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

The progression of infection with human immunodeficiency virus, type 1 (HIV-1), is associated with a loss of helper T cell function, but the mechanism for this loss (e.g., decreased absolute number of helper cells, altered function of helper cells, or both) has not been delineated. Many studies have suggested that T-cell production of and/or responsiveness to the T cell growth factor interleukin-2 (IL-2) declines over the course of HIV-1 infection. Using a highly quantitative 6-day limiting dilution assay (LDA), we investigated whether the number and the proliferative capacity of circulating IL-2 responsive cells in patients with AIDS differ from those in patients in earlier stages of HIV-1 infection (asymptomatic or AIDS-related complex) and healthy seronegative individuals. The frequency of IL-2 responsive cells declined progressively in asymptomatic seropositive subjects, those with ARC, and those with AIDS. In contrast, the proliferative capacity of individual IL-2 responsive cells, as reflected by the magnitude of thymidine uptake per precursor, was reduced only in patients with frank AIDS and was normal in asymptomatic subjects and in those with ARC. These results suggest that the development of AIDS in the setting of HIV-1 infection may reflect a combination of qualitative as well as quantitative changes in lymphocyte function. They also suggest that analysis of lymphocyte responsiveness to IL-2 may provide a useful approach to prediction of the development of AIDS in individuals infected with HIV-1.
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PMID:Limiting dilution analysis of in vivo-activated (IL-2 responsive) peripheral blood lymphocytes in HIV-1-infected subjects. 278 65

A study of the immunopathogenic characteristics of HIV infection was begun in 1984 at the National Reference Center on Clinical Immunology (CNRIC) in Caracas, Venezuela, on 240 individuals with a variety of clinical manifestations. The most important findings were depletion of the CD4 cells in HIV-infected individuals, including asymptomatic carriers; significant reduction of the CD3-, CD16+ large granular lymphocytes (LGL) in AIDS cases; decrease in LGL cytotoxic activity in infected persons versus controls, along with increased lytic function induced by stimulation with recombinant interleukin-2 in both groups; and reduction of the CD4 population in AIDS patients, independent of the presence or absence of free serum antigen. Such research is helping to clarify the immunopathogenic mechanisms of HIV and possible geographic and demographic variations.
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PMID:Immunopathogenic aspects of infection by the human immunodeficiency virus in Venezuela. 278 32

The human immunodeficiency virus (HIV) may interact with the Epstein Barr virus (EBV) indirectly by effects on the T4 lymphocyte or directly by effects on EBV transformed B lymphocytes. We have confirmed the susceptibility of EBV transformed B lymphocytes to productive HIV infection, and have evaluated the cytotoxic activity of HIV seronegative and seropositive donors after sensitization by their autologous EBV infected (monoinfected) or EBV and HIV infected (coinfected) transformed cell lines in a 51Cr release cytotoxicity assay. When sensitized by the coinfected cell line and assayed against monoinfected and coinfected cell lines, the cytotoxic activity of the seronegative donors was inhibited when compared to the cytotoxic effectors sensitized by the monoinfected B cell line. The inhibition appeared to be unrelated to direct HIV infection of the T4 effector cells and was reversible by addition of recombinant interleukin-2. Although deficient in their EBV cytotoxic activity in comparison to the seronegative donors, the HIV seropositive donors lysed the coinfected cell line better than the monoinfected cell line, whether or not HIV superinfected cells were used during the sensitization phase. In HIV seronegative donors, HIV may inhibit the immune response to EBV transformed B lymphocytes. This inhibition is not observed in HIV seropositive donors. These studies suggest the development of cytolytic effector mechanisms directed at HIV infected cells during HIV infection.
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PMID:Effects of human immunodeficiency virus (HIV) on the cytotoxic response to Epstein Barr virus (EBV) transformed B lymphocytes. 282 51

