HIV感染者肝功能损害的临床实验研究

研究HIV感染者肝功能损害情况 ,为临床治疗提供依据 ,对 2 8例HIV感染的静脉吸毒者、 3 4例HIV阴性的静脉吸毒者及 3 4例健康男性进行肝功能生化指标ALT ,AST ,m -AST ,GGT ,ALP ,TBA的检测 ,结果显示HIV感染组和吸毒组与对照组相比 ,ALT/AST/m -AST分别有统计学显著性差异 ,HIV感染组与吸毒组间ALT/AST/m -AST无统计学差异 (q检验 ,P >0 . 0 5 ) ,说明HIV为非嗜肝性病毒 ;静脉吸毒可导致肝功能损伤 ;ALT/AST/m -AST是反映静脉吸毒合并HIV感染者肝脏功能损害灵敏而有效的监测指标。     

CXCR5~+CD8~+ T细胞在HIV感染中的免疫特征及其与疾病进展关系的研究

目的探讨HIV感染者外周血CXCR5~+CD8~+T细胞的频率、功能变化及其与病情进展的相关性。方法收集40例HIV感染者和15例健康对照者,采用流式细胞分析术检测其外周血CXCR5~+CD8~+T细胞频率及IFN-γ和IL-10表达,并分析其与血浆HIV载量和外周血CD4~+T细胞计数的相关性。结果与健康对照组相比,HIV感染组外周血CXCR5~+CD8~+T细胞频率上调(P0.05),且与外周血CD4~+T细胞计数呈弱正相关(r=0.349,P=0.027),与血浆HIV载量呈弱负相关(r=-0.377,P=0.040);HIV感染者外周血CXCR5~+CD8~+T细胞IFN-γ表达与血浆HIV载量呈负相关(r=-0.514,P=0.002);而CXCR5~+CD8~+T细胞IL-10的表达在HIV感染者中明显上调(P0.05),与外周血CD4~+T细胞计数呈弱负相关(r=-0.317,P=0.046),与血浆HIV载量呈正相关(r=0.670,P=0.002)。结论 HIV感染者外周血CXCR5~+CD8~+T细胞频率功能变化与疾病进展密切相关。     

泡球蚴感染过程中宿主CD+4细胞凋亡和凋亡相关基因转录水平的研究

目的　为了探讨泡球蚴感染宿主CD+ 4 淋巴细胞缺失的机制 ,以及泡球蚴感染与宿主CD+ 4 淋巴细胞凋亡及凋亡相关基因转录水平的相关性。方法　利用尼龙柱和补体法从泡球蚴感染 12周 ,2 5周和正常对照组BALB/c小鼠脾脏分离出纯CD+ 4 ,CD+ 8细胞 ,在体外分别经EmAg ,anti-CD3 ,IL - 2 ,TNFα ,PWM刺激培养 16h ;Tunel和PI双染后 ,FCM分析凋亡细胞数 ;并用C -myc ,TGF - β ,bcl- 2cDNA探针检测感染 2 5周EmAg诱导CD+ 4 细胞的凋亡相关基因转录水平。结果　FCM分析 ,感染 12周组CD+ 4 ,CD+ 8细胞凋亡数同正常对照组无明显差别 (P >0 0 5 ) ,感染 2 5周组CD+ 4 细胞凋亡数较正常对照组显著增高 (P <0 0 1) ,也显著性高于同组CD+ 8细胞 (P <0 0 1)。CD+ 4 细胞内C -myc,TGF - βmRNA水平较正常对照组显著升高 (P <0 0 5 ) ,而bcl- 2mRNA水平则减弱 (P <0 0 5 )。结论　泡球蚴寄生宿主后期 ,可诱导宿主成熟T细胞中CD+ 4 细胞发生凋亡 ,使宿主处于免疫抑制状态。凋亡的形成与凋亡信号增加 ,抑制信号减弱所引起。     

