中草药“再生丹”对HIV感染者的疗效观察

目的　探讨中草药“再生丹”对ＨＩＶ感染者的治疗作用。方法　采用中药复合治疗方法，主药用于提高机体免疫力，辅药对症治疗。观察临床症状、实验室检测ＣＤ４ 和ＣＤ８ 淋巴细胞数，以及外周血中病毒载量的变化，并与治疗前比较。结果　２８ 例ＨＩＶ感染者服药后，体重有不同程度增加，平均增加５－４ ｋｇ。７ 例长期发热，４ 例腹泻，２ 例大面积皮肤溃烂和１ 例皮疹患者，服药１ 个月后症状消失；服药后５ 个月，１０ 例表现淋巴结肿大的患者中，３ 例肿大的淋巴结消失，７ 例显示不同程度的数量减少或体积缩小。治疗后２ 个月，４２－９％ 患者表现ＣＤ４ 淋巴细胞数增加，７１－４％ 患者病毒载量下降。治疗５ 个月后，ＣＤ４ 淋巴细胞增加者占５０－０％ ，８０－０％ 患者病毒载量下降，综合分析临床症状和实验室指标，总有效率达９４－０％ 。结论　中草药复合治疗ＨＩＶ感染者，可明显改善临床症状，提高ＣＤ４ 细胞数，使病毒载量下降，为用中草药控制ＨＩＶ感染和治疗艾滋病患者提供证据     

抗CD4及抗CXCR4抗体阻断HIV—1感染细胞作用的研究

为探讨抗ＣＤ４ 及抗ＣＸＣＲ４ 抗体在阻断Ｉ型人免疫缺陷病毒（ＨＩＶ－ １） 感染应用中的意义, 本文应用上述两种抗体分别与ＳｕｐＴ１ 细胞及人外周血单个核细胞（ＰＢＭＣ） 共培育, 以封闭ＨＩＶ－ １ 在上述细胞上的受体。然后, 以ＨＩＶ１ ＮＬ４３ 病毒株感染上述细胞, 通过测定感染细胞上清中ＨＩＶ－ １ 的Ｐ２４ 蛋白含量, 观察上述抗体对ＨＩＶ－ １ 感染细胞的阻断作用。结果显示, 无论是抗ＣＤ４ 或抗ＣＸＣＲ４ 的抗体单独应用或是两者联合应用, 均可明显地抑制ＨＩＶ－ １ 感染细胞的作用。该结果为今后开拓ＡＩＤＳ的抗体治疗提供了理论基础。     

CD26,人免疫缺陷病毒感染细胞的辅助分子

人免疫缺陷病毒（ＨＩＶ）感染并进入细胞是ＨＩＶ感染的关键步骤。ＣＤ４分子为ＨＩＶ感染并进入细胞的第一受体，ＣＤ２６分子为ＨＩＶ感染并进入细胞的第二受体。从ＨＩＶ感染细胞的ＣＤ２６分子量显著减少，ＤＰＰⅣ酶活性抑制剂、ＣＤ２６分子的单抗阻断ＨＩＶ感染并进入细胞，ＣＤ２６与ＣＤ４基因共转染使ＮＩＨ３Ｔ３变成ＨＩＶ易感的细胞系等方面证实了ＣＤ２６分子在ＨＩＶ感染中的作用管一发现对ＨＩＶ生活周期、细胞及动     

HIV/AIDS与肝炎病毒感染者CD4+、CD8+淋巴细胞数的比较

目的：探讨ＨＩＶ携带者或ＡＩＤＳ病人（简称ＨＩＶ／ＡＩＤＳ）与肝炎病毒感染者的ＣＤ４＾＋、ＣＤ８＾＋淋巴细胞变化,并进行比较。方法：用免疫磁珠法（ＤＹＮＡ ｂｅａｄｓ）检测ＣＤ４＾＋、ＣＤ８＾＋Ｔ淋巴细胞数,用双侧ｔ检验进行统计学处理。结果：全部ＨＩＶ／ＡＩＤＳ的ＣＤ４＾＋Ｔ淋巴细胞降低,且幅度大,８３．４％低于５００细胞／μｌ。在病毒性肝炎中降低的百分比和幅度均明显低于前者,只有２８．８％低于５     

