HAART对人类免疫缺陷病毒感染者淋巴细胞亚群的影响

应用流式细胞分析法通过分析检测41例AIDS患者与30例健康对照之间,以及21例AIDS患者在接受HAART治疗前后外周血淋巴细胞亚群的表达情况,研究感染HIV病毒以及HAART治疗对淋巴细胞亚群的影响。结果显示AIDS患者与健康对照相比,外周血CD4~+CD45RA~+、CD4~+CD28~+、CD4~+CD45RO~+、CD4~+CD95~+细胞比例明显低于正常对照,CD8~+CD95~+、CD8~+CD38~+、CD56~+细胞比例明显高于正常对照;经HAART治疗后,CD4~+CD45RA~+,CD4~+CD28~+细胞比例比治疗前升高,CD56~+细胞比例比治疗前显著下降。结果表明CD4~+T淋巴细胞表面CD45RA、CD28表达,以及CD56~+细胞能够预测AIDS患者HAART治疗效果。     

120例艾滋病合并结核发生免疫重建炎性综合征的胸部影像学分析

目的：探讨艾滋病合肺结核并发生免疫重建炎性综合征患者的胸部影像学特征。方法选取我院2013年1月~2014年6月120例艾滋病合并肺结核发生免疫重建炎性综合症患者,对其胸部影像学资料进行研究。结果艾滋病合并结核发生免疫重建炎性综合征,肺部病变出现或原有病灶增多,影像学表现院位于两肺野75例(62.50%,),上《和(或)下《背段17例(14.16%,),右中《和(或)下《28例(23.33%,),形态主要表现为斑片状72例(60.00%,),大片状16例(13.33%,),磨玻璃样影10例(8.33%,),结节状或肿块15例(12.53%,),条索状7例(5.83%,),伴空洞22例(18.33%,),钙化11例(9.16%,),纵隔淋巴结增多、增大69例(57.50%,),胸腔积液或胸膜增厚57例(47.5%,),心包积液18例(21.6%,)。随访中,好转87例(72.50%,);未治愈17例(14.16%,),死亡16例(13.93%,)。结论本病的影像资料特点多为弥漫性、多肺《性病变,病灶形态多样,空洞及钙化少见,纵隔淋巴结肿大常见多伴有液化坏死,通常会出现胸腔积液伴心包积液,在进行抗结核与抗病毒治疗后大部分病情明显好转。     

艾滋病患者T淋巴细胞表面归巢分子的表达在抗病毒治疗后升高

目的 探讨艾滋病(AIDS)患者高效抗反转录病毒治疗(HAART)前后T淋巴细胞表面归巢分子CD49d、CCR9、CD62L表达的变化情况.方法 采用流式细胞术检测42例艾滋病患者和18例HIV阴性健康对照的外周血T淋巴细胞表面CD49d、CCR9和CD62L表达,用BD FACSDiva软件分析计算各组细胞表达的百分率.结果 治疗后组外周血的平均CD4~+T淋巴细胞明显高于治疗前组(P<0.01);治疗前组CD3~+CD49d~+、CD3~+ CCR9~+、CD3~+CD62L~+、CD3~+CD4~+、CD4~+CD49d~+、CD4~+CCR9~+、CIM~+CD62L~+、CD8~+CD49d~+、CD8~+CD62L~+T淋巴细胞的百分率显著低于治疗后组和阴性对照组(P<0.05);CD3~+CD8~+T淋巴细胞的百分率高于治疗后组(P<0.05).治疗后组CD3~+CCR9~+、CD8~+CCR9~+、CD8~+CD62L~+T淋巴细胞的百分率均低于阴性对照组(P均<0.001).结论 AIDS患者外周血T淋巴细胞亚群不仅比例失调,而且其表面表达肠道归巢分子CD49d、CCR9,淋巴结归巢分子CD62L的数量发生异常改变.抗病毒治疗可以逆转以上部分免疫病理变化.建议肠道归巢分子CD49d、CCR9和淋巴结归巢分子CD62L可作为艾滋病疾病进展和评价机体HAART后免疫重建的指标.     