HIV-1慢性感染者CD39~+PD-1~+CD4~+T淋巴细胞特点与抗病毒治疗疗效的关系

目的通过分析1型艾滋病病毒(HIV-1)感染者不同疾病阶段CD39~+PD-1~+CD4~+T淋巴细胞(简称CD39~+PD-1~+CD4细胞)的特点及其与潜伏病毒库形成的关系,探讨CD39~+PD-1~+CD4细胞的临床意义。方法通过流式细胞术检测CD4细胞上CD39及PD-1的表达情况,分析CD39~+PD-1~+CD4细胞与CD4细胞计数、病毒载量及CD4细胞内病毒指标的相关性。通过实时荧光定量聚合酶链反应(PCR)检测免疫重建成功患者(CRs)和免疫重建失败患者(INRs)的HIV库,分析CD39~+PD-1~+CD4细胞与HIV库的关系。结果入组11例健康对照(HCs)和69例HIV-1感染者,其中包括38例未抗病毒治疗(ART)者(TNs)、21例CRs、10例INRs。1)与HCs相比,TNs组患者CD39~+PD-1~+CD4细胞亚群占比显著升高(平均值0.99%vs. 2.50%);与TNs组相比,ART后,CRs组患者的CD39~+PD-1~+CD4细胞亚群占比显著降低(平均值2.50%vs. 0.86%);而INRs组患者该细胞亚群占比显著高于CRs组(平均值2.74%vs. 0.86%);2)在TNs组患者中CD39~+PD-1~+CD4细胞亚群占比与CD4细胞计数呈负相关(r=-0.359 6, P=0.026 6),与病毒载量呈正相关(r=0.451 1, P=0.004 5);3)ART两年以上患者CD39~+PD-1~+CD4细胞亚群占比与HIV脱氧核糖核酸(HIV DNA)正相关(r=0.565 9,P=0.047 3),与细胞相关的未剪接HIV核糖核酸(HIV us RNA)正相关(r=0.675 8,P=0.013 7)。结论 CD39~+PD-1~+CD4细胞与ART后免疫重建失败相关,其机制可能是CD39~+PD-1~+CD4细胞促进HIV建立潜伏病毒库。     

人类免疫缺陷病毒感染者及艾滋病患者CD8+ CD38+ CD8+ HLA-DR+比IV载量的相关性研究

目的 研究人类免疫缺陷病毒(HIV)感染者和获得性免疫缺陷综合征(AIDS,艾滋病)患者CD8+ T细胞激活分子CD38、人类白细胞Ⅱ类抗原(HLA-DR)与血浆HIV载量的相关性,分析用CD8+ CD38+、CD8+ HLA-DR+的比例替代HIV载量的可行性.方法 采集1998-2006年期间在北京协和医院初诊的HIV感染者或AIDS患者236例和56名同期健康献血员的抗凝静脉血,用流式细胞术分析CD8+ T细胞分别表达CD38和HLA-DR的比例,用分支DNA技术(bDNA)检测血浆病毒载量(VL).用受试者工作特征曲线(ROC)分别预测VL＞1×103拷贝/mL、＞1×104拷贝/mL和＞1×105拷贝/mL时CD8+ CD38+、CD8+ HLA-DR+比例的临界值范围.结果 236例患者的CD4+ T细胞计数138(16,262)×106/L,显著低于对照组(P＜0.01);CD8+ T细胞计数618(353,879),显著高于对照组(P＜0.05);CD8+ CD38+、CD8+ HLA-DR+的比例分别为85.4%(72.5%,92.2%)和40.3%(17.5%,59.7%),显著高于对照组(P＜0.01),与HIV载量的相关性分别为0.429(P＜0.01)和0.282(P＜0.01).用CD8+ CD38+＞80.4%预测VL＞1×103拷贝/mL的敏感度和特异度为80.6%和75.0%;用CD8+ HLA-DR+预测VL＞1×105拷贝/mL的敏感度和特异度为78.7%和81.4%.结论 对HIV感染或AIDS初诊的患者可以尝试用CD38和HLA-DR激活亚群来预测血浆HIV载量,这种替代检测方法具有一定的可行性.     

