人类免疫缺陷病毒感染者CD4+T淋巴细胞计数与结核分枝杆菌共感染的相关性

目的 探讨HIV合并结核分枝杆菌感染患者外周血CD4+T淋巴细胞的变化及其对酶联免疫斑点试验(ELISPOT)的影响.方法 应用结核酶联免疫斑点试验(T-SPOT.TB)对云南省和上海地区193例明确诊断的HIV感染者的血标本进行结核分枝杆菌特异性T淋巴细胞检测,同时应用流式细胞仪检测外周血CD4+T淋巴细胞计数,采用t检验进行统计学分析.结果 HIV感染者中潜伏性结核发生率达30.6％.HIV合并活动性结核患者的外周血CD4+T淋巴细胞计数平均值为190×106/L,显著低于HIV合并潜伏性结核组的484×106/L(t=6.665,P＜0.01).根据CD4+T淋巴细胞计数＞500×106/L、200×106～500×106/L、＜200×106/L进行分层分析发现,活动性结核组和潜伏性结核组构成比依次为1∶16.2、1∶1.3、5.6∶1.79例T-SPOT.TB阳性的病例中,共有20例HIV合并活动性结核患者,其中14例患者CD4+T淋巴细胞计数平均值＜200×106/L,5例为200×106/L～500×106/L,1例＞500×106/L.59例潜伏性结核患者中,52例CD4+T淋巴细胞计数＞200×106/L.结论 我国HIV感染人群中有较高的潜伏性结核发生率,HIV合并活动性结核患者的总体细胞免疫应答功能严重受损,随着CD4ˉT淋巴细胞计数的下降,HIV患者合并的潜伏性结核更易进展为活动性结核.当CD4+T淋巴细胞＜200×106/L时,对T-SPOT.TB检测结果可能有影响.     

人类免疫缺陷病毒合并结核分枝杆菌感染者的抗结核细胞免疫功能

目的 评价HIV合并结核分枝杆菌潜伏感染或合并活动性结核患者的抗结核细胞免疫功能.方法 应用早期分泌性抗原靶蛋白(ESAT)-6和培养滤出蛋白(CFP)-10诱导的结核酶联免疫斑点法对云南地区100例明确诊断的HIV感染者的血液标本进行结核分枝杆菌特异性T淋巴细胞检测,同时应用流式细胞仪检测外周血CD3+CD4+T淋巴细胞和CD3+CD8+T淋巴细胞的绝对计数水平.采用Mann-Whitney检验进行非参数统计分析.结果临床上无活动性结核感染证据的HIV感染者中合并结核分枝杆菌潜伏感染的感染率高达67.6%.HIV合并结核分枝杆菌潜伏感染者的外周血CD3+CD4+T淋巴细胞(532×106/L)和CD3+CD8+T淋巴细胞(473×106/L)绝对计数与单纯HIV感染者(406×106/L和504 × 106/L)相比,差异无统计学意义.HIV合并活动性结核感染者的外周血CD3+CD4+T淋巴细胞绝对计数平均值为189 × 106/L,CD3+CD8+T淋巴细胞绝对计数平均值为293×106/L,均显著低于单纯HIV合并结核潜伏感染组和HIV组(U=168.0,U=163.0;U=147.0,U=374.0;均P<0.01).HIV合并活动性结核感染者的ESAT-6和CFP-10抗原特异性斑点形成细胞数(31/106细胞和82/106细胞)显著低于HIV合并结核分枝杆菌潜伏感染者(92/106细胞和109/106细胞.U=507.0,U=529.5,均P<0.01).结论 我国无活动性结核临床证据的HIV感染人群中有较高的结核潜伏感染率,HIV合并活动性结核感染者的总体细胞免疫应答功能及特异性抗结核免疫应答功能均严重受损.     