黄芪联合HAART治疗艾滋病22例疗效观察

目的使用黄芪联合高效抗逆转录病毒疗法（HAART）治疗艾滋病,与常规HAART治疗进行对比,观察其降低副作用及治疗艾滋病的效果。结论研究组收集22例艾滋病患者,用黄芪联合HAART治疗24周;对照组收集20例艾滋病患者,常规HAART治疗24周。观察两组治疗后药物副作用及抗艾滋病疗效对比情况。结果治疗24周后研究组在消化道反应、外周神经炎、皮疹、皮肤瘙痒及肝功能损害方面药物副作用较对照组发生少,差异有统计学意义。治疗后研究组CD4＋细胞数为（256.80±102.58）,对照组为（240.26±96.62）,差异有统计学意义。结论黄芪联合HAART治疗可以减少HAART治疗的副作用,提高CD4＋细胞数量,增强患者免疫力。     

湖南艾滋病患者Th17和Tr细胞及IL-17在抗病毒治疗过程中的变化

目的 观察HIV感染者和AIDS患者血IL-17、CD3+CD4+IL-17+细胞(Th17细胞)和CD4+CD25+Foxp3+T细胞(Tr细胞)的平衡状态及其在1年高效抗反转录病毒治疗(HAART)中的变化.方法 选取经HAART治疗的HIV/AIDS患者33例,同时选取33例健康志愿者为对照,分别于治疗0、6、12个月采集静脉血,检测血清IL-17水平、Th17细胞及Tr细胞百分比,并对比分析其相互关系.结果 HIV/AIDS在HAART治疗前、治疗6个月、12个月及健康对照外周血的Th17细胞在CD4+T细胞中的比例分别为(1.20±0.37)%、(2.50±1.03)%、(3.70±1.56)%和(4.70±1.43)%;Tr细胞在CD4+T细胞中的比例分别为(9.16±3.33)%、(7.19±2.91)%、(5.53±1.88)%和(4.43±0.97)%;血清IL-17水平分别为(5.3±2.5) pg/ml、(7.7±2.4) pg/ml、(10.4±3.1) pg/ml和(17.7±6.6) pg/ml.Th17细胞水平与CD4+T细胞计数正相关,与病毒载量负相关;Tr细胞水平与CD4+T细胞计数负相关,与病毒载量正相关.结论 HIV感染导致IL-17、Th17细胞和Tr细胞的失平衡,而HAART治疗可能逐渐恢复二者的免疫平衡状态.提示三者可能在艾滋病发病机制中起作用,并有可能成为观察艾滋病进展和HAART治疗效果的有效指标.

Abstract：

Objective To observe the Th17, IL-17 and Tr cells equilibrium state as well as their changes of HIV infected or AIDS suffered patients in one-year HAART treatment. Methods Select 33 HIV/AIDS patients received HAART treatment while 33 healthy volunteers as controls. Flow cytometry was used to analyze Th17 and Tr cells in venous blood at the time of pre-therapy, 6th, 12th month when IL-17 levels in serum are tested by ELISA. Results The ratio of Th17 cells in CD4 cells in HIV/AIDS patients and volunteers were (1.20±0.37)%, (2.50±1.03)%, (3.70±1.56)%, (4.70±1.43)%, respectively; The ratio of Tr cells were (9.16±3.33)%, (7.19±2.91)%, (5.53±1.88)%, (4.43±0.97)%, respectively; The levels of IL-17 in serum were (5.3±2.5) pg/ml, (7.7±2.4) pg/ml, (10.4±3.1) pg/ml, (17.7±6.6) pg/ml respectively. The Th17 cells' level was positively correlative with the amount of CD4 cells, negatively correlate with the count of viral load. However, the Tr cells level is positively correlative with the count of viral load, negatively relate to the quantity of CD4 cells. Conclusion HIV could make IL-17, Th17 cells and Tr cells lost their balance, but the immune equilibrium state may gradually recover after HAART treatment. Which indicates the IL-17, Th17 cells and Treg cells may play an important role in the pathogenesis of AIDS, and they are likely to be the effective indexes to observe the progress of AIDS and the treatment effect of highly active antiretroviral therapy(HAART).     