HIV感染者外周浅表淋巴结中CD4~+T淋巴细胞计数与胶原沉积的关系研究

目的通过对不同感染阶段HIV感染者外周浅表淋巴结中CD4+T淋巴细胞、胶原蛋白、白细胞介素(interleukin,IL)-7的检测,以及CD4+T淋巴细胞计数与胶原沉积的相关性分析,探讨HIV感染后胶原沉积对CD4+T淋巴细胞的影响。方法选择HIV感染者43例,分为HIV感染无症状组和AIDS组,留取外周浅表淋巴结活体组织检查(活检)组织;另外选择非HIV感染者12名为健康对照组,同样留取其外周浅表淋巴结活检组织。利用免疫组织化学方法检测研究对象淋巴结中CD4+T淋巴细胞、Ⅰ型胶原蛋白和IL-7定量及分布情况。结果 1随着病程进展,HIV感染者外周浅表淋巴结中胶原沉积逐渐增加,AIDS组高于无症状组,无症状组高于健康对照组,差异均有统计学意义(P均0.05);2HIV感染无症状组外周浅表淋巴结中CD4+T淋巴细胞计数与健康对照组相比差异无统计学意义(P0.05),而AIDS组则显著减少(P0.01);3HIV感染者外周浅表淋巴结中CD4+T淋巴细胞计数与胶原沉积量呈负相关(R2=0.724,P=0.000),与外周血中CD4+T淋巴细胞计数呈正相关(R2=0.702,P=0.000);43组IL-7的表达水平差异无统计学意义(P0.05),而AIDS组部分患者淋巴结中IL-7呈局部聚集性分泌。结论 HIV感染后外周浅表淋巴结中胶原沉积逐渐增加导致结构破坏,可能是CD4+T淋巴细胞进行性减少的一个重要原因,虽然IL-7有随病程进展而分泌增加的趋势,但仍不足以弥补淋巴结结构破坏对CD4+T淋巴细胞的影响。     

HIV感染者/AIDS患者外周血CD38 HLA-DR分子在CD4+ CD8+T淋巴细胞上的表达

目的　观察国内艾滋病病毒 (HIV)感染者 /艾滋病 (AIDS)患者外周血CD38、HLA DR分子在CD+4 、CD+8T淋巴细胞上表达的变化 ,并探讨这些变化的临床意义。方法　用流式细胞仪检测 5 1例正常对照、14例HIV感染者和 3 6例AIDS患者的外周血CD+4 、CD+8T淋巴细胞表面的CD38、HLA DR分子的表达 ,用分枝DNA(bDNA)法检测 11例HIV感染者和 18例AIDS患者的血浆病毒载量。结果　CD+4 HLA DR+细胞百分比显示 ,AIDS组显著高于正常组及HIV组 ;CD+8HLA DR+T细胞百分比显示HIV组与AIDS组间无差异 ,而它们均显著高于正常组。CD+8、CD38+细胞百分比则是AIDS组 >HIV组 >正常组 ,CD+8CD38+、CD+8HLA DR+、CD+4 HLA DR+细胞百分比与病毒载量显著正相关。结论　在HIV感染过程中 ,HLA -DR+、CD38+在CD+4 、CD+8T淋巴细胞上的表达均显著增加 ,反映T淋巴细胞异常激活 ;尤其是CD+8CD38+细胞百分比随着疾病进展逐渐升高 ,预示疾病进展程度。在评价HIV感染者和AIDS患者的免疫状况时 ,不仅要考虑免疫细胞数量和功能的变化 ,还应考虑免疫细胞的激活水平     

