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Query: UMLS:C0019693 (HIV)
 170,526 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In this report we have highlighted only a few examples of the extensive efforts underway to better understand the process of HIV pathogenesis, to develop new therapeutic agents to inhibit virus replication, and to identify strategies to restore damage done to the immune system during HIV disease progression. It is expected that progress in these areas will continue to advance, and that development of more effective therapies will lead to comprehensive multifaceted, multipronged treatment regimens.
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PMID:Conference summary: novel HIV therapies--from discovery to clinical proof of concept. 879 70

A follow-up study was carried out to evaluate the prognostic value of hairy leukoplakia (HL) and oral candidosis (OC) in a cohort of 111 asymptomatic Mexican HIV infected patients. Oral exams were performed at baseline and every 6 months, from September 1989 to March 1994. Chi-square contingency table test, the Kruskall-Wallis one-way analysis of variance, the Kaplan-Meier product-limit method and the log rank test were used for the analysis. Univariate and multivariate Cox's proportional hazards analysis were also performed. Fifty-four patients (51%) progressed to AIDS (initially 36 CDC-II and 18 CDC-III). Individuals with HL and/or OC, showed faster development to AIDS than subjects without lesions or other HIV-related manifestations (P = 0.008). The presence of OC, HL or both always remained significant despite adjustment for total lymphocytes, CDC stage, zidovudine therapy or its combinations. Oral lesions in HIV infection may be regarded with other clinical and laboratory studies as markers of HIV disease progression and as indicators to begin antiretroviral treatment.
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PMID:Prognostic value of oral candidosis and hairy leukoplakia in 111 Mexican HIV-infected patients. 883 16

Macrophage activation and tumor necrosis factor-alpha (TNF-alpha) production are critical in tuberculosis immunity but may result in increased human immunodeficiency virus (HIV) expression and accelerated HIV disease progression in HIV-infected persons. Pentoxifylline inhibits expression of TNF-alpha and HIV. A double-blind, placebo-controlled study of adjunctive therapy with pentoxifylline (1800 mg/day) as a timed-release formulation was done in Ugandan HIV-infected patients with pulmonary tuberculosis. Subjects had early HIV disease (mean CD4 cell count, 380/microL) and did not receive other antiretroviral drugs. Pentoxifylline resulted in decreased plasma HIV RNA and serum beta 2-microglobulin and, in a subset of moderately anemic patients, improved blood hemoglobin levels. Trends were noted toward reduced TNF-alpha production in vitro and improved performance scores, but these did not reach statistical significance. No effect was noted on body mass, CD4 cell count, or survival. Additional studies of more potent TNF-alpha inhibitors in HIV-positive subjects with tuberculosis are warranted.
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PMID:Pentoxifylline therapy in human immunodeficiency virus-seropositive persons with tuberculosis: a randomized, controlled trial. 884 9

IL-2 administration in vivo has been shown to increase CD4+ T cell counts in HIV+ patients. We have previously reported that PBMC from HIV-infected patients undergo marked spontaneous apoptosis in vitro. In this study, we examined the effect of IL-2 added in vitro upon culture-induced apoptosis in PBMC from 80 HIV-infected patients by flow cytometry. IL-2 at concentrations of > or = 10 U/ml significantly reduced spontaneous apoptosis in CD3+ T lymphocytes in patients but not in healthy volunteers. Interestingly, we observed that Bcl-2 expression in patient lymphocytes decreased rapidly upon in vitro culture while that in cells of healthy volunteers was relatively unaffected. The most significant decrease in Bcl-2 expression was noted in the apoptotic cell population. The IL-2-mediated reduction in lymphocyte apoptosis was found to be associated with the blocking of this culture-induced down-modulation of Bcl-2 expression. IL-2 did not induce significant expansion of lymphocytes during the culture period nor did it affect Fas Ag expression in patient cells, which were already expressing Fas maximally. These findings strongly suggest that IL-2 mediates its apoptosis-blocking effects via suppressing down-modulation of Bcl-2. Our findings also provide an experimental basis for the ongoing therapies utilizing this cytokine for slowing HIV disease progression.
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PMID:IL-2 rescues in vitro lymphocyte apoptosis in patients with HIV infection: correlation with its ability to block culture-induced down-modulation of Bcl-2. 889 56