艾滋病与超抗原的关系

人类免疫缺陷性病毒（ＨＩＶ）引发艾滋病的主要原因是ＣＤ４￣＋Ｔ细胞进行性耗竭和功能异常，但ＨＩＶ损伤ＣＤ４￣＋Ｔ细胞的确切机制仍不十分清楚，对此机制的了解是治疗及预防艾滋病的基础。近年来，越来越多的研究结果表明，超抗原（ｓｕｐｅｒａｎｔｉｇｅｎ）可能与艾滋病的发生有关，ＨＩＶ基因很可能表达一些具有超抗原活性的蛋白质致ＣＤ４￣＋Ｔ细胞损伤而引发艾滋病。     

在免疫细胞亚群中用超敏荧光原位杂交监测HIV-1治疗

ＨＩＶ－１病毒动力学研究已经显示在细胞内ＨＩＶ－１每天复制产生１百万以上颗粒，高效抗逆转录病毒治疗（ＨＡＡＲＴ）在数周内减少血浆ＨＩＶ－１ＲＮＡ数量，而且，存在于淋巴结和扁桃腺细胞内病毒宿主起到第二次序病毒衰弱，当治疗失败或病人不依从后，细胞宿主的ＨＩＶ－１仍然保持可以恢复病毒载量到治疗前水平。 血样本来自５例病人治疗前，用齐多夫定２００ｍｇ（ｔｉｄ）、拉夫咪啶１５０ｍｇ（Ｂｉｄ）和Ｉｎｄｉｎａｖｉｒ ８００ｍｇ（ｔｉｄ）治疗后４周、１２周和２４周。校正扩增逆转录酶（Ａｍｐｌｉｃｏｒｒｅｖｅｒｓｅ…     

用流式细胞仪检测HIV感染者和AIDS患者的T细胞亚群

目的用流式细胞仪（ｆｌｏｗｃｙｔｏｍｅｔｅｒ,ＦＣＭ）检测周围血中ＣＤ４＋、ＣＤ８＋淋巴细胞,结合临床情况对ＨＩＶ感染者和ＡＩＤＳ患者的免疫状况进行评价。方法将抗凝全血进行白细胞分类计数,用双色荧光标记的单克隆抗体染色,经溶血和固定后,用ＦＣＭ计数,从而得出ＣＤ４＋、ＣＤ８＋淋巴细胞数。结果ＨＩＶ感染者和ＡＩＤＳ患者的ＣＤ４＋淋巴细胞数都比正常人低,特别是ＡＩＤＳ患者,他们的ＣＤ４＋淋巴细胞数都低于２００个／ｍｍ３,临床表现也很差。结论ＦＣＭ检测结果与临床评价高度一致,而且ＦＣＭ比一般人工计数法更准确、方便、迅速,同时也证明ＦＣＭ是监测ＨＩＶ感染者和ＡＩＤＳ患者的免疫状况的最佳方法。     

中国人类免疫缺陷病毒（HIV—1）D亚型毒株gag,env和t …

目的 通过对ＨＩＶ－１毒株ｇａｇ,ｔａｔ,ｅｎｖ基因的序列分析,阐明Ｄ亚型ＨＩＶ－１毒株已在中国出现。方法 从１名四川非洲回国营务人员ＨＩＶ感染者（ＳＣ９ ７１２）淋巴细胞（ＰＢＭＣ）中提取前病毒ＤＮＡ,使用套式ＰＣＲ方法分别扩增ＨＩＶ－１的ｇａｇ基因区,ｅｎｖ基因的Ｃ２Ｖ３区和ｔａｔ基因的第一外显子。结果 发现ＳＣ９ ７１２在ｇａｇ区,ｅｎｖ区和ｔａｔ区与国际标准Ｄ亚型毒株的基因距离最近,其中在     