12例中国汉族人艾滋病相关型皮肤Kaposi肉瘤临床病理特征及治疗分析

 目的： 观察12例汉族人艾滋病（AIDS）相关型皮肤Kaposi肉瘤患者的临床、病理学特点及免疫学表型,探讨其有效治理的方法及预后因素。方法：回顾分析12例汉族人AIDS相关型皮肤Kaposi肉瘤患者临床、病理学特征及免疫学表型。结果：12例汉族人AIDS相关型皮肤Kaposi肉瘤患者HIV均阳性;12例患者的皮损主要表现为暗红或紫黑色的丘疹、斑块;病理表现为真皮内见片状或弥漫分布的棱形细胞浸润,增生活跃的血管多呈裂隙状,组织间隙见红细胞渗出,含铁血黄素沉积,有炎症细胞浸润;免疫组化结果如下：T细胞UCHL1(+),局部CD31(+),增生的血管内皮细胞factor Ⅷ(+),血管壁HHF-35(+), vimentin (+++), S-100蛋白(-),6例梭形细胞CD34 (+++),1例梭形细胞CD34（-）。12例患者均使用高效抗反转录病毒治疗（HAART）,4例皮损局限者手术切除,局部辅以微波,预后良好; 另2例皮损局限者辅以微波治疗,皮损消退;6例全身泛发皮损者,其中5例辅以微波、1例联合化疗,5例患者的皮损缓解,1例死亡。结论：12例汉族人AIDS相关型皮肤Kaposi肉瘤患者与其他人群的AIDS相关型皮肤Kaposi肉瘤患者的临床、组织病理学及免疫学表现无明显差异。HAART是治疗AIDS相关型皮肤Kaposi肉瘤的必要手段。早期患者肉瘤直径小于2 cm,可给予手术切除肿物,微波治疗;肿物直径大于2 cm,可给予化疗和微波治疗。     

43例血友病/艾滋病患者经高效抗逆转录病毒治疗三年后免疫功能的观察

研究对43例血友病/艾滋病患者用高效抗逆转录病毒治疗三年,定期采用流式细胞仪检测CD4、CD3、CD8和NK细胞;病毒载量仪(bDNA)检测血浆病毒载量;同时检测血清免疫球蛋白及白细胞介素。结果表明,43例血友病/艾滋病患者在治疗三年后CD4+平均上升257/mm3(P<0.001),HIV RNA下降,治疗后平均降至(2.26±1.10)log/ml(P<0.0001),同时伴有IgA下降(P<0.05)IL-10,sIL-2R上升(P<0.05)。HAART能快速抑制HIV RNA的复制,纠正机体免疫功能紊乱和重建免疫功能。     

骁悉在GVHD防治作用机制的初步研究

移植物抗宿主病(GVHD)是骨髓移植术后的主要并发症,是影响移植成功及患者长期生存的主要因素.尽管环孢素A(CSA)联合短程甲氨蝶呤(MTX)或/和固醇类激素是目前国内外预防GVHD的经典方案,但移植物抗宿主病的发生率仍高达38%～68%.MMF是一种新型免疫抑制剂,能选择性抑制T、B细胞增殖,已广泛应用于实体器官移植后排斥反应的预防与治疗[1].为了进一步探索降低GVHD的有效方法,我们使用MMF联合CSA和MTX预防GVHD,并与传统的CSA联合MTX预防GVHD的方案进行对照研究,观察GVHD的患者在使用MMF治疗前后T细胞亚群的变化,现将结果报道如下.     

女性慢性生殖道炎症与抗精子免疫的相关研究

目的 :研究生殖道慢性感染状态下抗精子免疫应答的机制 ,为防治抗精子免疫性不孕提供依据。方法 :①病例选择 :诊断为慢性宫颈炎或 和慢性盆腔炎 ,有正常性生活的妇女 5 0例。对照组为有正常性生活并排除急慢性生殖道炎症的妇女 10例 ;②观察指标 :宫颈粘液病原体检测 :包括细菌、真菌、解脲支原体 (UU)与人型支原体 (MH)培养 ,沙眼衣原体(CT) ;血清ASAb总Ig测定 (ELISA法 ) ;外周血淋巴细胞亚群 (红细胞花环法 ) ;宫颈粘液白细胞介素 2 (IL 2 )。结果 :①慢性生殖道炎症组血清抗精子抗体 (ASAb)水平显著高于对照组 (P <0 0 5 ) ;解脲支原体 (UU)或 和沙眼衣原体 (CT)感染与ASAb有高度相关性 (P <0 0 1) ;②慢性生殖道炎症并抗精子抗体阳性组的妇女CD8+ 细胞减少 ,CD4 + CD8+ 比值升高 ,而宫颈粘液中IL 2水平显著升高 ,与ASAb阴性患者及正常对照组比较均有显著差异 (P <0 0 1)。结论 :女性慢性生殖道炎症可导致体内体液免疫与细胞免疫异常 ,并诱导抗精子抗体的产生。     