HIV病毒载量与HCV病毒载量间及与CD3,CD4和CD8细胞免疫功能的相关性研究

目的研究静脉吸毒人群HIV/HCV混合感染者病毒载量间的相关性及与CD3,CD4,CD8细胞计数的关系.方法采用荧光定量PCR技术和流式细胞技术分别检测HIV和HCV病毒载量及CD3,CD4,CD8细胞计数,并采用多元统计方法进行分析.结果综合分析显示,在HIV和HCV混合感染的静脉吸毒人群中,HIV病毒载量与CD3和CD4细胞计数存在有统计学负相关关系,HCV病毒载量与CD3和CD4细胞计数存在统计学正相关关系,两病毒载量均与CD8细胞计数和CD4/CD8比值无统计学关系,HIV病毒载量与HCV病毒载量间存在统计学负相关关系.进一步逐步回归分析表明,CD3和CD8细胞计数对HIV病毒载量影响较小,CD4细胞计数和CD4/CD8比值及HCV病毒载量对HIV病毒载量水平则产生决定性的影响.结论静脉吸毒人群HIV/HCV混合感染者病毒载量间存在一定程度的内在联系和相互干扰, CD3,CD4,CD8 T淋巴细胞免疫水平和作用机制有待于进一步研究.     

HIV-1感染者CD73~+CD8~+ T细胞减少与T细胞异常活化的相关性研究

目的探讨HIV-1感染者外周血CD8~+T细胞上CD73的表达特点及其与T细胞异常活化和疾病进展的关系。方法研究入选65例HIV-1感染者和27例健康对照。通过流式细胞术检测研究对象外周血CD73~+CD8~+T细胞的频率和绝对计数,并将患者CD73~+CD8~+T细胞绝对计数和频率与其CD4~+T细胞计数、HIV-1载量以及CD38~+CD8~+T细胞频率进行相关性分析。结果与健康对照相比,HIV-1感染者外周血CD73~+CD8~+T细胞绝对计数和频率均明显降低(P均0.05);HIV-1感染者外周血CD73~+CD8~+T细胞绝对计数和频率与CD4~+T细胞计数呈正相关(r=0.555,P=0.001;r=0.342,P=0.005),与CD38~+CD8~+T细胞频率呈负相关(r=-0.384,P=0.002;r=-0.387,P=0.001);HIV-1感染者CD73~+CD8~+T细胞的绝对计数与HIV-1载量呈弱负相关(r=-0.261,P=0.035)。结论 HIV-1感染者外周血CD73~+CD8~+T细胞的减少不但与患者T细胞的活化程度呈显著负相关,而且与AIDS疾病进展相关。     

CD1d~(hi)CD5~+CD19~+B细胞在HIV-1感染者外周血中的表达

目的研究艾滋病病毒1型(HIV-1)感染者外周血中调节性B细胞(Breg)与T淋巴细胞数量、病毒载量及白介素-10(IL-10)的表达水平,分析其相关性并探讨Breg在HIV发病机制中的作用。方法选择30例未经抗病毒治疗的HIV-1感染者,分离外周血单个核细胞(PBMC),用流式细胞术(FCM)检测CD1dhi CD5+CD19+B细胞的比例、CD+4T淋巴细胞(简称CD4细胞)数量、CD+8T淋巴细胞(简称CD8细胞)数量,用酶联免疫吸附试验法(ELISA)测定其PBMC培养液上清中IL-10的表达水平,经反转录聚合酶链反应(RT-PCR)检测病毒载量,与同期选择的健康对照组比较。结果与健康对照组相比,HIV-1感染者的CD1dhi CD5+CD19+B细胞的比例均明显升高(P0.0001),其培养液上清中IL-10的表达水平也显著升高(P=0.0005)。另外,HIV-1感染者PBMC中的CD1dhi CD5+CD19+B细胞的比例与CD4细胞数量(r=-0.6084,P=0.0004)及CD4细胞/CD8细胞的比值(r=-0.8715,P0.0001)均呈显著负相关性,与血浆中病毒载量的水平(r=0.6825,P0.0001)及IL-10的水平均呈正相关性(r=0.7656,P0.0001),而与CD8细胞数量未见相关性(r=0.1183,P=0.5334)。结论CD1dhi CD5+CD19+B细胞比例与其相关细胞因子IL-10表达水平的上调可能参与HIV的发病机制。     

Immune restoration by combination of a cytostatic drug (hydroxyurea) and anti-HIV drugs (didanosine and indinavir).

