Weidle Paul J, Downing Robert, Sozi Catherine, Mwebaze Raymond, Rukundo Gideon, Malamba Samuel, Respess Richard, Hertogs Kurt, Larder Brendan, Ochola Dorothy, Mermin Jonathan, Samb Badara, Lackritz Eve
Division of HIV/AIDS Prevention, National Center for HIV, STD, and TB Prevention (NCHSTP), Centers for Disease Control and Prevention (CDC), Atlanta, Georgia 30333, USA.
AIDS. 2003 Jul;17 Suppl 3:S39-48. doi: 10.1097/00002030-200317003-00006.
We describe phenotypic drug resistance, response to therapy, and genotypic mutations among HIV-infected patients in Uganda taking antiretroviral medications for > or = 90 days who had a viral load > or = 1000 copies/ml.
HIV-1 group and subtype, virologic and immunologic responses to antiretroviral therapy, phenotypic resistance to antiretroviral drugs, and associated genotypic mutations among patients at three treatment centers in Uganda between June 1999 and August 2000 were assessed. Therapy was two nucleoside reverse transcriptase inhibitors (NRTIs) or highly active antiretroviral therapy (HAART).
All HIV identified was HIV-1, group M, subtypes A, C, and D. Sixty-one (65%) of 94 patients with a phenotypic resistance result had evidence of phenotypic resistance including resistance to a NRTI for 51 of 92 (55%) taking NRTIs, to a non-nucleoside reverse transcriptase inhibitor (NNRTI) for nine of 16 (56%) taking NNRTIs, and to a protease inhibitor (PI) for eight of 37 (22%) taking PIs. At the time of the first specimen with resistance, the median change from baseline viral load was -0.56 log copies/ml [interquartile range (IQR), -1.47 to +0.29] and CD4+ cell count was +35 x 10(6) cells/l (IQR, -18 to +87). Genotypic resistance mutations, matched with phenotypic resistance assay results and drug history, were generally consistent with those seen for HIV-1, group M, subtype B infections in industrialized countries.
Initial phenotypic resistance and corresponding genotypic mutations among patients treated in Uganda were similar to those with subtype B infections in North America and Europe. These data support policies that promote the use of HAART regimens against HIV-1, group M, non-B subtypes in a manner consistent with that used for subtype B infections.
我们描述了乌干达接受抗逆转录病毒药物治疗≥90天且病毒载量≥1000拷贝/毫升的HIV感染患者的表型耐药性、治疗反应和基因变异情况。
评估了1999年6月至2000年8月期间乌干达三个治疗中心患者的HIV-1组和亚型、对抗逆转录病毒治疗的病毒学和免疫学反应、对抗逆转录病毒药物的表型耐药性以及相关基因变异。治疗方案为两种核苷类逆转录酶抑制剂（NRTIs）或高效抗逆转录病毒治疗（HAART）。
所有鉴定出的HIV均为HIV-1，M组，A、C和D亚型。94例有表型耐药结果的患者中，61例（65%）有表型耐药证据，包括92例服用NRTIs的患者中有51例（55%）对NRTI耐药，16例服用非核苷类逆转录酶抑制剂（NNRTIs）的患者中有9例（56%）对NNRTI耐药，37例服用蛋白酶抑制剂（PIs）的患者中有8例（22%）对PI耐药。在首次出现耐药的标本时，与基线病毒载量相比的中位数变化为-0.56 log拷贝/毫升[四分位间距（IQR），-1.47至+0.29]，CD4+细胞计数为+35×10⁶个/升（IQR，-18至+87）。与表型耐药检测结果和用药史相匹配的基因耐药突变通常与工业化国家HIV-1 M组B亚型感染所见的情况一致。
乌干达接受治疗患者的初始表型耐药性和相应的基因变异与北美和欧洲B亚型感染患者相似。这些数据支持以与B亚型感染相同的方式推广使用针对HIV-1 M组非B亚型的HAART方案的政策。