特发性血小板减少性紫癜患者T细胞及B细胞亚群变化的研究

目的 探讨特发性血小板减少性紫癜(idiopathic thrombocytopenic purpura,ITP)患者T、B淋巴细胞亚群的变化.方法 从大理州人民医院收集ITP患者和健康者的外周血,用Sysmex血液分析仪及流式细胞术分析T细胞及B细胞亚群.结果 与健康人群比较,ITP患者CD3+T细胞百分率无明显变化,CD4+T细胞百分率降低(42.39％±12.12％,P＜0.05),CD8+T细胞百分率升高(46.93％±11.99％,P＜0.05);CD19+B细胞百分率升高(14.11％±10.28％,P＜0.05),T2B细胞百分率(34.51％±9,70％,P＜0.05)、成熟B细胞百分率(30.91％±7.12％,P＜0.05)及记忆性B细胞百分率(23.31％±8.23％,P＜0.05)增多,差异均有统计学意义.ITP患者T1 B细胞、Kappa+B细胞、Lambda+B细胞百分率与健康人差异无统计学意义.结论 ITP患者外周血T细胞亚群和B细胞亚群分布发生了变化,这种变化在ITP发病中的作用尚需进一步研究.     

Challenges in diagnosis and management of Cryptococcal immune reconstitution inflammatory syndrome (IRIS) in resource limited settings

In many resource-limited settings, cryptococcal meningitis (CM) contributes up to 20% of all deaths with further complications due to Immune Reconstitution Inflammatory Syndrome (IRIS). We present a case report on a patient who developed CM-IRIS and then subsequent CM-relapse with a fluconazole-resistant organism and then later CM-IRIS once again, manifesting as cystic cryptococcomas, hydrocephalus, and sterile CSF. In this case we, demonstrate that CM-IRIS and persistent low level cryptococcal infection are not mutually exclusive phenomena. The management of IRIS with corticosteroids may increase the risk of culture positive CM-relapse which may further increase the risk of recurrent IRIS and resulting complications including death. We also highlight the role of imaging and fluconazole resistance testing in patients with recurrent meningitis and the importance of CSF cultures in guiding treatment decisions.     

Immunopathological characteristics of immune reconstitution inflammatory syndrome caused by Mycobacterium parascrofulaceum infection in a patient with AIDS

Immune reconstitution inflammatory syndrome (IRIS) caused by mycobacterium in patients with AIDS is often experienced in clinical practice. There is, however, a paucity of data documenting the histopathological findings and the pathogenesis. We determined the immunopathological characteristics of IRIS associated with Mycobacterium parascrofulaceum infection in an AIDS patient. A patient presented with pulmonary lymphadenitis and involvement of the pulmonary lingular segment. Portions of the involved lymph nodes and lung were excised, and the immunological properties were analyzed by immunohistochemical assays. The histological characteristics of lymph nodes showed a caseous necrosis. Histopathologically, the pulmonary lesion was composed of exudative and proliferative lesions. CD4⁺, CD8⁺, CD57⁺, and CD25⁺/FoxP3⁺ cells were observed in both types of lesions. Clusters of CD20⁺ cells and GATA3⁺ cells were predominantly observed in exudative lesions, while T-bet⁺ cells were dominant in proliferative lesions. ROR-γ⁺ cells were also observed in exudative lesions. These results indicate that the cellular immunity to mycobacteria was recovering in the lung tissue. In M. parascrofulaceum pulmonary infection, the exudative lesion had characteristics of Th2 and Th17-type immunities. In contrast, the proliferative lesion had characteristics of Th-1 type immunity. Our data provide the first evidence to reveal the status of the axis of distinctive immunity in the process of granuloma formation caused by a mycobacterium-related infection.     

The immunopathogenesis of the HIV tuberculosis immune reconstitution inflammatory syndrome

HIV‐1 patients co‐infected with some pathogens are at risk of developing the immune reconstitution inflammatory syndrome (IRIS) when initiating antiretroviral therapy (ART). IRIS is characterized by inflammation leading to the clinical worsening of a treated infection or the unmasking of a previously undiagnosed condition or infection. It is commonly associated with tuberculosis (TB), 8–43% of the HIV‐TB co‐infected patients prescribed with antitubercular treatment and ART develop TB‐IRIS. Although IRIS has been recognized for over 20 years, relatively little was known until recently about its pathogenesis. Despite these advances in understanding IRIS, there remains no immune biomarker for diagnostic or prognostic purposes. Here, we review the risk factors associated with TB‐IRIS, the challenges in studying this syndrome, and how T lymphocytes, dysregulated cytokine responses, and innate immunity may contribute to the development of TB‐IRIS.     

