染者，尽管长期感染仍无症状，为了解艾滋病发病机制中涉及的病毒学和宿主因素提供了独特的机会。我们之前已经确定了10名长期幸存者（LTS），尽管13至15年的HIV-1感染，但临床健康且免疫正常。在这项研究中，我们在这些LTS中检测了HIV-1的三个辅助基因vif、vpr和vpu。从这些患者的外周血单个核细胞中共获得52vif、54vpr和55vpun核苷酸序列。分析这些序列没有发现明显的缺失或插入。大多数克隆是全长的，具有完整的开放阅读框。LTS的vif、vpr和vpusx序列的系统发育分析表明，研究对象中发现的HIV-1毒株与艾滋病患者中发现的HIV-1毒株没有显著差异，LTS中的病毒不太可能具有共同的遗传起源。此外，来自LTS和艾滋病患者的病毒之间的总体遗传多样性程度相似，这表明遗传多样性程度与疾病发展速度之间不太可能存在显著相关性。除遗传差异外的其他因素，如病毒载量和表型，可能对疾病状态有更大的影响。
The identification of HIV-1-infected individuals who remain asymptomatic despite prolonged infection presents a unique opportunity to understand virologic and host factors involved in the pathogenesis of AIDS. We have previously identified 10 long-term survivors (LTS) who are clinically healthy and immunologically normal despite 13 to 15 years of HIV-1 infection. In this study, we examined three accessory genes of HIV-1,vif, vpr,andvpu,in these LTS. A total of 52vif,54vpr,and 55vpunucleotide sequences were obtained from the peripheral blood mononuclear cells of these patients. Analysis of these sequences revealed no gross deletions or insertions. Most of the clones were full-length with an intact open reading frame. Phylogenetic analyses of thevif, vpr,andvpusequences from the LTS suggested that the HIV-1 strains found in the study subjects are not significantly different from those found in patients with AIDS and that the viruses in the LTS are unlikely to share a common genetic origin. Furthermore, a similar degree of overall genetic diversity between viruses from the LTS and AIDS patients suggests that there is unlikely a significant correlation between the degree of genetic diversity and the rate of disease development. Factors other than genetic divergence, such as viral load and phenotype, are likely to impact more on disease status.