BC Centre for Excellence in HIV/AIDS, Vancouver, British Columbia, Canada.
PLoS One. 2011;6(6):e21189. doi: 10.1371/journal.pone.0021189. Epub 2011 Jun 20.
Human immunodeficiency virus type 1 (HIV-1) genomes often carry one or more mutations associated with drug resistance upon transmission into a therapy-naïve individual. We assessed the prevalence and clinical significance of transmitted drug resistance (TDR) in chronically-infected therapy-naïve patients enrolled in a multi-center cohort in North America. Pre-therapy clinical significance was quantified by plasma viral load (pVL) and CD4+ cell count (CD4) at baseline. Naïve bulk sequences of HIV-1 protease and reverse transcriptase (RT) were screened for resistance mutations as defined by the World Health Organization surveillance list. The overall prevalence of TDR was 14.2%. We used a Bayesian network to identify co-transmission of TDR mutations in clusters associated with specific drugs or drug classes. Aggregate effects of mutations by drug class were estimated by fitting linear models of pVL and CD4 on weighted sums over TDR mutations according to the Stanford HIV Database algorithm. Transmitted resistance to both classes of reverse transcriptase inhibitors was significantly associated with lower CD4, but had opposing effects on pVL. In contrast, position-specific analyses of TDR mutations revealed substantial effects on CD4 and pVL at several residue positions that were being masked in the aggregate analyses, and significant interaction effects as well. Residue positions in RT with predominant effects on CD4 or pVL (D67 and M184) were re-evaluated in causal models using an inverse probability-weighting scheme to address the problem of confounding by other mutations and demographic or risk factors. We found that causal effect estimates of mutations M184V/I (-1.7 log₁₀pVL) and D67N/G (-2.1[³√CD4] and 0.4 log₁₀pVL) were compensated by K103N/S and K219Q/E/N/R. As TDR becomes an increasing dilemma in this modern era of highly-active antiretroviral therapy, these results have immediate significance for the clinical management of HIV-1 infections and our understanding of the ongoing adaptation of HIV-1 to human populations.
人类免疫缺陷病毒 1 型(HIV-1)基因组在传播给未经治疗的个体时,通常会携带一个或多个与耐药性相关的突变。我们评估了在北美的一个多中心队列中,慢性感染未经治疗的患者中传播的耐药性(TDR)的流行率和临床意义。治疗前的临床意义通过基线时的血浆病毒载量(pVL)和 CD4+细胞计数(CD4)来量化。用世界卫生组织监测清单定义的耐药突变对 HIV-1 蛋白酶和逆转录酶(RT)的原始群体序列进行筛选。TDR 的总体流行率为 14.2%。我们使用贝叶斯网络来识别与特定药物或药物类别相关的耐药突变簇的共同传播。根据斯坦福 HIV 数据库算法,通过对根据 TDR 突变加权求和的线性模型拟合,估计药物类别中突变的聚合效应。对两类逆转录酶抑制剂的传播耐药性与 CD4 降低显著相关,但对 pVL 的影响相反。相比之下,TDR 突变的位置特异性分析显示,在几个残基位置对 CD4 和 pVL 有实质性影响,这些影响在总体分析中被掩盖了,并且存在显著的相互作用效应。对 CD4 或 pVL 有主要影响的 RT 残基位置(D67 和 M184)在因果模型中使用逆概率加权方案进行了重新评估,以解决由其他突变和人口统计学或风险因素引起的混杂问题。我们发现突变 M184V/I(-1.7log₁₀pVL)和 D67N/G(-2.1[³√CD4]和 0.4log₁₀pVL)的因果效应估计值被 K103N/S 和 K219Q/E/N/R 补偿。随着 TDR 在现代高效抗逆转录病毒治疗时代成为一个越来越大的困境,这些结果对 HIV-1 感染的临床管理以及我们对 HIV-1 对人类群体的持续适应的理解具有直接意义。