The association between stressful life events, psychiatric symptoms, coping, and social support and HIV disease progression one year later were studied in 51 HIV-infected asymptomatic and early symptomatic homosexual men. Dependent variables were CD4 counts and clinical progression. No associations between the psychosocial parameters and CD4 counts were found. Active confrontation with HIV infection as a coping strategy was predictive of decreased clinical progression at one year follow-up, after taking into account baseline biomedical and behavioral variables. These results show that active coping strategies may have an effect on disease progression, possibly mediated by greater compliance with medical treatments or by psychoneuroimmunological mechanisms.
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PMID:Active confrontational coping predicts decreased clinical progression over a one-year period in HIV-infected homosexual men. 892 5

Human T-cell lymphotropic virus (HTLV) types I and II were the first discovered human retroviruses. While HTLV-I has been clearly associated with disease, the health implications of HTLV-II infection are still unsettled. A prospective epidemiological study of 409 HIV-infected subjects of different transmission categories was performed to study the presence of HTLV-II antibodies, and whether HTLV-II antibodies are associated with the progression to AIDS and to death of any cause. Of 409 subjects, 30 (7.3%) were HTLV-II positive at study entry; 2 subjects seroconverted during follow-up. In the HTLV-II-positive group 2 were heterosexually HIV infected, 28 (of whom 2 were seroconverters) were IDUs and 2 were homosexual men. When controlling for transmission category, gender, age and CD4+ lymphocyte count at study entry, the relative risk of AIDS progression for the HTLV-II-positive group was 2.1 (0.8-5.1, 95% confidence interval (CI)) as compared to the HTLV-II-negative group. The adjusted relative risk of dying was 2.1 (1.0-4.3, 95% CI). When studying IDUs separately, the adjusted relative risk of AIDS progression was 2.3 (0.8-6.9, 95% CI) and the relative risk of dying was 2.0 (0.9-4.6, 95% CI). The results of this study suggest that HTLV-II is a cofactor in HIV disease progression. The number of HTLV-II-infected subjects, was, however, small, and insufficient control of confounding factors must be taken into consideration.
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PMID:Co-infection with HIV-1/HTLV-II and the risk of progression to AIDS and death. The Oslo HIV Cohort Study Group. 897 91

Optimal stimulation and prevention of anergy in T cells requires signaling through the CD28 molecule. During HIV disease progression, CD28 expression is lost, particularly on CD8+ T cells. Because alterations in cytokine production patterns occur during HIV infection, we determined whether CD8+ T cell phenotype or function was affected by cytokine environment. Treatment of CD8+ T cells with IL-4 decreased levels of both CD28 surface expression and message and increased CD8 expression. Furthermore, CD8+ T cells that had down-regulated CD28 had reduced proliferative capacity. The inhibitory effects of CD28 reduction could be compensated either by increased anti-CD3 or by exogenous IL-2, suggesting that the strength of T cell signaling necessary for the production of IL-2 and subsequent proliferation is negatively regulated by IL-4. CD8+ subpopulations with differential CD28 expression produced different patterns of cytokines, particularly IL-2 and IFN-gamma. Furthermore, CD8+ T cells that had reduced CD28 levels but made their own IL-2 were able to proliferate in response to TCR stimulation. These results suggest that loss of CD28 expression and CD8 T cell function can be regulated by the cytokine environment, which may be altered during HIV disease progression. Whether the dysfunction of CD8+ T cells in HIV infection occurs by such a mechanism is the subject of future investigation.
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PMID:Regulation of CD28 costimulation in human CD8+ T cells. 902 89

To investigate the possible role of Cryptococcus neoformans var. neoformans in HIV disease progression, and to identify the responsible cryptococcal components, an in vitro cell culture model was set up to study the C. neoformans-induced enhancement of HIV replication in HIV-1-infected PBMC. Similar to whole C. neoformans, cell-wall membrane fraction and mannoproteins induced proliferation of PBMC and enhancement of lymphotropic HIV replication in HIV-infected PBMC, while galactoxylomannan did not. MoAbs capable of interfering with MHC class II-mediated antigen presentation prevented the induction of cell proliferation by whole C. neoformans or cryptococcal mannoproteins. MoAb binding to adhesion molecules intercellular adhesion molecule-1 (ICAM-1) and lymphocyte function-associated antigen-1 (LFA-1) also inhibited C. neoformans-induced cell proliferation. In addition, anti-MHC class II MoAb inhibited the enhancement of HIV replication by C. neoformans. The results suggest that: (i) C. neoformans may accelerate HIV disease progression by stimulation of HIV replication through MHC class II-mediated antigen presentation; and (ii) cryptococcal mannoprotein may be one of the responsible components. The ability to enhance HIV replication in PBMC in vitro is not unique for C. neoformans. However, this is the first report to study in detail a yeast-induced enhancement of HIV replication in PBMC.
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PMID:Mannoproteins of Cryptococcus neoformans induce proliferative response in human peripheral blood mononuclear cells (PBMC) and enhance HIV-1 replication. 903 Aug 66

