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

The purpose of the study was to examine how immune parameters related to non-major histocompatibility complex (MHC) restricted cytotoxicity changed with respect to progression and duration of human immunodeficiency virus (HIV) infection. Forty-one HIV seropositive subjects with a known time for seroconversion were included. The major finding was that a low percentage and number of natural killer (NK) cells were found in the group who had a rapid progression to acquired immune deficiency syndrome (AIDS) (less than 70 months following seroconversion) compared with those progressing more slowly to AIDS (more than 70 months following seroconversion). Furthermore, a significant correlation was found between the number of months from seroconversion to the diagnosis of AIDS and percentages of CD16+ cells (rs = 0.811, P < 0.01), CD56+ cells (rs = 0.647, P < 0.05), and CD16+CD56+ cells (rs = 0.839, P < 0.01) as well as the concentration of CD16+CD56+ cells in the blood (rs = 0.699, P < 0.05) No differences were found in percentages and concentrations of NK cell subsets between subjects with a long history (more than 6 years) versus a short history (less than 6 years) of HIV infection without AIDS. Furthermore, no negative correlations were found between the concentration of any NK subsets and the number of months since seroconversion in HIV seropositive individuals without AIDS. The total concentration of CD16+, CD56+, and CD16+CD56+ cells was lower in the group of HIV seropositive subjects compared with HIV seronegative subjects (age and sex matched), and the concentration of CD16+ cells was lower in those with AIDS than in those without AIDS. In conclusion, low concentration of NK cells in the blood was associated with a more rapid disease progression, indicating that defective non-MHC restricted cytotoxicity may be associated with HIV disease progression.
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PMID:Clinical progression of HIV infection: role of NK cells. 924 13

An interesting aspect of HIV disease is the immunoendocrine dialogue, via the hypothalamo-pituitary-adrenal axis, between glucocorticoids and cytokines and its potential role in HIV disease progression. This study reports recent data on the interaction between glucocorticoids and the immune system in AIDS patients with an acquired form of glucocorticoid resistance. Clinically, glucocorticoid-resistant AIDS patients (AIDS-GR; about 12% in our series of patients) present Addisonian symptoms (weakness, weight loss, hypotension, hyponatremia and intense mucocutaneous melanosis) in spite of elevated values of plasma cortisol and urinary free cortisol. Monocytes from these patients have a significantly lower receptor affinity (higher Kd) for glucocorticoids and a higher receptor density than other patients and controls. Such receptor alteration is associated with higher values of plasma interferon alpha (IFN alpha). In AIDS-GR there is a significant correlation between the values of receptor Kd and of plasma IFN alpha (r = 0.77). After poly(I):poly(C) stimulation, monocytes from AIDS-GR produce much more IFN alpha than other AIDS patients. While in patients with no resistance and in control patients, monocyte production of IFN alpha is inhibited by dexamethasone (the effect being reversed by RU-486), a very slight inhibition of dexamethasone on IFN alpha production is observed in monocytes from AIDS-GR. In conclusion, these data demonstrate that the immunosuppressive mechanisms acting in AIDS may be reversed, as shown by the increased stimulus on IFN alpha production found in cortisol-resistant patients. These data also suggest that antiglucocorticoid drugs may be helpful in HIV disease as they antagonize the excessive immunosuppression induced by the increased production of glucocorticoids found at every stage of HIV disease.
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PMID:Glucocorticoids and the immune system in AIDS. 926 43

Reports indicate that there is a dissociation between markers of HIV disease progression and clinical stage among subjects coinfected with human T-cell lymphotropic virus type I (HTLV-I) and HIV. HTLV-I coinfection does not appear to affect HIV viral load, currently considered to be the best marker of HIV disease progression. We measured HIV RNA levels in stored serum samples from 23 subjects with coinfection and 92 subjects with HIV single infection and examined the correlation with the CD4+ lymphocyte count. Subjects were recruited from an ongoing HIV cohort study in Rio de Janeiro, Brazil. In both groups, CD4+ lymphocyte counts declined with increasing levels of HIV RNA. In a linear regression analysis adjusting for HIV RNA serum level, coinfected individuals had an estimated 78% higher CD4+ lymphocyte count than those with single infection. Simultaneous adjustment for beta2-microglobulin level increased the difference, with coinfected individuals having 146% (p = 0.005, 95% CI: 32% to 359%) higher CD4+ counts. These data suggest that the higher CD4+ lymphocyte counts associated with coinfection do not provide immunologic benefit and may reflect HTLV-I-associated nonspecific lymphocyte proliferation. The results of this and other studies suggest that the CD4+ count cutoff values used in making clinical decisions in HIV infection may not be appropriate in coinfection. As with HIV single infection, HIV virus load may be the optimal surrogate marker for subjects with coinfection.
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PMID:HIV viral load and CD4+ lymphocyte counts in subjects coinfected with HTLV-I and HIV-1. 929 91