HLA多态性与HIV感染及AIDS发病相关性的研究

为研究人类白细胞抗原（ＨＬＡ）和人免疫缺陷病毒（ＨＩＶ）易感性的关系，本文分析比较了以下三组人群的ＨＬＡ表型频率和单倍型频率：①１７２例正常人；②１７例血清ＨＩＶ阴性高危人群；③１８０例血清ＨＩＶ阳性患者，其中２１例发展为艾滋病（ＡＩＤＳ），３７例６个月内ＣＤ４＋淋巴细胞降低至少２０％（ＣＤ４ｄｅｃｌｉｎｅ）。在１７２例对照和１８０例血清ＨＩＶ阳性受试者的比较中发现，其ＨＬＡ表型频率和单倍型频率没有显著差别，提示ＨＩＶ感染与ＨＬＡ无关联。然而，ＨＬＡ－Ｂ２１、ＨＬＡ－Ｂ８、ＨＬＡ－Ｂ３５表型及ＨＬＡ－Ａ１－Ｂ８、ＨＬＡ－Ｂ８－ＤＲ３、ＨＬＡ－Ａ１－Ｂ８－ＤＲ３单倍型与ＣＤ４阳性淋巴细胞下降，或与血清ＨＩＶ感染发展成ＡＩＤＳ病显著相关。１７例ＨＩＶ血清阴性高危人群中，无一携带单倍型ＨＬＡ－Ａ１－Ｂ８－ＤＲ３，提示该单倍型可能与ＨＩＶ感染的抗性相关。     

人类免疫缺陷病毒感染辅助因子的研究状况

人类免疫缺陷病毒（ＨＩＶ）进入感染细胞的过程一直是ＨＩＶ研究的焦点之一。最近，一种称为“融和素”的表面蛋白被发现，它的基因已被克隆。此蛋白被认为是ＨＩＶ－１感染ＣＤ４Ｔ淋巴细胞所必需的辅助因子。     

HIV/AIDS患者CD28在外周血CD4+、CD8+ T细胞上的表达变化

目的　研究国内HIV AIDS患者CD2 8在外周血CD4 + 、CD8+ T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 36例AIDS患者的外周血CD4 + 、CD8+ T淋巴细胞表面的CD2 8分子的表达 ,用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　CD4 + CD2 8+ T细胞的绝对计数与百分比、CD8+ CD2 8+T细胞的百分比均显示为正常对照组 >HIV感染组 >AIDS组 ;而CD8+ CD2 8+ T细胞的绝对计数显示HIV感染组和对照组显著大于AIDS组 ,HIV感染组与对照组间差异无显著性。CD4 + 、CD2 8+ CD4 + T淋巴细胞计数与血浆病毒载量显著负相关。结论　HIV AIDS患者外周血CD2 8在CD4 + 、CD8+ T淋巴细胞上表达随着病情进展而降低 ,反映了细胞免疫功能随着疾病进展损害逐渐加重 ,是判断病情进展的指标。     

Plasma viremia in human immunodeficiency virus infection

To determine which markers of human immunodeficiency virus type 1 (HIV) replication correlate most closely with progressive disease, we compared the following: (1) the frequency of isolation of HIV from peripheral-blood mononuclear cells (PBMC), (2) the frequency of isolation of the virus from cell-free plasma (plasma viremia), (3) the presence and titer of p24 antigen in plasma, and (4) the presence and titer of antibody to p24 antigen. We studied 213 persons who were positive for HIV antibody and 71 who were negative. HIV was isolated from PBMC from 207 of the 213 antibody-positive patients (97 percent), regardless of the clinical stage of the infection. Plasma viremia, in contrast, was correlated with the clinical stage of the infection. It was detected in 11 of 48 patients (23 percent) with asymptomatic infection, 32 of 71 (45 percent) in Class IVa of the Centers for Disease Control (those with AIDS-related complex), and 75 of 92 (82 percent) in Class IVc (those with AIDS) (P less than 0.01). Plasma HIV titers ranged from 10(0) to 10(4.3) and rose from a mean of 10(1.4) in asymptomatic patients to 10(2.5) in those with AIDS (P less than 0.02). Only 45 percent of patients with plasma viremia had HIV p24 antigen in either serum or plasma, and no correlation was found between the amount of p24 antigen in plasma and the plasma HIV titers. Follow-up tests indicated that plasma viremia was associated with a more marked decline in the CD4-lymphocyte cell count and the development of symptomatic disease (P = 0.034). We conclude that plasma viremia is a more sensitive virologic marker of the clinical stage of HIV infection and viral replication than the presence of p24 antigen or antibody in plasma. Not only whole blood but cell-free plasma from HIV-infected patients should be considered potentially infectious.     