Cell activation is essential for HIV infection. CD4+ T lymphocyte activation allows virus replication and CD8+ T lymphocyte activation may contribute to pathogenesis. We combined hydroxyurea, a cytostatic drug that inhibits cell activation and proliferation, with two drugs that inhibit HIV (didanosine and indinavir), to block the "cell activation-virus production-pathogenesis" cycle. HIV was strongly suppressed in treated patients, and the average CD4 count increased to 224/mm3. Compared with a matched group of patients who had declined antiretroviral treatment, treated patients had a significantly lower proportion of activated CD8+ T lymphocytes and a significantly higher number of naive CD8+ and CD4+ T lymphocytes. The proliferative responses to allogeneic and influenza virus antigens were increased in treated patients, and a defect in CD3-zeta expression, the signaling chain of the T cell receptor complex, was reversed. The use of a cytostatic drug was not detrimental to the immune system; on the contrary, the combination of antiviral and cytostatic treatment improved all of the immune parameters tested.     

Late diagnosis of HIV infection: the role of age and sex

Background

Late diagnosis of human immunodeficiency virus (HIV) infection is detrimental to infected persons and to the public health. The objective of this study was to identify factors associated with late diagnosis of HIV infection, defined as an initial CD4 count <200 cells/μL, in a cohort of recently diagnosed persons. Additionally, we evaluated factors associated with HIV infection being diagnosed during hospitalization.

Methods

This was a cross-sectional study of a university-based HIV clinic in the southeastern US. Patients with newly diagnosed HIV infection evaluated at the Duke University HIV clinic between October 2002 and August 2004 were included in this analysis. Socio-demographic variables, site of HIV diagnosis, opportunistic infections present at diagnosis, initial CD4 count, and initial HIV RNA level were recorded for study subjects.

Results

Forty-nine percent of subjects met the immunologic definition of AIDS at the time of HIV diagnosis (CD4 count <200 cells/μL). In multivariable logistic regression analyses, older patients were more likely to be diagnosed with a CD4 count <200 cells/μL (adjusted odds ratio [AOR] 1.72, 95% confidence interval [CI], 1.12-2.64, P = .01), and older patients (AOR 1.79, 95% CI, 1.07-3.12, P = .03) and women (AOR 6.74, 95% CI, 2.08-21.81, P = 0.001) were more likely to be diagnosed during hospitalization.

Conclusions

Late diagnosis of HIV infection is a considerable problem, particularly for older patients. Inpatient diagnosis of HIV infection is significantly more common among women and older patients. Improved HIV testing strategies may allow for more timely diagnosis of HIV infection, which may benefit both the infected individual and society.     

Immune status at presentation to care did not improve among antiretroviral-naive persons from 1990 to 2006.

BACKGROUND: Human immunodeficiency virus (HIV) prevention initiatives to improve access to HIV services have increased over time. Despite this, >250,000 cases of HIV infection in the United States are undiagnosed, and many infected persons do not present for care until their HIV infection is advanced. Late presentation may increase the risk of HIV transmission and make HIV infection more difficult to treat effectively. With more effective HIV therapy, it was hoped that patients might present earlier in their disease course. METHODS: To assess immune status and time of HIV diagnosis in patients who newly presented for care, we analyzed data for the period 1990-2006 from patients who were antiretroviral naive at presentation to the Johns Hopkins HIV Clinic in Baltimore, Maryland. We compared CD4(+) cell count and time from HIV diagnosis at presentation by demographic characteristics at enrollment. RESULTS: The median presenting CD4(+) cell count decreased from 371 cells/mm(3) during 1990-1994 to 276 cells/mm(3) during 2003-2006 (P<.01) overall and decreased within individual demographic groups. There was also a decrease in the median time from HIV diagnosis to presentation for care (271 days in 1990-1994 to 196 days in 2003-2006; P<.01). Multivariate analysis revealed that, in addition to CD4(+) cell count at presentation, male sex was associated with lower CD4(+) cell counts (-93 cells/mm(3)), as was black race (-71 cells/mm(3)) and older age (-20 cells/mm(3) per 10 years). CONCLUSIONS: There has been a decrease in time from diagnosis of HIV infection to presentation for care, coupled with an increase in the severity of immunocompromise at time of presentation, over the past 16 years in Maryland. New strategies to provide earlier HIV testing and referral into care are urgently needed.     