The addition of both live and ultraviolet-inactivated preparations of human T lymphotropic virus type I (HTLV-I) and HIV to cultures of human peripheral lymphocytes impeded the ability of these cells to respond to phytohaemagglutinin (PHA). This inhibition depended on the concentration of the virus and seemed due, in part at least, to interference with the generation of interleukin-2 (IL-2) activity in the PHA-stimulated cultures. However, the addition of exogenous IL-2 did not effectively restore the lymphocyte proliferative responsiveness of cells which had been co-incubated with these human retroviruses. Exposure to the viruses did not affect expression on co-incubated cells of the Tac antigen, an epitope of the IL-2 receptor, as determined by an indirect immunofluorescence assay. These results suggest that one mechanism through which human retroviruses may be able to impede cellular proliferative responsiveness is interference with the ability of target cells to respond to IL-2, even though IL-2 receptors continue to be expressed under the conditions tested.
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PMID:Inhibition of human lymphocyte mitogenesis by human and other retroviruses. Differential effect of interleukin-2 in restoration of responsiveness. 283 64

The binding of antigen or monoclonal antibody to the T cell receptor for antigen or the closely associated CD3 complex causes increases in the concentration of intracellular ionized calcium and subsequent cell proliferation. By measuring second messenger production in primary cultures of human immunodeficiency virus (HIV-1)--infected T cells stimulated with monoclonal antibodies specific for either CD3 or CD2, a specific impairment of membrane signaling was revealed. The HIV-1--infected T cells were unable to mobilize Ca2+ after stimulation with anti-CD3, whereas CD2-induced calcium mobilization remained intact. Furthermore, the HIV-1--infected cells proliferated poorly after CD3 stimulation, although the cells retained normal DNA synthesis in response to interleukin-2 stimulation. These results show that the signals initiated by CD2 and CD3 can be regulated independently within the same T cell; uncoupling of signal transduction after antigen-specific stimulation provides a biochemical mechanism to explain, in part, the profound immunodeficiency of patients with HIV-1 infection.
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PMID:HIV-1-infected T cells show a selective signaling defect after perturbation of CD3/antigen receptor. 289 8

The effect of cyclosporine A (CyA) on the ability of the human immunodeficiency virus type 1 (HIV-1) to infect the H-9 T-cell leukemic line, as well as interleukin-2 (IL-2)-grown human peripheral blood-derived lymphocytes, has been studied. Pretreatment of H-9 cells and human lymphocytes with CyA over 24 hours completely prevented viral infection over a 21-day period, whereas the addition of drug at two hours postinfection with HIV-1 had a significant inhibitory effect on viral replication and expression of the virus-specific antigens p17 and p24. However, if CyA was added at later times to these lymphocytic cells, this inhibitory effect was lost. Indeed, the removal of CyA from cultures that had been treated from two hours after infection led to the rapid production of progeny virus. HIV-1 was able to infect peripheral blood lymphocytes obtained from each of four kidney allograft recipients on long-term CyA antirejection therapy, as long as drug was not included in the culture medium. In addition, we asked what effect pretreatment with CyA of cells of the U-937 monocytic line and primary cultures of human monocytes/macrophages might have on infection by HIV-1. CyA had no demonstrable effect on the ability of HIV-1 to infect cells of either type.
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PMID:The effect of cyclosporine A on infection of susceptible cells by human immunodeficiency virus type 1. 290 90

Mononuclear leukocytes from human immunodeficiency virus (HIV)-seronegative and -seropositive homosexual men lysed HIV-infected U937 cells to a significantly greater degree than uninfected U937 cells. Depletion of cell subsets with monoclonal antibodies and complement indicated that the effector cells were primarily of the CD16+ phenotype. Acid-stable alpha interferon (IFN-alpha) production induced by the HIV-infected cells correlated with, although was not an absolute requisite for, preferential lysis of the infected targets. The activity of these CD16+, natural killer (NK) cells decreased in relation to the duration of HIV infection and the presence of acquired immunodeficiency syndrome. Pretreatment of peripheral blood mononuclear cells from HIV-seronegative subjects, but not HIV-seropositive men, with IFN-alpha or recombinant interleukin-2 enhanced lysis of both uninfected and HIV-infected U937 cells. These results suggest that IFN-alpha-associated, NK-like mechanisms are active in the cytotoxic response against HIV-infected cells and that HIV infection results in an early and progressive depression of such responses. Prospective investigations may be useful in determining the role of this NK cell response in the natural history and pathogenesis of HIV infection and the efficacy of therapeutic modalities.
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PMID:Association of alpha interferon production with natural killer cell lysis of U937 cells infected with human immunodeficiency virus. 291 35