HIV-1-infected long-term nonprogressors are a heterogeneous group of individuals with regard to immunologic and virologic markers of HIV-1 disease. CC chemokine receptor 5 (CCR5) has recently been identified as an important coreceptor for HIV-1 entry into CD4+ T cells. A mutant allele of CCR5 confers a high degree of resistance to HIV-1 infection in homozygous individuals and partial protection against HIV disease progression in heterozygotes. The frequency of CCR5 heterozygotes is increased among HIV-1- infected long-term nonprogressors compared with progressors; however, the host defense mechanisms responsible for nonprogression in CCR5 heterozygotes are unknown. We hypothesized that nonprogressors who were heterozygous for the mutant CCR5 gene might define a subgroup of nonprogressors with higher CD4+ T cell counts and lower viral load compared with CCR5 wild-type nonprogressors. However, in a cohort of 33 HIV-1-infected long-term nonprogressors, those who were heterozygous for the mutant CCR5 gene were indistinguishable from CCR5 wild-type nonprogressors with regard to all measured immunologic and virologic parameters. Although epidemiologic data support a role for the mutant CCR5 allele in the determination of the state of long-term nonprogression in some HIV-1- infected individuals, it is not the only determinant. Furthermore, long-term nonprogressors with the wild-type CCR5 genotype are indistinguishable from heterozygotes from an immunologic and virologic standpoint.
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PMID:Heterozygosity for a defective gene for CC chemokine receptor 5 is not the sole determinant for the immunologic and virologic phenotype of HIV-infected long-term nonprogressors. 929 27

Cytotoxic T cells are believed to be an important immune response in HIV infection, both in the initial response to viraemia, and in controlling HIV replication and maintaining clinical stability. We report here the detailed findings in two vertically infected children, from the Edinburgh perinatal cohort. Both were clinically stable for the first 7 years of life. One had vigorous HIV-specific cytotoxic T lymphocyte (CTL) responses, and non-lytic suppression, measured in vitro, while the second had no CTL activity against HIV. Despite her HIV-specific immunity, the first child had a declining CD4 count, and a high and fluctuating viral load, whereas the second child maintained a stable CD4 count, a low viral load and had a virus which could not be cultured in peripheral blood mononuclear cells (PBMC) in vitro. The first child subsequently progressed to AIDS and has now died, while the second remains clinically well. More detailed investigations showed the clinically stable child to be heterozygous for the CCR5 receptor, and to be HLA-B49--both of which markers have been associated with slow HIV disease progression. These findings question the role of CTL in maintaining stable HIV disease, and stress the need for immunological investigations to be considered in the light of the genetic make-up of the patient. They may also reflect a different immunopathogenesis of HIV disease in children compared with adults.
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PMID:In vitro measurement of cytotoxic T cell activity does not predict clinical progression in paediatric HIV disease--two case studies. 935 43

In a previous investigation, we demonstrated that certain human leukocyte antigens (HLA) may be associated with human immunodeficiency virus type I (HIV-1) infection or protection from infection among regional African Americans and Caucasians. We demonstrated that HLA-DQB1*0605 was associated with a possible increased risk of susceptibility to infection in African Americans and that DQB1*0602 was associated with a possible increased risk of infection in Caucasians. The present study was designed to demonstrate possible HLA associations with HIV-1 disease progression and AIDS in regional African American and Caucasian populations. To differentiate rapid from slow progressors, immune parameters of the HIV-1-positive patient population were monitored over a mean follow-up period of 23 +/- 2 months for African Americans (n = 30) and 25 +/- 5 months for Caucasians (n = 22). To determine significance, HLA allele frequencies among rapid progressors were compared to those of slow progressors, separated by race. Results were analyzed by chi 2 analysis, with Fisher's exact test where applicable, linear logistic regression and Kaplan-Meier survival analysis. In the HIV-1-positive African American group, a better prognosis was associated with HLA-DQB1*0602. In the HIV-1-positive Caucasian group, HLA-DQB1*0302 was associated with rapid HIV disease progression, but no marker was associated with a more favorable prognosis.
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PMID:HLA-DQB1 markers associated with human immunodeficiency virus type I disease progression. 939 45