艾滋病免疫重建炎性综合征与基线CD_4~+T淋巴细胞计数的相关性及治疗分析

目的探讨艾滋病(AIDS)免疫重建炎性综合征(IRIS)与基线CD+4T淋巴细胞(简称CD4细胞)计数的相关性及治疗方法。方法将选取的艾滋病病毒(HIV)感染者/艾滋病(AIDS)病人(HIV/AIDS病人),根据不同基线CD4细胞水平分为两组,观察这两组在高效抗反转录病毒治疗(HAART)后,发生IRIS的情况,以及糖皮质激素在治疗IRIS中的作用。结果共选取HIV/AIDS病人312例,A组157例,CD4细胞计数≤100个/μL:B组155例,CD4淋巴细胞计数100个/μL。A组IRIS发生率为40.1%(63/157),死亡率为6.3%(4/63);B组IRIS发生率为3.9%(6/155),无死亡病例;两组IRIS发生率差异有统计学意义(P0.01),死亡率虽有差异,但无统计学意义(P0.05)。两组IRIS最常见并发结核病,分别为71.4%(45/63)和33.3%(2/6)。糖皮质激素治疗重症病人症状的有效率为90.2%。结论基线CD4细胞低下是IRIS发生的重要因素,CD4细胞计数≤100个/μL的病人发生IRIS合并结核的较多见,糖皮质激素治疗有效。     

有效的高效抗反转录病毒治疗后低CD4/CD8比值HIV/AIDS患者免疫学特征分析

目的对比研究有效的高效抗反转录病毒治疗(highly active antiretroviral therapy,HAART)后低CD4/CD8比值组与高CD4/CD8比值组患者相关免疫学特征。方法选择接受HAART≥96周、CD4~+T淋巴细胞≥500/μl、HIV载量低于检测值下限的HIV感染者/AIDS患者(HIV/AIDS患者)109例,从中选出CD4/CD8比值≥0.82的患者28例及CD4/CD8比值≤0.48的患者28例,对比分析2组T淋巴细胞上CD38、人类白细胞抗原DR(HLA-DR)、CD27、CD28、CD45RA及CD31的表达,进而分析2组外周血T淋巴细胞的免疫活化与免疫老化状况。结果①低CD4/CD8比值组的基线CD4~+T淋巴细胞计数和基线CD4/CD8比值较高CD4/CD8比值组低(P0.05);②低CD4/CD8比值组HLA-DR~+CD8~+T淋巴细胞频率、处于中期分化阶段(CD27~-CD28~+)的CD4~+T淋巴细胞频率及处于晚期分化阶段(CD27~-CD28~-)的CD4~+和CD8~+T淋巴细胞频率高于高CD4/CD8比值组(P均0.05),而处于早期分化阶段(CD27~+CD28~+)的CD4~+和CD8~+T淋巴细胞频率低于高CD4/CD8比值组(P均0.05);③低CD4/CD8比值组纯真CD4~+和与CD8~+T淋巴细胞频率以及CD31~+纯真CD8~+T淋巴细胞的频率低于高CD4/CD8比值组(P均0.05)。结论①低基线CD4~+T淋巴细胞计数和低基线CD4/CD8比值HIV/AIDS患者有效HAART后CD4/CD8比值仍然相对较低,应及早起始HAART,预防CD4/CD8低比值持续的发生;②有效HAART后低CD4/CD8比值的HIV/AIDS患者表现出更为严重的免疫活化和免疫老化现象,针对这些免疫紊乱应给予除HAART外新的干预措施。     

HAART对HIV/HCV合并感染者PBMCs中MxA表达水平及其对后续抗HCV疗效的影响

目的纵向研究高效抗逆转录病毒治疗(HAART)对HIV单一感染者和HIV/HCV合并感染者外周血单个核细胞(PBMCs)中粘病毒抵抗蛋白Mx A mRNA表达水平的影响,分析HAART后HIV/HCV合并感染者抗HCV前基线Mx A mRNA水平是否与后续干扰素抗HCV疗效有关。方法以广州市第八人民医院收治的艾滋病患者(HIV单一感染组,HAART前CD4+T淋巴细胞200个/mm3,42例)和HIV/HCV合并感染患者(HIV/HCV合并感染组,HAART前CD4+T淋巴细胞200个/mm3,33例)为研究对象,并以22名健康自愿者作为对照;观察患者在抗HCV治疗前的HAART的不同时间点(0 W、4 W、12 W、24 W、48 W、72 W、96 W)PBMCs中Mx A mRNA表达水平;对比分析后继抗HCV治疗效果(有早期病毒学应答EVR,无早期病毒学应答NEVR)与Mx A mRNA表达水平的关系。结果 HIV单一感染组PBMCs中Mx A mRNA水平在HAART 4 W后下降(P0.05),其他各时间点及与健康对照组之间差异均无统计学意义(P0.05);HIV/HCV合并感染组PBMCs中HAART各时间点及与健康对照组之间差异均无统计学意义(P0.05);HAART 96 W后进行抗HCV治疗,EVR组抗HCV治疗前Mx A mRNA水平较NEVR组高(P0.05)。结论长期HAART对HIV/HCV合并感染者PBMCs中Mx A mRNA表达水平无显著影响;但HAART后抗HCV治疗前PBMCs中Mx A mRNA水平可作为HIV/HCV合并感染者抗HCV疗效的预测指标之一。     

