Bratt G, Karlsson A, Leandersson A C, Albert J, Wahren B, Sandström E
Department of Dermatovenereology (Venhälsan), Södersjukhuset, Stockholm, Sweden.
AIDS. 1998 Nov 12;12(16):2193-202. doi: 10.1097/00002030-199816000-00015.
The efficacy of highly active antiretroviral treatment (HAART) in HIV-1 disease may vary between nucleoside-naive and experienced patients as well as between patients with different viral phenotypes and in different stages of disease.
To investigate variables of importance for successful long-term viral suppression by analysing virological, clinical and immunological characteristics at initiation of protease inhibitor treatment on suppression of HIV RNA over 1 year.
An open, non-randomized, observational clinical study.
Venhälsan, Department of Dermatovenereology, Söder Hospital, Stockholm, Sweden.
A total of 147 unselected advanced patients with known HIV-1 infection for a mean of 7 years, of whom 37% had AIDS and who started treatment with a protease inhibitor during 1996.
All patients received HAART with at least two nucleoside analogues in combination with either indinavir (81%) or ritonavir (19%). The majority (77%) had been previously treated with nucleoside analogues for a mean of 39 months.
CD4+ lymphocyte count, plasma HIV-1 RNA, viral phenotype and HIV-1 coreceptor CCR-5 genotype at baseline. Viral load and CD4+ lymphocyte count were determined every 3 months.
Patients were analysed on an intention-to-treat basis. The mean CD4+ lymphocyte count at baseline was 170 x 10(6)/l and the median viral load was 68 600 copies/ml. Heterozygosity for the delta32 deletion of the CCR-5 gene (delta32/wt) was found in 27%. MT-2 positive virus (syncytium-inducing) was isolated in 46%. Logistic regression revealed that nucleoside analogue experience and baseline log10 HIV-1 RNA were the only factors independently related to plasma HIV-1 RNA levels below 500 copies/ml after 1 year of treatment, which was found in 69%.
The virological outcome after 1 year of HAART was strongly correlated to prior treatment history and baseline viral load, whereas CD4+ lymphocyte count, CCR-5 genotype and viral biological phenotype had less influence. The long-term antiviral efficacy of HAART was lowest in individuals with previous nucleoside analogue treatment and a high baseline viral load. In these individuals an even more aggressive treatment should be considered.
高效抗逆转录病毒治疗（HAART）在HIV-1疾病中的疗效在核苷初治患者和经治患者之间、不同病毒表型患者之间以及疾病不同阶段可能有所不同。
通过分析蛋白酶抑制剂治疗开始时的病毒学、临床和免疫学特征对1年以上HIV RNA抑制情况，研究成功长期病毒抑制的重要变量。
一项开放、非随机、观察性临床研究。
瑞典斯德哥尔摩南医院皮肤病与性病科Venhälsan。
共147例未筛选的已知HIV-1感染的晚期患者，平均感染7年，其中37%患有艾滋病，于1996年开始使用蛋白酶抑制剂治疗。
所有患者接受HAART，至少两种核苷类似物联合茚地那韦（81%）或利托那韦（19%）。大多数（77%）患者此前曾接受核苷类似物治疗，平均治疗39个月。
基线时的CD4+淋巴细胞计数、血浆HIV-1 RNA、病毒表型和HIV-1共受体CCR-5基因型。每3个月测定病毒载量和CD4+淋巴细胞计数。
按意向性分析对患者进行分析。基线时CD4+淋巴细胞计数平均为170×10⁶/l，病毒载量中位数为68600拷贝/ml。CCR-5基因δ32缺失杂合子（δ32/wt）占27%。46%分离出MT-2阳性病毒（合胞体诱导型）。逻辑回归显示，核苷类似物治疗经验和基线log₁₀HIV-1 RNA是治疗1年后血浆HIV-1 RNA水平低于500拷贝/ml的唯一独立相关因素，69%的患者达到该水平。
HAART治疗1年后的病毒学结果与既往治疗史和基线病毒载量密切相关，而CD4+淋巴细胞计数、CCR-5基因型和病毒生物学表型影响较小。既往接受核苷类似物治疗且基线病毒载量高的个体，HAART的长期抗病毒疗效最低。对于这些个体，应考虑更积极的治疗。