Association of CD4 T cell count and optimal timing of antiretroviral therapy initiation with immune reconstitution inflammatory syndrome and all-cause mortality for HIV-infected adults with newly diagnosed pulmonary tuberculosis: a systematic review and meta-analysis

Aims: CD4 T cell count and optimal timing of antiretroviral therapy (ART) during tuberculosis (TB) treatment are challenging. We conducted a meta-analysis to assess the association of CD4 T cell count and timing of ART initiation with immune reconstitution inflammatory syndrome (IRIS) and all-cause mortality of patients co-infected with HIV/TB. Methods: We conducted an electronic search of clinical studies dated from January 1980 to December 2019 in PubMed and EMBASE. Randomized, controlled trials evaluating low-base CD4 T cell count (< 50 cells/μL) versus high-base CD4 T cell count (≥ 50 cells/μL), and/or early ART initiation (1 to 28 days after starting TB treatment) versus delayed ART initiation (≥ 28 days after starting TB treatment) were included. The primary endpoints were all-cause mortality and TB-related immune reconstitution inflammatory syndrome (IRIS-TB). The risk ratio (RR) was calculated as a measure of intervention effect. Mantel-Haenszel method was used to estimate the RR. Results: Ten trials (n = 5226) were conducted in North America, Africa, and Asia. We found that low-baseline CD4 T cell count increased the incidence of TB-associated IRIS (RR, 1.47; 95% CI, 1.24-1.75; I² = 58%) and all-cause mortality (RR, 2.42; 95% CI, 1.71-3.42; I² = 41%) compared with high baseline CD4 T cell count, and early ART initiation increased the incidence of TB-associated IRIS compared with delayed ART initiation (RR, 1.80; 95% CI, 1.57-2.07; I² = 74%). However, early ART initiation did not reduce all-cause mortality (RR, 0.91; 95% CI, 0.74-1.12; I² = 49%) compared with delayed ART initiation.Conclusions: The present study demonstrates that low-baseline CD4 T cell count (< 50 cells/μL) in patients co-infected with TB-HIV increases the incidence of TB-associated IRIS and all-cause mortality. Early ART initiation (≤ 28 days) in patients co-infected with TB-HIV increases the incidence of TB-associated IRIS. However, evidence is insufficient to refute or support a survival benefit conferred by the comparison between early ART initiation (≤ 28 days) and delayed ART initiation.     

A novel experimental model of Cryptococcus neoformans‐related immune reconstitution inflammatory syndrome (IRIS) provides insights into pathogenesis

Antiretroviral therapy (ART) has yielded major advances in fighting the HIV pandemic by restoring protective immunity. However, a significant proportion of HIV patients co‐infected with the opportunistic fungal pathogen Cryptococcus neoformans paradoxically develops a life‐threatening immune reconstitution inflammatory syndrome (IRIS) during antiretroviral therapy. Despite several clinical studies, the underlying pathomecha‐nisms are poorly understood. Here, we present the first mouse model of cryptococcal IRIS that allows for a detailed analysis of disease development. Lymphocyte‐deficient RAG‐1^?/? mice are infected with C. neoformans and 4 weeks later adoptively transferred with purified CD4⁺ T cells. Reconstitution of CD4⁺ T cells is sufficient to induce a severe inflammatory disease similar to clinical IRIS in C. neoformans‐infected RAG‐1^?/? mice of different genetic backgrounds and immunological phenotypes (i.e. C57BL/6 and BALB/c). Multiorgan inflammation is accompanied by a systemic release of distinct proinflammatory cytokines, i.e. IFN‐γ, IL‐6, and TNF‐α. IRIS development is characterized by infection‐dependent activation of donor CD4⁺ T cells, which are the source of IFN‐γ. Interestingly, IFN‐γ‐mediated effects are not required for disease induction. Taken together, this novel mouse model of cryptococcal IRIS provides a useful tool to verify potential mechanisms of pathogenesis, revealing targets for diagnosis and therapeutic interventions.     