人脐带间充质干细胞治疗慢性HIV感染者的回顾性研究

目的明确人脐带间充质干细胞(human umbilical cord-derived mesenchymal stem cells,UC-MSC)治疗慢性HIV感染者的长期安全性和有效性。方法回顾性分析2009年3月—2012年7月在我院接受UC-MSC治疗的57例慢性HIV感染者随访3年的资料。根据UC-MSC治疗前CD4+T淋巴细胞水平,将所有患者分为≤200个/mm3组(免疫重建失败组)和200个/mm3组(免疫重建成功组)。分析UC-MSC治疗的长期安全性和有效性。结果 2组患者接受UC-MSC治疗1、2、3年,其外周血CD4+T淋巴细胞计数及CD4/CD8比值均较基线水平显著升高。进一步分析发现,免疫重建失败组UC-MSC治疗1年和2年的有效率(以CD4+T淋巴细胞计数较基线水平升高30%为有效)显著高于免疫重建成功组。2组随访中未发现明显不良事件,安全性好。结论 UC-MSC治疗慢性HIV感染者3年安全性好,可显著持续升高外周血CD4+T淋巴细胞计数和CD4/CD8比值,UC-MSC治疗免疫重建失败患者疗效更为显著。本研究提示慢性HIV感染者免疫重建失败可能是UC-MSC治疗的适应证。     

艾滋病合并结核病与CD4 T淋巴细胞计数的相关性研究

目的通过对AIDS合并结核病例的回顾性分析,探讨AIDS合并结核病临床特征与CD4 T淋巴细胞计数的相关性。方法对95例AIDS并发结核感染的病例CD4 T淋巴细胞计数进行检测,同时选择30例近期入院的HIV阴性肺结核病人CD4 T淋巴细胞计数的检测,AIDS合并结核病与HIV阴性肺结核病CD4 T淋巴细胞水平对比分析;AIDS合并结核中PPD、结明试验、结核分型与CD4 T不同水平进行相关性分析。结果AIDS合并结核病与HIV阴性结核病CD4 T淋巴细胞水平相比,二者有显著性差异;CD4 T淋巴细胞计数与艾滋病合并结核病的影象学表现;PPD、结明试验、痰涂片抗酸染色阳性率、结核病分型有相关性,CD4&lt;100/mm3与CD4&gt;100/mm3相比,影象学中斑片实变影、多发空洞、多发结节、纵隔和(或)腋下淋巴结肿大有显著性差异;单发空洞,胸腔积液的机率,无显著性差异。CD4&lt;100/mm3与CD4&gt;100/mm3相比,PPD、结明试验、痰涂片抗酸染色阳性率相比均有显著性差异;Ⅱ、Ⅴ型结核发生率有明显差异。结论AIDS患者合并结核病发病率高,尤其以肺外结核和血型播散性结核多见,CD4 T淋巴细胞计数低于100/mm...     