泡状棘球蚴病宿主淋巴细胞的变化及意义

目的　为探讨泡状棘球蚴病宿主体内淋巴细胞在免疫调节和发病中的作用。方法　对泡球蚴感染BALB/c小鼠观察至 2 5周 ,在不同时间取脾制备细胞悬液 ,检测CD+ 4 ,CD+ 8细胞数量。对 2 5例泡球蚴病患者和 18例健康人群 ,用FCM分析了CD+ 3 ,CD+ 4 ,CD+ 8,CD+ 19,CD+ 3 8,CD+ 56和HLA -DR+ 细胞的变化。结果　泡球蚴感染BALB/c小鼠后 ,1～ 8周以CD+ 4 细胞为主 ,随后CD+ 4 细胞减少 ,CD+ 8细胞增加 ,2 0周后改变显著 (P <0 0 5 ) ,CD+ 4 /CD+ 8比值迅速倒置。泡状棘球蚴病患者CD+ 3细胞未发生改变 ,CD+ 4 细胞较正常对照组下降 (P <0 0 5 ) ,CD+ 8细胞上升 (P <0 0 5 ) ,使CD+ 4 /CD+ 8比值降低 (P <0 0 5 )。CD+ 56细胞较正常对照组显著性降低 (P <0 0 1) ,CD+ 19,CD+ 3 8和HLA -DR+ 细胞未发生改变 (P >0 0 5 )。结论　泡球蚴感染小鼠前 8周 ,以CD+ 4 细胞反应为主 ,具有保护性免疫。感染后期逐渐以CD+ 8细胞为主 ,使机体呈免疫抑制状态 ,有利于泡球蚴生存。泡状棘球蚴病患者机体呈免疫抑制状态 ,有利于泡状棘球蚴在体内的生长     

Impact of treatment with direct-acting antivirals on inflammatory markers and autoantibodies in HIV/HCV co-infected individuals

HCV infection could have extrahepatic manifestations due to an aberrant immune response. HCV/HIV co-infection increases such persistent immune activation. Aim of the present study is to describe the evolution of inflammatory markers used in clinical practice, mixed cryoglobulinemia (MC) and autoantibody reactivity in co-infected individuals who achieved sustained virological response (SVR) after DAA treatment. This prospective, observational study included all HIV/HCV co-infected subjects who started any DAA regimen from 2015 to 2020. Samples for laboratory measurements (ferritin, C reactive protein, C3 and C4 fractions, rheumatoid factor, MC, anti-thyroglobulin Ab, anti-thyroid peroxidase Ab, ANCA, ASMA, anti-LKM, anti-DNA, AMA, ANA, T CD4+ and CD8+ cell count, and CD4/CD8 ratio) were collected at baseline, after 4 weeks, at end of treatment, and at SVR12. The analysis included 129 individuals: 51.9% with a F0–F3 fibrosis and 48.1% with liver cirrhosis. Cryocrit, C3 fraction, and rheumatoid factor significantly improved at week 4; ferritin, anti-thyroglobulin Ab, and C4 fraction at EOT; total leukocytes count at SVR12. MC positivity decreased from 72.8% to 35.8% (p < .001). T CD4+ cell slightly increased at SVR12, but with an increase also in CD8+ resulting in stable CD4/CD8 ratio. Autoantibody reactivity did not change significantly. ANA rods and rings positivity increased from 14.8% to 28.6% (p = .099): they were observed in three subjects without exposure to RBV. DAA therapy may lead to improvement in inflammatory markers and MC clearance but without significant changes in autoantibodies reactivity and CD4/CD8 ratio over a follow up of 12 weeks.     