In vitro anti-HIV-1 antibody production in subjects in different stages of HIV-1 infection.

We evaluated the in vitro antibody production from peripheral blood mononuclear cells (PBMC) against HIV-1 proteins in infected adults. Fifty-four HIV-1 infected patients (four recent seroconverters, 15 asymptomatics with a CD4 count higher than 500/microliters, 27 asymptomatics with a CD4 count between 200 and 500/microliters and eight symptomatic patients) were tested. PBMC were incubated in the presence or absence of 1% pokeweed mitogen (PWM) at 37 degrees C for 8 days. Western blot assay, p24 antigen ELISA and anti-p24 antibody ELISA were performed on serum and culture supernatants. Spontaneous production of anti-env antibody in culture supernatants was evidenced in all subjects. All the positive supernatants for anti-core antibodies (18/54) were derived from asymptomatic patients. PBMC from recent seroconverters and from symptomatic patients did not produce any anti-core antibody. Antibody production decreased after stimulation with PWM. The concentration of p24 antigen did not significantly increase in p24 positive supernatants following acidification (P = 0.1), suggesting that the inability to detect p24 antibody was not due to the anti-p24 antibody complexed to p24 antigen in culture supernatants. In vitro production of anti-p24 antibodies was significantly more frequent in asymptomatic subjects with high CD4+ cell counts (P = 0.02) and was absent in recent seroconverters. This last finding suggests that during the initial phases of the infection, anti-p24 antibody production may be restricted to cells residing in lymphoid organs. In addition, the lower percentage of anti-core antibody in people with low CD4+ cell counts is not merely a consequence of the binding of the antibody to an increased amount of antigen, but probably reflects an impaired production or a sequestration of producing cells in lymphoid tissue during the late stages of the infection.     

Estimated biological markers of progression in human immunodeficiency virus infection]

The biological markers for determining as early as possible the progression in the infection by the human immunodeficiency virus (HIV) are very important for the health care of patients, and to adapt their anti-retroviral treatment. Among those, four independent biological markers for predicting a pejorative evolution in the following 36 months are used in medical practice: two specific for HIV, p24 antigenemia and serum titre of antibodies to the p24 core antigen, and two non-HIV specific surrogate markers, the beta 2-microglobulinemia and the absolute number of CD4 T cell in blood. P24 antigenemia corresponds to an active retroviral in vivo replication. The cut off for detection is about 10 pg/ml. It is difficult to detect in black people, and in the asymptomatic or pauci-symptomatic stages of the disease. The apparition or the increase of the serum p24 antigen levels suggest the occurrence of opportunistic infections. P24 antigenemia decreases or disappears during the treatment by zidovudine. The diminution or the disappearance of serum antibodies directed to the p24 core protein are secondary to the deficiency of the humoral immunity, and to an increase of the viral replication, which occur at the late stage of the disease. The diminution or the disappearance of serum antibodies to p24 precede the occurrence of AIDS by several months. The increase of the serum beta 2-microglobulin level is associated with the severity of the disease. In the San Francisco prospective cohort, the progression to AIDS in 36 months was 69% when beta 2-microglobulinemia was more than 5 mg/l, 33% when it was between 3.1 to 5 mg/l, and 12% when it was less than 3 mg/l. The beta 2-microglobulin intra-thecal synthesis level could serve as a marker for the specific HIV encephalitis. The CD4 lymphocyte count constitutes an independent provisional marker for progression to AIDS, probably the most important, but mainly of statistical value. A lymphocyte count of 200 CD4/mm3 is considered as the threshold of full blown AIDS. Beside these classic biological markers, numerous other parameters have been evaluated, without knowing their practical interest. Although the predictive markers for AIDS have a real statistical significance, their interpretation could be difficult or hazardous when applied to a sole individual. In a relatively short delay, the actual biological markers will probably be completed or changed, in the routine medical practice, by the use of direct virological markers evaluating the viral load (plasmatic or cellular viremia).     