未接受HAART的HIV/AIDS患者血清隐球菌抗原阳性率调查

目的调查未接受高效抗反转录病毒治疗(highly active antiretroviral therapy,HAART)的HIV/AIDS患者血清隐球菌抗原的阳性率。方法回顾性调查我院感染科2012年1—9月住院的77例未接受HAART的HIV/AIDS患者外周血CD4+T淋巴细胞计数及血清隐球菌抗原阳性率,比较隐球菌抗原阳性患者与阴性患者的CD4+T淋巴细胞计数。结果 77例(男53例,女24例)中,血清隐球菌抗原阳性48例,阳性率为62.34%,阴性29例,阴性率为37.66%。其中,CD4+T淋巴细胞计数≤50个/mm3的患者血清隐球菌抗原阳性率为72.73%。血清隐球菌抗原阳性患者外周血CD4+T淋巴细胞计数显著低于阴性患者(P=0.022)。结论未接受HAART的外周血CD4+T淋巴细胞计数较低的HIV/AIDS患者血清隐球菌抗原阳性率高,血清隐球菌抗原阳性患者CD4+T淋巴细胞水平低于阴性患者(P<0.05)。     

云南省德宏州1039例成人艾滋病患者抗病毒治疗效果评价

目的 评价德宏州成人HIV感染者、AIDS患者接受国家免费高效抗反转录病毒治疗(HAART)的效果.方法 回顾性分析德宏州5个县市2004年7月1日至2008年6月30 H期间规范HAART的1039例HIV感染者、AIDS患者的临床资料,评估治疗不同时间段患者的病毒学及免疫学应答情况.数据行卡方检验或F检验.结果 1039例HIV感染者、AIDS患者中,男611例,女428例,平均年龄(37.0±9.9)岁,平均治疗(22.41±12.69)个月.其中781例患者病毒得到完全抑制,HIV载量＜50拷贝/mL,占75.17%.接受HAART 6～12、13～24、25～36个和≥37个月时,病毒完全抑制率分别为76.95%、76.49%、70.65%、77.73%,不同治疗时间病毒完全抑制率比较,差异无统计学意义(x2=8.646,P=0.194).患者基线CD4+T淋巴细胞计数为(164.93±118.05)×106/L,接受HAART 6～12、13～24、25～36和≥37个月时分别为(330.85±201.73)×106/L、(356.24±205.49)×106/L、(434.53±250.65)×106/L和(396.31±202.62)×106/L,其中治疗时间为25～36个月和≥37个月时CD4+T淋巴细胞计数比较,差异无统计学意义;其余各治疗时间段间CD4+T淋巴细胞计数比较,差异有统计学意义(F=19.423,P＜0.01).随访1020例患者CD4+T淋巴细胞情况,其中927例出现免疫学应答,占90.88%.病毒学应答和免疫学应答均成功者717例,占70.29%,均失败者40例,占3.92%.结论 云南省德宏地区HIV感染者、AIDS患者对HAART有较好的病毒学及免疫学应答.     

HIV感染者外周血淋巴细胞总数与CD4+T淋巴细胞计数相关性研究

目的 分析HIV感染者外周血淋巴细胞总数(total lymphocyte count,TLC)与CD4+T淋巴细胞计数相关性,探讨将外周TLC作为监测HIV感染者病情变化指标的可行性.方法 回顾性分析我院54例HIV感染者TLC与CD4+T淋巴细胞计数相关性,判断CD4+T淋巴细胞计数分别＜100× 106/L、＜2...     

Tuberculosis immune reconstitution inflammatory syndrome in countries with limited resources.

Mycobacterium tuberculosis infection accounts for probably one third of human immunodeficiency virus (HIV) related immune reconstitution inflammatory syndrome (IRIS) events, particularly in developing countries where HIV and tuberculosis (TB) co-infection is very common. Small cohort studies of HIV-positive patients with active TB treated with antiretroviral therapy (ART) suggest an incidence of TB IRIS varying between 11% and 45%. Risk factors for TB IRIS that have been suggested in certain studies but not in others include: starting ART within 6 weeks of starting TB treatment; extra-pulmonary or disseminated disease; a low CD4+ lymphocyte count and a high viral load at the start of ART; and a good immunological and virological response during highly active antiretroviral therapy (HAART). It is important to agree on a clinical case definition of TB IRIS that could be used in resource-limited settings. Such a case definition could be used to determine the exact incidence and consequences of TB IRIS and would be valuable worldwide in clinical trials that are needed to answer questions on how this phenomenon could be prevented and treated.     