T淋巴细胞激活亚群在HIV感染中的变化及其临床意义

目的：研究HIV／AIDS患者T淋巴细胞激活亚群的变化，探讨其临床意义。方法：用流式细胞仪检测59例HIV／AIDS患者和51例健康献血员的T淋巴细胞，对其中40例患者的所有健康献血员进一步分析T淋巴细胞激活亚群（HLA－DR^ CD4^ 、HLA-DR^ CD8^ 和CD38^ CD8^ ）；用bDNA病毒定量检测仪检测59例HIV／AIDS患者的血浆HIV病毒载量。结果：与正常人组相比，HIV组和AIDS组的T淋巴细胞各激活亚群的百分比均显著升高，所有激活亚群均与T4细胞计数成反比，而与病毒载量成正比。其中，CD38^ CD8^ 亚群的百分比与T4细胞计数和病毒载量的相关性最为密切，相关系数分别为r=-0.603和r=0.523，（P＜0．01）。结论；HIV／AIDS患者的T淋巴细胞发生持续和异常的免疫激活，细胞激活程度与疾病进展高度相关，测定这些激活的T细胞亚群变化不仅有助于评价HIV／AIDS患者的免疫状况、判断病毒复制的活跃程度，而且对预示疾病进展和临床疗效评价方面均具有重要价值。     

AIDS合并结核病患者HIV RNA定量和CD4+T淋巴细胞计数特点分析

目的 总结AIDS合并结核病的临床特点,进一步提高对AIDS合并结核病的认识.方法 将AIDS合并结核病患者分为肺内结核组、肺内结核并肺外结核组和肺外结核组,比较和分析3组之间HIV RNA定量、CD4+T淋巴细胞计数的差异.结果 肺内结核组的HIV RNA定量明显低于肺内并肺外结核组和肺外结核组(P均＜0.05).肺内结核组的CD4+T淋巴细胞计数明显高于肺内并肺外结核组和肺外结核组(P均＜ 0.05).结论 患者的HIV RNA载量越高、CD4+T淋巴细胞计数越低,免疫功能越差,越易发生肺外结核和肺内并肺外结核,越易导致结核分枝杆菌播散性传播.     

Pilot study of the effects of intermittent interleukin-2 on human immunodeficiency virus (HIV)-specific immune responses in patients treated during recently acquired HIV infection.

Highly active antiretroviral therapy (HAART) initiated during acute human immunodeficiency virus (HIV) infection may preserve HIV-specific CD4+ T cell responses that are thought to enhance HIV-specific CD8+ T cell function. The present pilot study was designed to determine whether preserved HIV-specific immune responses are augmented by the administration of the immunomodulatory agent interleukin (IL)-2. Nine persons recently (<6 months) infected with HIV were randomized to receive HAART alone or HAART plus 3 cycles of intermittent IL-2 during a 12-month period. Although HAART plus IL-2 significantly increased counts of total and naive CD4+ T cells, compared with HAART alone, there was no increase in CD4+ or CD8+ HIV-specific immune responses. In addition, adjuvant IL-2 therapy did not reduce the pool of HIV-infected resting CD4+ T cells. Thus, although intermittent IL-2 plus HAART quantitatively increased CD4+ T cells, this increase was not selective for HIV-specific CD4+ or CD8+ T cell responses in recently infected persons.     

Profile of immunologic recovery in HIV-infected Ugandan adults after antiretroviral therapy

HIV infection is characterized by a decrease in total CD4 cell count, rising viral load, as well as an increase in immune activation levels. Increased activation can lead to an increase in apoptosis and contribute to CD4 depletion. We evaluated the clinical and immunologic responses of 23 HIV-positive Ugandan volunteers following initiation of antiretroviral therapy (ART). All volunteers achieved and maintained complete viral suppression within the first 3 months of therapy (p > 0.05). CD4+ and CD8+ T cell activation also decreased significantly, although it never reached the level of HIV negative Ugandan volunteers. Viral suppression and CD4 cell recovery were also associated with an improved profile in CD8+ T cell functional markers, but had no effect on HIV-specific proliferation. We conclude that ART in a cohort of therapy-naive Ugandans with AIDS partially restores but does not fully reverse the immune dysfunction observed in chronic HIV infection.