存放温度及时间对于HIV/AIDS患者外周血CD4+、CD8+细胞测定结果的影响

目的　研究HIV AIDS患者外周血CD4 、CD8 淋巴细胞数在不同条件下 (时间、温度和处理过程 )的变化。方法　选取HIV AIDS患者 34例 ,用流式细胞术检测在 4℃条件下放置不同时间(2、2 4、4 8、72h)的外周血CD4 、CD8 细胞数的变化 ,对经过处理的外周血 (处理过的血样 )CD4 、CD8 细胞数的变化进行比较 ;对室温条件下放置不同时间 (2、2 4、4 8、72h)处理过的血样CD4 、CD8 细胞数的变化进行比较。结果　在 4℃时 ,全血放置 2、2 4、4 8、72h的CD4 细胞计数差异无显著意义(P >0 0 5 ) ,而CD8 细胞数放置 72h时则差异有显著意义 (P <0 0 5 ) ;处理过的样品放置 72hCD4 细胞计数差异才有显著意义 (P <0 0 5 ) ,而CD8 细胞数在 2 4h时差异就有显著意义 (P <0 0 5 )。在室温时 ,处理过血样放置 2、2 4、4 8、72h的CD4 细胞计数差异无显著意义 (P >0 0 5 ) ,而CD8 细胞数在 4 8h则差异有显著意义 (P <0 0 5 )。结论　抗凝全血在 4℃放置 4 8h ,检测CD4 、CD8 淋巴细胞数 ,结果是可靠的。处理过血样在室温放置 2 4h ,检测CD4 、CD8 淋巴细胞数 ,结果是可靠的。 2 4～4 8h虽然CD4 淋巴细胞没有变化 ,但CD8 淋巴细胞却发生明显的变化 ,两者比例必然发生变化。     

Detection of TT virus in HIV-1 exposed but uninfected individuals and in HIV-1 infected patients and its influence on CD4+ lymphocytes and viral load

The TT virus (TTV) was detected for the first time in the serum of a patient with post-transfusion hepatitis of unknown origin. TTV was subsequently, also found in the serum of blood donors with no history of blood transfusion. In the present study, the percentage of TTV carriers among HIV-infected and noninfected patients was determined. The study was conducted to evaluate CD4 count and HIV viral load in 100 asymptomatic patients infected with HIV-1, 100 symptomatic patients with AIDS, 100 HIV-1 exposed but uninfected individuals and 100 normal healthy blood donors. In this work, the presence of TTV was investigated by nested-PCR. TTV was detected in 6% of normal donors, 12.5% of HIV-infected individuals and 21% of exposed individuals. The presence of TTV was statistically significant in the HIV-exposed individuals (21/100) compared with blood donors (6/100). Odds ratio = 4.16 (95%CI 1.60–10.83). No inter-group relations were found for CD4 and CD8 counts or HIV viral load. In the symptomatic group, patients with TTV presented minor viral load. This work demonstrated that TTV was detected in HIV-exposed individuals and no relation was verified for CD4, CD8 and viral load in the asymptomatic and symptomatic HIV patients.     