Immune reconstitution inflammatory syndrome in an HIV/TB co-infected patient four years after starting antiretroviral therapy

The Immune reconstitution inflammatory syndrome (IRIS) after starting antiretroviral therapy for HIV is well known. We describe an HIV seropositive woman, presenting 2 IRIS episodes associated with Mycobacterium tuberculosis. Exceptional was that the last episode occurred 4 years after initiating antiretroviral treatment, when her CD4+ lymphocyte count had been around 300 cells/mm3 for one year.     

Improved outcomes with earlier initiation of highly active antiretroviral therapy among human immunodeficiency virus-infected patients who achieve durable virologic suppression: longer follow-up of an observational cohort study

On the basis of studies with relatively short follow-up, treatment guidelines currently recommend that highly active antiretroviral therapy (HAART) be initiated in asymptomatic human immunodeficiency virus-infected patients when the CD4+ lymphocyte count is < or =200 cells/mm3. We assessed the development of a new opportunistic infection or death among 1173 patients initiating HAART. Durable virologic suppression was defined as having more undetectable (<400 copies/mL) than detectable virus loads after the initiation of therapy. The median durations of therapy and follow-up were 29 and 36 months, respectively. Among patients who achieved durable virologic suppression, those with baseline CD4+ lymphocyte counts of <200 cells/mm3 tended to progress faster than those with baseline CD4+ lymphocyte counts of 201-350 cells/mm3 (P=.09) and progressed faster than those with baseline CD4+ lymphocyte counts of >350 cells/mm3 (P=.01). Among those with durable virologic suppression, there was no difference in disease progression between those with baseline CD4+ lymphocyte counts of 201-350 cells/mm3 and those with durable virologic suppression with baseline CD4+ lymphocyte counts of >350 cells/mm3 (P=.40). Initiating HAART with a CD4+ lymphocyte count of <200 cells/mm3 was associated with a higher risk of disease progression, even with durable virologic suppression. HAART should be initiated at CD4+ lymphocyte counts of >200 cells/mm3.     

Tuberculosis after HAART initiation in HIV-positive patients from five countries with a high tuberculosis burden

BACKGROUND: HAART reduces tuberculosis (TB) incidence in people living with HIV/AIDS but those starting HAART may develop active TB or subclinical TB may become apparent in the immune reconstitution inflammatory syndrome. OBJECTIVE: To measure the incidence rate of notified TB in people receiving HAART in five HIV programmes occurring in low-resource countries with a high TB/HIV burden. METHODS: A retrospective review in five Médecins Sans Frontières programmes (Cambodia, Thailand, Kenya, Malawi and Cameroon) allowed incidence rates of notified TB to be calculated based on follow-up time after HAART initiation. RESULT: Among 3151 patients analysed, 90% had a CD4 cell count of < 200 cells/mul. Median follow-up time ranged from 3.7 months in Thailand or Kenya to 11.1 months in Cambodia. Incidence rates were 7.6, 10.4, 17.6, 14.3 and 4.8/100 person-years for pulmonary TB and 12.7, 4.3, 6.9, 2.1 and 0/100 person-years for extra-pulmonary TB in the programmes in Cambodia, Thailand, Kenya, Malawi and Cameroon, respectively. Overall, 62.3% of pulmonary TB and 54.9% of extra-pulmonary TB were diagnosed within 3 months after HAART initiation. CONCLUSION: High incidence rates of notified TB under HAART in programmes held in poor-resource countries were observed; these were likely to include both undiagnosed prevalent TB at HAART initiation and subclinical TB developing during the immune reconstitution inflammatory syndrome. This raises operational issues concerning TB diagnosis and treatment of TB/HIV-coinfected patients and prompts for urgent TB and HIV care integration.     

Cytokine responses induced by Mycobacterium tuberculosis in patients with HIV-1 infection and tuberculosis.

