Nicastri Emanuele, Sarmati Loredana, d'Ettorre Gabriella, Parisi Saverio G, Palmisano Lucia, Galluzzo Clementina, Montano Marco, Uccella Ilaria, Amici Roberta, Gatti Francesca, Vullo Vincenzo, Concia Ercole, Vella Stefano, Andreoni Massimo
Department of Public Health, University of Rome Tor Vergata, Rome, Italy.
J Clin Microbiol. 2003 Jul;41(7):3007-12. doi: 10.1128/JCM.41.7.3007-3012.2003.
Whether highly active antiretroviral therapy (HAART) should be modified in patients with persistent increases in CD4(+) T cells despite detectable viral loads is an unresolved question. Forty-three heavily pretreated human immunodeficiency virus (HIV)-infected patients with virologic failure during HAART were studied before a change of therapy guided by genotypic analysis and during follow-up. Patients with an increase in CD4(+) cell count (>100 cells/ml) over pre-HAART values were considered to be discordant patients (20 individuals), whereas patients with a lower increase or no increase in CD4(+) cell count were considered failing patients (23 individuals). Based on univariate analysis, a high CD4(+) cell count before antiretroviral treatment, homosexual behavior as a risk factor for HIV infection, reduced drug exposure to nonnucleoside reverse transcriptase inhibitors, low replicative capacity of HIV isolates, and more frequent detection of HIV isolates with a non-B subtype, an R5 biological phenotype, and M184V and T215Y/F mutations were factors associated with a discordant response to HAART. Based on multivariate analysis, only the M184V mutation remained significantly associated with a viroimmunologic discordant response (odds ratio, 25.48; 95% confidence interval, 1.43 to 453.93). No difference in lamivudine exposure was found between discordant (95%) and failing (91%) patients. Twelve months after the genotypic analysis-guided change of therapy, 3 discordant (15%) and 6 failing patients (26%) achieved undetectable viral loads (<50 copies/ml), whereas in patients with HIV RNA loads of >500 copies/ml, discordant responses were observed in 5 out of 15 discordant patients and in 4 out of 16 failing patients. A relationship between the M184V mutation and a viroimmunologic discordant response to HAART was found. After the genotypic analysis-driven change of therapy, similar rates of virologic suppression were detected in the two groups.
对于那些尽管病毒载量可检测到但CD4(+) T细胞持续增加的患者,高效抗逆转录病毒疗法(HAART)是否应进行调整仍是一个未解决的问题。在基于基因型分析指导治疗改变之前及随访期间,对43例在HAART期间病毒学治疗失败且接受过大量治疗的人类免疫缺陷病毒(HIV)感染患者进行了研究。CD4(+)细胞计数较HAART治疗前增加(>100个细胞/ml)的患者被视为反应不一致患者(20例),而CD4(+)细胞计数增加较少或未增加的患者被视为治疗失败患者(23例)。基于单变量分析,抗逆转录病毒治疗前较高的CD4(+)细胞计数、同性恋行为作为HIV感染的危险因素、非核苷类逆转录酶抑制剂的药物暴露减少、HIV分离株的低复制能力以及更频繁检测到具有非B亚型、R5生物学表型以及M184V和T215Y/F突变的HIV分离株,这些因素与对HAART的反应不一致有关。基于多变量分析,只有M184V突变仍与病毒免疫反应不一致显著相关(优势比,25.48;95%置信区间,1.43至453.93)。反应不一致患者(95%)和治疗失败患者(91%)之间的拉米夫定暴露没有差异。在基因型分析指导治疗改变12个月后,3例反应不一致患者(15%)和6例治疗失败患者(26%)实现了不可检测的病毒载量(<50拷贝/ml),而在HIV RNA载量>500拷贝/ml的患者中,15例反应不一致患者中有5例、16例治疗失败患者中有4例出现了反应不一致情况。发现M184V突变与对HAART的病毒免疫反应不一致之间存在关联。在基因型分析驱动治疗改变后,两组中病毒学抑制率相似。