中国HIV-1感染者CD4+CD25+Foxp3+调节性T细胞与疾病进展相关性研究

目的对中国HIV-1感染者CD4~ CD25~ Foxp3~ 调节性T细胞水平及与疾病进展相关性进行研究,探讨CD4~ CD25~ Foxp3~ 调节性T细胞在HIV-1疾病进程中发挥的作用。方法选取35名HIV-1感染者及14名健康对照,应用流式细胞仪胞内染色技术在单细胞水平检测CD~ CD25~ Foxp3~ 调节性T细胞表达及淋巴细胞活化、凋亡水平。结果中国HIV-1感染者CD4~ CD25~ Foxp3~ T细胞水平与CD4~ T细胞显著负相关(r=-0.544,P=0.001),与病毒载量明显正相关(r=0.484,P= 0.026),与CD4~ T细胞凋亡(CD95表达)水平明显正相关(r=0.431,P=0.011)。艾滋病人CD4~ CD25~ Foxp3~ T细胞水平明显高于无症状HIV感染者(P<0.05),与健康人相比差异无统计学意义。艾滋病人CD4~ 、CD8~ T细胞凋亡水平明显高于无症状HIV感染者及健康人(P<0.05),艾滋病人及无症状HIV感染者CD4~ 、CD8~ T细胞活化明显高于健康人(P<0.05)。结论中国HIV-1感染者CD4~ CD25~ Foxp3~ 调节性T细胞水平与疾病进展明显相关。     

中国HIV-1病毒分离株的生物学特性与疾病进展关系的研究

目的　从HIV AIDS患者应用微量全血法分离中国HIV 1毒株 ,研究HIV 1的生物学特性与HIV AIDS疾病进展相关性。方法　建立微量全血法 ,从HIV AIDS全血标本中分离 17株HIV 1病毒分离株 ;检测这 17株病毒分离株嗜性和复制动力。结果　从 2 6例HIV AIDS病例中分离出HIV 1病毒 ,分离率为 6 5 .4 % (17 2 6 ) ,其中 17例HIV 1感染者的病毒分离率为 5 2 .9% (9 17) ,均为巨噬细胞嗜性 (M嗜性 ,NSI) ;9例AIDS患者的HIV 1病毒分离率为 88.9% (8 9) ,其中 7株为T细胞嗜性 (T嗜性 ,SI) ,1株为巨噬细胞嗜性。通过检测P2 4抗原确定 17株HIV 1病毒分离株的复制动力。在分离到的 17株HIV 1中 ,SI型病毒分离株与AIDS组显著相关 (P <0 .0 5 ) ;AIDS期的病毒分离株的复制动力明显高于HIV感染期 (P <0 .0 5 )。结论　微量全血法可用于病毒分离。 17株分离株的HIV 1复制动力与CD4 + T淋巴细胞计数呈线性负相关 ,与病毒载量呈正相关。     

Impact of inversion of the CD4/CD8 ratio on the natural history of HIV-1 infection

BACKGROUND: HIV-1 infection is characterized by an inverted CD4/CD8 T-cell ratio, but the distribution of inversions over time after seroconversion and whether delay of inversion is associated with a favorable prognosis are not known. METHODS: T-cell counts and clinical outcomes among men in the Multicenter AIDS Cohort Study who had incident HIV-1 infection before December 31, 1995 were analyzed by Kaplan-Meier and Cox proportional hazards methods. Results were also analyzed by time-dependent multivariate methods to adjust for CD4 lymphocyte counts, viral loads, age, race, and polymorphisms in host chemokine receptor genes (CCR5-Delta32 and CCR2-64I). RESULTS: Among 424 cases whose date of seroconversion was known to within +/-4.5 months, 317, 52, and 55 inverted their CD4/CD8 ratio within less than 1, 1 to 2, and more than 2 years of seroconversion, respectively. Longer time to inversion was significantly associated with longer time to AIDS, even after adjusting for CD4 lymphocyte count and viral load at the first seropositive visit and over the first 3 seropositive visits. Of the 6 seroconverters who had more than 500 CD4 lymphocytes 10 years after seroconversion without receiving highly active antiretroviral therapy, 5 took more than 2 years to invert their CD4/CD8 ratio. CONCLUSIONS: Time from HIV-1 seroconversion to inversion of the CD4/CD8 ratio independently predicted time to AIDS. Early measurements of the CD4/CD8 ratio until inversion occurs may identify people likely to become long-term nonprogressors or slow progressors, thus facilitating detailed studies of the mechanism of HIV-1 disease progression.