A case-control, prospective, open-label, clinical trial to evaluate efficacy and safety of a combined zidovudine/Thymus Humoral Factor Gamma-2 (THF) therapy in HIV-infected subjects was conducted in 13 patients. Twenty-six patients were included as controls receiving only zidovudine. The two groups of patients were matched according to sex, age, CDC stage of HIV infection, number of CD4+ T cells and type of previous opportunistic infections (if any) and all patients and controls were naive for antiretroviral therapy at the moment they entered the trial. The observation period was protracted up to 47 months (mean 28 +/- 13 months). No significant difference was observed between the two groups as far as surrogate markers of HIV disease progression are concerned. However, patients receiving zidovudine and THF showed a lower number of opportunistic complications. Only one patient in this group progressed to manifest AIDS while 9 of 18 controls presented disease progression. Four patients died in the case group, all of them were CDC stage IV at admission, and 15 of 26 died in the control group (all CDC stage IV at admission, and four patients who presented disease progression during the study period). Survival time was increased in the case group. The exact immunological effect of thymus hormones in HIV infection has still to be elucidated, but a possible therapeutic role of these agents is foreseeable.
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PMID:Zidovudine and thymus humoral factor gamma-2 in the treatment of HIV infection: preliminary clinical experience. 903 36

Therapeutic observations suggest that azidothymidine (AZT)-resistant HIV+/AIDS patients are frequently offered AZT/dideoxycytidine (DDC) or dideoxyinosine (DDI) therapy. The latter therapies have been associated with the development of acute pancreatitis. During the initial portion of this study, when patients reported limiting ethanol consumption, an increase in CD4+, a decrease in amylase, and a decrease in lipase was observed in patients on DDI monotherapy. Marinol/marijuana usage was associated with depressed CD4+ counts and elevated amylase levels within the DDI subgroup. The purpose of this study was to follow these patients over 1 year and compare clinical indicators of pancreatitis and HIV progression. After 1 year, the remaining 56 patients were reexamined in the follow-up portion for clinical indicators of HIV disease progression and pancreatoxic/hepatotoxic effects. Those in the AZT group, who remained on this therapy throughout the year, had significantly increased amylase values from 55.3 to 69.3 IU/liter (p < 0.05). In the AZT/DDC group, those who remained on combination therapy throughout the year, 4 of the 5 clinical indicators of disease progression changed. Amylase, ALT, and AST all increased significantly from 55.2 to 77.8 IU/liter (p < 0.01), from 38.0 to 92.3 IU/liter (p < 0.05), and from 55.2 to 97.0 IU/liter (p < 0.05), respectively. Lipase levels decreased significantly (106.0 to 74.6 IU/liter, p < 0.05). The most remarkable changes occurred in the AZT/DDC group (who reduced ethanol consumption), wherein clinical indicators of pancreatitis and liver dysfunction declined, including amylase (65.0 to 20.0 IU/liter, p < 0.05), ALT (350.0 to 100.0 IU/liter, p < 0.01), and AST (240.0 to 95.0 IU/liter, p < 0.01). No significant changes were noted in the DDI or AZT groups. Marinol/marijuana use was associated with declining health status in both the AZT and AZT/DDC groups. In contrast, all clinical indicators of pancreatitis improved in the DDI patients who utilized Marinol/marijuana, including amylase (-34%), lipase (-30.8%), ALT (-21.4%), and AST (-20.1%). This paired follow-up study suggests that HIV+/AIDS patients on antiretroviral therapies should restrict their ethanol consumption. In HIV+/AIDS patients with the lowest CD4+ counts (those on DDI monotherapy), utilization of Marinol/marijuana does not seem to have a deleterious impact.
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PMID:The impact of ethanol and Marinol/marijuana usage on HIV+/AIDS patients undergoing azidothymidine, azidothymidine/dideoxycytidine, or dideoxyinosine therapy. 904 84


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