OBJECTIVE: Tuberculosis (TB) is an important opportunistic infection in HIV patients. Immune responses to Mycobacterium tuberculosis in HIV/TB patients were evaluated. METHODS: Fifteen patients with HIV/TB, ten with HIV, four with TB, and five controls were enrolled. Peripheral blood mononuclear cells were isolated and stimulated with mycobacterial antigen (PPD). Interferon (IFN)-gamma and TNF-alpha in culture supernatants were measured by ELISA. RESULTS: IFN-gamma and TNF-alpha production after PPD stimulation was markedly decreased in HIV patients, but not in HIV/TB patients. In HIV patients with a CD4 cell count of less than 200/mm3, IFN-gamma and TNF-alpha production after PPD stimulation was higher in HIV/TB patients than in HIV patients. Cytokine responses to M. tuberculosis reconstituted after highly active antiretroviral therapy (HAART) and were prominent in HIV/TB patients. CONCLUSIONS: Cytokine responses to M. tuberculosis were retained in HIV-infected patients with tuberculosis, even in patients with a CD4 cell count of less than 200/mm3, and reconstituted after HAART.     

Long-term changes in circulating CD4 T lymphocytes in virologically suppressed patients after 6 years of highly active antiretroviral therapy

Highly active antiretroviral therapy (HAART) initiated in advanced HIV disease is associated with CD4 lymphocyte increases (200-300 cells/mm3 after 2-4 years), although longer-term cellular dynamics have not been studied. We observed a significant median CD4 lymphocyte increase of 126 cells/mm3 and 54 naive CD4 lymphocytes from year 3 to 6 of HAART among 20 individuals with pre-HAART CD4 cell counts of 100-300 cells/mm3. This cohort represents the longest prospective immunological follow-up of virologically suppressed patients on HAART.     

Long-term clinical benefit after highly active antiretroviral therapy in advanced HIV-1 infection, even in patients without immune reconstitution

Our objective was to assess, in the clinical setting, the predictors of immune reconstitution (IR) and its relation with long-term clinical benefit, in HIV patients with advanced disease after highly active antiretroviral therapy (HAART) through an observational study. A retrospective cohort study in a clinical setting of 383 consecutive adult patients with advanced HIV infection (CD4+ cells <200/mm(3) at baseline), starting their first protease inhibitor (PI)-containing regimen was observed. Immune reconstitution was defined as CD4 count >200 cells/mm(3) and an increase > or =100 cells from baseline, anytime since starting HAART. Clinical benefit was defined as decreased mortality and reduction in AIDS-defining events, AIDS-related complex (ARC) events, major infections and hospitalization (days spent in hospital). During a mean follow-up of 808 days, 261 patients (68.1%) achieved IR. About 50% of these patients reached this result within one year after starting HAART. In multivariate analysis, predictors of immune recovery were sex (female) and baseline CD4 count higher than 50 cells/mm(3). The group of patients with IR had greater clinical benefit with lower mortality, fewer AIDS-defining events, shorter lengths of stay in hospital, fewer ARC events and fewer major infections during all the follow-up (P < 0.0001, tests for trends). However, although they did less remarkably than the first group of patients, even those patients who did not achieve IR experienced a significant decrease in the incidence of all the above events, as compared with the first and sometimes the second trimester after starting their HIV therapy. About 70% of HIV patients with advanced disease achieved IR after starting HAART. Such a benefit is a time-dependent effect and may even take more than 2 years to occur. Predictors of IR were sex (female) and higher baseline CD4 count (>50 cells/mm(3)). The patients who achieved immune recovery performed clinically better than patients who did not. Also the patients who failed to gain such a strong immunological recovery experienced a long-term clinical benefit. This suggests that PI-containing regimens, in advanced HIV disease, may produce a significant clinical benefit, at least temporary, even for patients who do not achieve a substantial immune response.     

