Kyeyune Fred, Gibson Richard M, Nankya Immaculate, Venner Colin, Metha Samar, Akao Juliet, Ndashimye Emmanuel, Kityo Cissy M, Salata Robert A, Mugyenyi Peter, Arts Eric J, Quiñones-Mateu Miguel E
Center for AIDS Research Uganda Laboratories, Joint Clinical Research Centre, Kampala, Uganda Department of Molecular Biology and Microbiology, Case Western Reserve University, Cleveland, Ohio, USA.
Department of Microbiology and Immunology, University of Western Ontario, London, Ontario, Canada.
Antimicrob Agents Chemother. 2016 May 23;60(6):3380-97. doi: 10.1128/AAC.00038-16. Print 2016 Jun.
Most patients failing antiretroviral treatment in Uganda continue to fail their treatment regimen even if a dominant drug-resistant HIV-1 genotype is not detected. In a recent retrospective study, we observed that approximately 30% of HIV-infected individuals in the Joint Clinical Research Centre (Kampala, Uganda) experienced virologic failure with a susceptible HIV-1 genotype based on standard Sanger sequencing. Selection of minority drug-resistant HIV-1 variants (not detectable by Sanger sequencing) under antiretroviral therapy pressure can lead to a shift in the viral quasispecies distribution, becoming dominant members of the virus population and eventually causing treatment failure. Here, we used a novel HIV-1 genotyping assay based on deep sequencing (DeepGen) to quantify low-level drug-resistant HIV-1 variants in 33 patients failing a first-line antiretroviral treatment regimen in the absence of drug-resistant mutations, as screened by standard population-based Sanger sequencing. Using this sensitive assay, we observed that 64% (21/33) of these individuals had low-frequency (or minority) drug-resistant variants in the intrapatient HIV-1 population, which correlated with treatment failure. Moreover, the presence of these minority HIV-1 variants was associated with higher intrapatient HIV-1 diversity, suggesting a dynamic selection or fading of drug-resistant HIV-1 variants from the viral quasispecies in the presence or absence of drug pressure, respectively. This study identified low-frequency HIV drug resistance mutations by deep sequencing in Ugandan patients failing antiretroviral treatment but lacking dominant drug resistance mutations as determined by Sanger sequencing methods. We showed that these low-abundance drug-resistant viruses could have significant consequences for clinical outcomes, especially if treatment is not modified based on a susceptible HIV-1 genotype by Sanger sequencing. Therefore, we propose to make clinical decisions using more sensitive methods to detect minority HIV-1 variants.
在乌干达,大多数抗逆转录病毒治疗失败的患者即使未检测到主要的耐药HIV-1基因型,其治疗方案仍会持续失败。在最近的一项回顾性研究中,我们观察到,基于标准的桑格测序,乌干达联合临床研究中心(坎帕拉)约30%的HIV感染者出现了对敏感HIV-1基因型的病毒学失败。在抗逆转录病毒治疗压力下,选择少数耐药HIV-1变异体(桑格测序无法检测到)可导致病毒准种分布发生变化,这些变异体成为病毒群体的主要成员,最终导致治疗失败。在此,我们使用了一种基于深度测序(DeepGen)的新型HIV-1基因分型检测方法,对33例一线抗逆转录病毒治疗方案失败且经标准群体桑格测序筛查无耐药突变的患者中低水平耐药HIV-1变异体进行定量。使用这种灵敏的检测方法,我们观察到这些个体中有64%(21/33)在患者体内的HIV-1群体中存在低频(或少数)耐药变异体,这与治疗失败相关。此外,这些少数HIV-1变异体的存在与患者体内较高的HIV-1多样性有关,这表明分别在有或无药物压力的情况下,耐药HIV-1变异体在病毒准种中存在动态选择或逐渐消失。本研究通过深度测序在抗逆转录病毒治疗失败但桑格测序方法确定无主要耐药突变的乌干达患者中鉴定出低频HIV耐药突变。我们表明,这些低丰度耐药病毒可能对临床结果产生重大影响,特别是如果不根据桑格测序的敏感HIV-1基因型调整治疗方案。因此,我们建议使用更灵敏的方法来检测少数HIV-1变异体以做出临床决策。