The phenotype and functions of T lymphocytes and of natural killer (NK) cells have been investigated in four children and five adults from three Italian families infected with HIV (LAV/HTLV III). The results show a heterogeneous pattern of immunological derangements involving distribution of T and natural killer subsets, proliferation in response to T cell mitogens and natural killer activity. However, all infected patients tested showed a very low or absent phytohaemagglutinin induced interleukin-2 production regardless of age and clinical conditions, while concanavalin A-induced interleukin-2 production was within the normal range. The impaired interleukin-2 production in response to phytohaemagglutinin in some patients is not related to phytohaemagglutinin-induced proliferation, to clinical conditions or to a defective distribution of T cell subsets. These results suggest that, in our patients, both adults and children, HIV (LAV/HTLV III) has an "early" tropism for a subset of T cells involved in interleukin-2 production.
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PMID:Acquired immune deficiency syndrome in childhood: impaired production of interleukin-2 by HIV (LAV/HTLV III) infected patients. 295 15

Enkephalins have been shown to enhance T cell-mediated immune responses and natural killer-cell activity in vitro. We have studied the effects of infusions of methionine-enkephalin on immune functions and clinical courses in seven patients with various stages of infection with human immunodeficiency virus (HIV). All patients were clinically stable at the time of entry into the study. Each received 10 micrograms/kg of methionine-enkephalin in an intravenous infusion three times weekly for up to 12 weeks. Evaluation of cellular immunity (T-cell subsets, in vitro interleukin-2 production and interleukin-2 receptor expression, T-cell responses to mitogens and antigens, and delayed-hypersensitivity skin tests) as well as clinical and toxicity monitoring was performed prior to treatment, at 2-week intervals during treatment, and after the cessation of treatment. Increases in interleukin-2 receptor expression were seen on lymphocytes collected on one occasion from each of two patients 30 min postinfusion. Studies done 24 hr after infusions revealed increases in interleukin-2 production in one patient, but when pre- and posttreatment values were compared there were no significant changes in numbers of circulating T cells of any phenotype or in T-cell responses to mitogens or antigens. None of the patients with Kaposi's sarcoma had regression of tumor; one patient dropped out of the study at week 5 because of deteriorating clinical status and progression of tumor. There were no adverse reactions or evidence of toxicity. We conclude that methionine-enkephalin appears to enhance temporarily selected immune responses in patients with HIV infection, however, in the schedule used in this study it was not clinically efficacious.
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PMID:Methionine-enkephalin as immunomodulator therapy in human immunodeficiency virus infections: clinical and immunological effects. 296 9

To investigate if serial measurement of T helper (CD4) lymphocyte number in peripheral blood is of prognostic value, we determined lymphocyte function in asymptomatic and symptomatic HIV antibody positive and negative homosexual males and related the results to absolute number of CD4 lymphocytes in peripheral blood. Lymphocyte function was determined by measuring streptolysin O (SLO)-induced proliferative responses of peripheral blood lymphocytes (PBL) and of PBL depleted of CD8 lymphocytes. Phytohemagglutinin (PHA) induced interleukin-2 (IL-2) production was also measured. In all functional tests values were significantly lower in HIV antibody-positive subjects than in HIV antibody-negative subjects. Results lower than the 95% confidence limit in HIV antibody-negative individuals were therefore defined as "decreased." Decreased functional responses were most frequent (83-100%) in individuals with a number of CD4 lymphocytes of less than 400/microliters, and were least frequent (3-21%) in subjects with a CD4 lymphocyte count of greater than 600/microliters. Frequency of decreased functional responses was intermediate in the population with 600-400/microliters CD4 lymphocytes. The magnitude of functional responses differed significantly between groups with less than 400, 400-600, and greater than 600 CD4 lymphocytes per microliter, indicating that T helper cell number decreases with loss of immune function.
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PMID:Analysis of absolute T helper cell number and cellular immune defects in HIV antibody positive and negative homosexual men. 297 9


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