HIV disease progression and the effect of replacement therapy with clotting factor concentrates (CFCs) were studied in 100 Swedish haemophiliacs, mean age at seroconversion 29 years (range, 4-72). On average 16 years after seroconversion, 67 per cent of the patients had CD4+ cell counts of < 200 x 10(6)/l, 50 per cent had developed AIDS, and 58 per cent had died. HIV disease progression was significantly slower in those aged less than 28 (median age) at seroconversion (P = 0.004). Moreover, mortality was inversely correlated to total annual CFC consumption after adjustment for age and HIV-related therapy, i.e., Pneumocystis carinii prophylaxis and antiretroviral drugs (P = 0.014), but unrelated to the purity of the CFCs used. After adjustment for age, annual CFC consumption and HIV-therapy, prophylactic replacement therapy was not associated with significantly better survival than on-demand treatment. It is concluded that in HIV-positive haemophiliacs replacement therapy may have a beneficial effect on the immune system, and that CFC purity and the regimen (prophylaxis vs on-demand) would seem to be factors of minor importance.
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PMID:[Hemophiliacs with HIV. Slower progression of the infection among younger patients and at higher dosages of factor concentrates]. 945 46

Selenium deficiency has been demonstrated to be a significant predictor of HIV-related mortality, independent of CD4 over time, CD4 < 200 at baseline, and antiretroviral treatment. Although selenium deficiency in healthy humans is relatively rare (Cohen et al. 1989, Lockitch, 1989), a number of studies have documented a decline in plasma selenium levels and decreased glutathione peroxidase activity in individuals with HIV/AIDS (Dworkin et al. 1988, Cirelli et al. 1991, Mantero-Atienza et al. 1991, Staal et al. 1992, Allavena et al. 1995). These findings are of particular concern in light of selenium's influence on immune function, viral replication, and survival. As recent investigations (Delmas-Beauvieux et al. 1996) indicate that supplementation with selenium may help to increase the enzymatic defense systems in HIV-infected patients, further studies to determine possible mechanisms and clinical trials to evaluate the effect of selenium supplementation on HIV disease progression are essential.
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PMID:Micronutrient status in relationship to mortality in HIV-1 disease. 948 Nov 35

To determine whether Epstein-Barr virus (EBV) constitutes a contributing factor in AIDS and, conversely, whether the human immunodeficiency virus (HIV) alters the course of primary EBV infection in a pediatric population, 62 children born to HIV-infected mothers and prospectively followed were evaluated. EBV infection was documented by EBV-specific serology and polymerase chain reaction and by clinical history. HIV infection status was determined according to the Centers for Disease Control and Prevention pediatric classification system. Demographics from HIV-infected and HIV-uninfected children were comparable. The data suggest that HIV-infected children may acquire primary EBV infection earlier in life. The incidence of accompanying splenomegaly or hepatomegaly (or both) around the time of EBV seroconversion was higher among HIV-infected children than among HIV-uninfected children. In contrast, HIV disease progression and HIV-1 RNA load did not seem to be influenced by primary EBV infection.
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PMID:Natural history of Epstein-Barr virus infection in a prospective pediatric cohort born to human immunodeficiency virus-infected mothers. 953 89

A 25-year old woman with rapid HIV disease progression had been receiving zidovudine (ZDV) for two years, when she became pregnant. She had a high viral load and carried out zidovudine-resistant viral strains. For these reasons, and with the main objective to maximally reduce viremia, the association of DDI to ZDV was introduced a few weeks before delivery. The virological follow-up for one year has confirmed the lack of HIV infection in the child. Combined antiretroviral therapy during the last weeks of pregnancy might be considered for the prevention of vertical transmission of HIV in cases of high risk of newborn infection, without adding relevant toxicity.
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PMID:[Combined antiretroviral therapy for prevention of vertical HIV-1 transmission]. 956 23


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