Palmer Sarah, Kearney Mary, Maldarelli Frank, Halvas Elias K, Bixby Christian J, Bazmi Holly, Rock Diane, Falloon Judith, Davey Richard T, Dewar Robin L, Metcalf Julia A, Hammer Scott, Mellors John W, Coffin John M
HIV Drug Resistance Program, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA.
J Clin Microbiol. 2005 Jan;43(1):406-13. doi: 10.1128/JCM.43.1.406-413.2005.
To investigate the extent to which drug resistance mutations are missed by standard genotyping methods, we analyzed the same plasma samples from 26 patients with suspected multidrug-resistant human immunodeficiency virus type 1 by using a newly developed single-genome sequencing technique and compared it to standard genotype analysis. Plasma samples were obtained from patients with prior exposure to at least two antiretroviral drug classes and who were on a failing antiretroviral regimen. Standard genotypes were obtained by reverse transcriptase (RT)-PCR and sequencing of the bulk PCR product. For single-genome sequencing, cDNA derived from plasma RNA was serially diluted to 1 copy per reaction, and a region encompassing p6, protease, and a portion of RT was amplified and sequenced. Sequences from 15 to 46 single viral genomes were obtained from each plasma sample. Drug resistance mutations identified by single-genome sequencing were not detected by standard genotype analysis in 24 of the 26 patients studied. Mutations present in less than 10% of single genomes were almost never detected in standard genotypes (1 of 86). Similarly, mutations present in 10 to 35% of single genomes were detected only 25% of the time in standard genotypes. For example, in one patient, 10 mutations identified by single-genome sequencing and conferring resistance to protease inhibitors (PIs), nucleoside analog reverse transcriptase inhibitors, and nonnucleoside reverse transcriptase inhibitors (NNRTIs) were not detected by standard genotyping methods. Each of these mutations was present in 5 to 20% of the 20 genomes analyzed; 15% of the genomes in this sample contained linked PI mutations, none of which were present in the standard genotype. In another patient sample, 33% of genomes contained five linked NNRTI resistance mutations, none of which were detected by standard genotype analysis. These findings illustrate the inadequacy of the standard genotype for detecting low-frequency drug resistance mutations. In addition to having greater sensitivity, single-genome sequencing identifies linked mutations that confer high-level drug resistance. Such linkage cannot be detected by standard genotype analysis.
为了研究标准基因分型方法遗漏耐药性突变的程度,我们使用一种新开发的单基因组测序技术,对26例疑似多药耐药1型人类免疫缺陷病毒患者的相同血浆样本进行了分析,并将其与标准基因分型分析进行比较。血浆样本取自先前至少接触过两类抗逆转录病毒药物且抗逆转录病毒治疗方案失败的患者。通过逆转录酶(RT)-PCR和大量PCR产物测序获得标准基因分型。对于单基因组测序,将源自血浆RNA的cDNA连续稀释至每个反应1拷贝,扩增并测序包含p6、蛋白酶和部分RT的区域。从每个血浆样本中获得15至46个单病毒基因组的序列。在研究的26例患者中,有24例通过单基因组测序鉴定出的耐药性突变未被标准基因分型分析检测到。在标准基因分型中,单基因组中出现频率低于10%的突变几乎从未被检测到(86个中1个)。同样,单基因组中出现频率为10%至35%的突变在标准基因分型中仅25%的时间被检测到。例如,在一名患者中,单基因组测序鉴定出的10个赋予蛋白酶抑制剂(PIs)、核苷类逆转录酶抑制剂和非核苷类逆转录酶抑制剂(NNRTIs)耐药性的突变未被标准基因分型方法检测到。这些突变中的每一个在分析的20个基因组中出现频率为5%至20%;该样本中15%的基因组包含连锁的PI突变,而标准基因分型中均未出现。在另一名患者样本中,33%的基因组包含五个连锁的NNRTI耐药性突变,标准基因分型分析均未检测到。这些发现说明了标准基因分型在检测低频耐药性突变方面的不足。除了具有更高的灵敏度外,单基因组测序还能鉴定出赋予高水平耐药性的连锁突变。这种连锁无法通过标准基因分型分析检测到。