背景与目的 高效抗逆转录病毒治疗的问世帮助患者实现了对体内人类免疫缺陷病毒（Human Immunodeficiency Virus, HIV）水平的控制，但感染早期建立的病毒储存库的存在，病毒仍无法得到根除。大量研究表明 HIV 感染引起的异常免疫激活对早期病毒储存库的形成和维持有至关重要的作用。对于急性期 HIV 感染患者，强化 ART 治疗和强化 ART 联合雷公藤治疗对于异常免疫激活和病毒储存库的影响尚不明确。本研究旨在对比接受三联标准治疗、四联 ART 强化治疗和四联联合雷公藤多甙治疗的急性期 HIV 感染患者的炎症因子水平和外周血病毒储存库水平，比较不同治疗方法对 HIV 相关异常免疫激活指标与病毒储存库的影响。 研究方法 本研究采用回顾性研究方法，为单中心对照临床试验。入组时筛选出处于急性期接受 ART 治疗的患者，分别纳入三联治疗组、四联 ART 强化治疗组或四联强化 ART 联合雷公藤多甙治疗组。四联治疗组在三联治疗的基础上应用整合酶抑制剂进行治疗，而雷公藤治疗组在 ART 治疗第 24 周开始口服雷公藤至 72 周。对入组患者在 ART 基线、24、48、72、96 周随访，采用 Luminex 液相平台测定血浆炎症因子水平，并使用 PCR 荧光探针法检测外周血中整合在 PBMC 中的 HIV-DNA 储存库，观察受试者免疫激活水平与病毒储存库情况的改变。主要观察终点为两组患者血浆炎症标记物、外周血病毒储存库的改变。 结果 共纳入 28 例急性期 HIV 感染患者，其中三联治疗组 9 例，四联治疗组 11例，雷公藤治疗组 8 例。炎症指标方面：所检测的 14 种炎症因子中 12 种未观察到随访期相对于基线的差异；IP-10、TNF-α在接受四联强化与雷公藤干预后出现明显下降。第 24、48、72 周，雷公藤治疗组的 TNF-α水平相较于基线有显著差异（P 分别为 0.008、0.029、0.019），而三联、四联治疗组则未观察到该差异；给药第 48、72 周，雷公藤组患者 IP-10 水平显著性下降（P=0.019、0.034），雷公藤组血浆 IP-10 水平较低患者的比例高于四联与三联治疗组（分别为 6/8vs3/9，6/8vs2/9）。储存库方面：病毒储存库在四联治疗后出现明显下降，第 72、96周，四联治疗组外周血 PBMC 中 HIV-DNA 储存库水平出现显著下降（P 分别为0.034、0.038）。 结论 雷公藤多甙可以有效抑制急性期 HIV 感染相关的炎症因子，表明其对 HIV 相关异常免疫激活指标有抑制作用。急性期 HIV 感染患者使用四联 ART 强化治疗，外周血病毒储存库出现显著下调。雷公藤多甙治疗与病毒储存库的动态变化相关。

BACKGROUND AND PURPOSE: The introduction of HAART has dramatically changed patients’ control over the HIV virus. However, due to the presence of an early established HIV reservoir, current treatment has not been able to eradicate the virus from our system. Evidence is accumulating for the dependent relationship between the immue activation caused by HIV infection and HIV reservoir. For patients with primary HIV infection, the effect of early use of intense antiretroviral therapy and TwHF on the immune activation and reservoir is under investigation. Changes in serum inflammation markers and virus reservoir levels were investigated to compare the effect of intense therapy and TwHF on primary HIV infection patients. METHODS: Patients with primary HIV infection are enrolled in our single-centered study. The treatment arms are divided as standard therapy arm, intense therapy arm (Standard therapy+integrase inhibitor), and the TwHF therapy arm. Patients in the TwHF arm received ART to begin with and oral TwHF was later added week 24th to 72nd. All immune activation and HIV reservoir levels were assessed at week 24th, 48th, 72n, and 96th. The main endpoints were changes in serum inflammation markers and peripheral viral reservoirs. RESULTS: A total of 28 patients were enrolled (9 in standard arm, 11 in intense arm, and 8 in TwHF arm). A decrease in the level of IP-10 and TNF-α was observed in intensive and TwHF arms. The TNF-α level in TwHF arm showed significant difference from baseline (P=0.008, 0.029, 0.019 respectively, for week 24th, 48th, and 72n,). Significant intergroup diffenrece was observed among three arms on week 48th and 72n (P=0.019, 0.034 respectively). More recepients with low IP-10 level were found in TwHF arm than intense therapy arm (75%vs33.3%, 75%vs22.2% respectively). HIV reservoir declined significantly after intense treatment. Difference among arms was observed at week 72nd and 96th (P =0.034, 0.038* respectively). CONCLUSION: TwHF shows efficacy in suppressing levels of serum inflammatory markers in primary infection of HIV, which suggests its potential nature of reining the abnormal immune activation in HIV patients. Intense therapy during the early phase of HIV infection is related to a decline in peripheral HIV reservoir. A relationship between TwHF therapy and dynamic changes of virus reservoir is also observed.