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HIV-1 viral rebound dynamics after a single treatment interruption depends on time of initiation of highly active antiretroviral therapy.

机译:单一治疗中断后,HIV-1病毒反弹的动力学取决于开始进行高效抗逆转录病毒治疗的时间。

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OBJECTIVE: An important pending question is whether temporary highly active antiretroviral therapy during primary HIV infection can influence viral rebound dynamics and the subsequently established viral setpoint, through preservation and enhancement of HIV-1-specific immune responses, or through other mechanisms. METHODS: We included all patients from two prospective studies who underwent a single treatment interruption while being well suppressed on highly active antiretroviral therapy. One group started highly active antiretroviral therapy during primary HIV infection, and the other group started it during chronic HIV infection with CD4 cell counts above 350 cells/microl. Data were collected up to 48 weeks from treatment interruption. The median time to viral rebound was analysed for three levels of viraemia: 50, 500 and 5000 copies HIV-RNA/ml plasma. RESULTS: The median time to viral rebound was significantly longer in primary HIV infection patients (n = 24) than in chronic HIV infection patients (n = 46): 8 versus 4 weeks (P < 0.001 for all three endpoints). In two primary HIV infection patients, no rebound of plasma HIV-1 RNA over 50 copies/ml occurred. In the first 4 weeks after treatment interruption, CD4+ T-cell counts declined with a median of -5.0 cells/microl blood per week in the primary HIV infection group and -45 cells/microl blood per week in the chronic HIV infection group (P < 0.05). From week 4 to 48, the decline in CD4+ T-cell count was similar in both groups. CONCLUSION: Plasma viral load and CD4 dynamics after a single interruption of highly active antiretroviral therapy were different for primary HIV infection and chronic HIV infection patients. Viral rebound is delayed or absent and early CD4 cell count decline after treatment interruption is less pronounced in primary HIV infection patients.
机译:目的:一个重要的悬而未决的问题是,在原发性HIV感染期间进行临时的高效抗逆转录病毒治疗是否会通过保存和增强HIV-1特异性免疫反应或通过其他机制来影响病毒的反弹动力学和随后确定的病毒设定点。方法:我们纳入了来自两项前瞻性研究的所有患者,这些患者均接受了单次治疗中断,但在高活性抗逆转录病毒治疗中被良好抑制。一组在原发性HIV感染期间开始高活性抗逆转录病毒疗法,另一组在慢性HIV感染期间以大于350细胞/微升的CD4细胞计数开始治疗。从治疗中断起长达48周收集数据。分析了三种病毒血症水平的病毒反弹中位时间:50、500和5000拷贝HIV-RNA / ml血浆。结果:原发性HIV感染患者(n = 24)的病毒反弹时间的中位数明显长于慢性HIV感染患者(n = 46):8周比4周(所有三个终点的P <0.001)。在两名原发性HIV感染患者中,血浆HIV-1 RNA没有反弹超过50拷贝/ ml。在治疗中断后的头4周内,主要HIV感染组的CD4 + T细胞计数下降,中位数为每周-5.0细胞/微血,而慢性HIV感染组则为-45细胞/微血(P <0.05)。从第4周到第48周,两组的CD4 + T细胞计数下降相似。结论:原发性HIV感染和慢性HIV感染患者单次中断高活性抗逆转录病毒治疗后血浆病毒载量和CD4动力学是不同的。在原发性HIV感染患者中,治疗中断后病毒反弹被延迟或不存在,并且早期CD4细胞计数下降不明显。

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