人类免疫缺陷病毒合并结核感染患者外周血Vγ2Vδ2+T淋巴细胞的数量与功能变化

目的 探讨外周血Vγ2Vδ2+T淋巴细胞数与功能变化对HIV合并结核感染状态的影响.方法 将76例HIV/AIDS合并结核感染患者分为活动性结核感染组(HIV+TB组)和潜伏结核感染组(HIV+LTB组).流式细胞仪测定外周血淋巴细胞分类情况.酶联斑点免疫法(ELISPOT)和胞内细胞因子染色(ICS)方法 检测在PPD和磷酸化抗原(HMBPP)的刺激下T淋巴细胞亚群分泌IFN-γ功能的情况.统计学处理采用t检验.结果 HIV+TB组CD3+T淋巴细胞绝对计数(t=-3.67,P<0.01)和Vγ2Vδ2+T淋巴细胞所占CD3+T淋巴细胞比例(t=-2.06,P<0.05)均显著低于HIV+LTB组.PPD刺激时,HIV+LTB组分泌特异性IFN-γ的T淋巴细胞和参与分泌IFN-γ的CD4+T淋巴细胞所占CD3+T淋巴细胞比例,与HIV+TB组比较差异均无统计学意义.HMBPP刺激时,HIV+LTB组与HIV+TB组比较,分泌IFN-γ的特异性T淋巴细胞计数(t=2.71,P<0.01)和产生IFN-7的特异性Vy2'T淋巴细胞比例(t=3.003,P<0.01)均显著增加.结论 Vγ2Vδ2+T淋巴细胞在HIV/AIDS合并活动性结核患者中的数量和功能都有受损,提示该类细胞在CD4+T淋巴细胞受到抑制的情况下可能是人体内抵御结核感染的重要免疫细胞.     

Development of opportunistic infections after diagnosis of active tuberculosis in HIV-infected patients

Despite advances in highly active antiretroviral therapy (HAART), its use during tuberculosis (TB) treatment is fraught with challenges, often leading to delayed therapy. This report describes the course of HIV infection and outcomes of 26 consecutive TB/HIV coinfected patients who received TB treatment in Rhode Island. HIV infection was diagnosed in 26 (4%) of 598 TB cases in during a 10-year period. Of these patients, TB was the first indication of HIV infection in 15 patients (58%). Of the 21 patients who were not on antiretrovirals at the time of TB diagnosis, 17 (81%) met criteria for immediate initiation of HAART. The median CD4 cell counts and HIV-1 plasma viral load were 80 cells per microliter (range, 2-800 cells per microliter) and 255,631 copies per milliliter (range, 50,000 to > 500,000 copies per milliliter), respectively, for the patients whose baseline measurements were available. CD4 lymphocyte count was less than 200 cells per microliter in 13 (76%) of the 17 patients whose measurements were available. Three (30%) of the 10 patients whose CD4 cell count was less than 100 cells per microliter developed subsequent AIDS-defining illness prior to the initiation of HAART and a fourth patient, within 30 days of starting HAART. None of the patients who had CD4 cell counts 100 cells per microliter or greater developed subsequent AIDS-defining illness during TB treatment. The median time to starting HAART after starting TB treatment was 12 weeks (range, 3-36 weeks). From our limited experience based on this case series, we recommend early initiation of HAART in coinfected patients with CD4 cell counts less than 100 cells per microliter.     

AIDS-related Mycobacterium avium infection dissemination in a patient with endobronchial lesions associated with immune reconstitution inflammatory syndrome

Highly active antiretroviral therapy (HAART) has dramatically decreased the incidence of HIV-1-associated morbidity and mortality. During the initial months of HAART, immune reconstitution inflammatory syndrome (IRIS), an adverse consequence of restoration of the pathogen-specific immune response, often occurred in terminal-stage in patients, with MAC infection the most frequently implicated in IRIS. In August 2004, a 26-year-old Japanese woman with fever and general lymphadenopathy was diagnosed with AIDS (HIV-1 RNA 5.7 x 10(5) copies/mL, CD4+ T cell count 10/microL) and disseminated Mycobacterium avium (M. avium) infection, for which antimycobacterial treatment was initiated. The M. avium infection responded well to two months of this treatment, and HAART was begun. Despite good virologic response to HAART (HIV-1 RNA <50 copies/mL), she contracted pulmonary disease with parenchymal lung changes, endobronchial lesions, and localized supraclavicular lymphadenitis, which are M. avium-associated IRIS. Good immunological response (CD4+ T cell count 136/microL) and a stronger antimycobacterial treatment helped her overcoming M. avium-associated IRIS without systemic corticosteroids or the discontinuation of HAART. The possibility of IRIS should always be watched for when treating AIDS patients with HAART and an antimycobacterial treatment regimen formulated that considers potential drug interactions with HAART.