Fatal meningitis by Cryptococcus laurentii in a post-partum woman: A manifestation of immune reconstitution inflammatory syndrome

Cryptococcal meningitis in immunocompetent post-partum women has been rarely reported. Immune restoration during post-partum period leads to unmasking of many opportunistic infections that may have been acquired during pregnancy but manifest itself in the post-partum period due to immune reconstitution inflammatory syndrome. This case highlights the importance of considering opportunistic pathogens in immunocompetent patients who may be undergoing immune restoration. We report here a fatal case of post-partum immunocompetent women who presented with clinical features of meningitis. Prognosis of the cryptococcal meningitis not only depends on the immune status of the patient but also on how early the disease is diagnosed in the course of illness.     

Regulatory T cells generated during cytomegalovirus in vitro stimulation of mononuclear cells from HIV-infected individuals on HAART correlate with decreased lymphocyte proliferation

HIV-infected patients fail to fully recover cell-mediated immunity despite HAART. To identify regulatory factors, we studied the phenotype and function of in vitro cytomegalovirus (CMV)-stimulated T cells from HAART recipients. CFSE-measured proliferation showed CD4⁺ and CD8⁺ cells dividing in CMV-stimulated cultures. Compared with healthy controls, CMV-stimulated lymphocytes from HAART recipients had lower ³H-thymidine incorporation; lower IFNγ and TNFα production; higher CD4⁺CD27⁻CD28⁻ and CD8⁺CD27⁻CD28⁻ frequencies; lower CD4⁺CD25^hi; and higher FoxP3 expression in CD8⁺CD25^hi cells. CMV-specific proliferation correlated with higher IFNγ, TNFα and IL10 levels and higher CD4⁺perforin⁺ and CD8⁺perforin⁺ frequencies. Decreased proliferation correlated with higher CD4⁺CD27⁻CD28⁻ frequencies and TGFβ1 production, which also correlated with each other. Anti-TGFβ1 neutralizing antibodies restored CMV-specific proliferation in a dose-dependent fashion. In HIV-infected subjects, decreased proliferation correlated with higher CMV-stimulated CD8⁺CD25^hi frequencies and their FoxP3 expression. These data indicate that FoxP3- and TGFβ1-expressing regulatory T cells contribute to decreased immunity in HAART recipients.     

HIV/AIDS患者高效抗逆转录病毒治疗后免疫重建不良的特征及相关因素分析

目的 通过回顾性研究,描述免疫重建不良HIV/AIDS患者的基本特征,探讨免疫重建不良的相关因素,发现HIV/AIDS患者免疫重建不良的预示指标.方法 以2005年1月-2011年8月在北京地坛医院起始HAART治疗≥96w的HIV/AIDS患者（503例）为研究对象,比较其中免疫无应答者（76例）与免疫应答良好者（427例）临床资料（人口学资料、基线CD4＋T细胞计数、机会性感染的合并情况、HAART（高效抗逆转录病毒治疗）方案和各种化验指标的差异,分析HIV/AIDS患者免疫重建不良的相关因素.结果 入组病例中免疫重建不良的发生率为15.11％;免疫重建不良组的基线CD4＋T细胞数、总淋巴细胞数目（TLC）及血红蛋白（Hb）显著低于免疫重建良好组（z=-9.056,P＜0.001;z=-5.541,P＜0.001;z=-3.014,P=0.003）.免疫重建不良组基线机会性感染合并率显著高于重建良好组（x2=14.834,P=0.037）.结论 低基线CD4＋T细胞数目、TLC及Hb均为免疫重建不良的相关因素,应对HIV感染的患者及早进行治疗,预防免疫重建不良的发生.     

高效抗病毒治疗促使艾滋病患者免疫功能重建

艾滋病的特征是ＨＩＶ 1感染人体后 ,造成ＣＤ4 +Ｔ淋巴细胞数量进行性减少、细胞免疫功能损害 ,最后导致艾滋病 (ＡＩＤＳ)。先前的研究表明这种免疫功能的丧失是不可逆转的 ,抗ＨＩＶ病毒治疗仅能控制或减缓其进展。近年来 ,由于强效联合抗病毒治疗 (ＨＡＡＲＴ)的应用 ,艾滋病的发病率和死亡率均较前明显下降 (指西方国家 )。说明ＨＡＡＲＴ不仅能有效的控制ＨＩＶ 1的复制 ,并能使艾滋病病人的免疫功能得到恢复。这种ＨＡＡＲＴ使艾滋病病人免疫功能重建的假说最近被一组法国研究人员证实 ,艾滋病的免疫重建规律是 :(1)治疗早期ＣＤ4 +…