Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019693 (HIV)
 170,526 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study evaluates genetic influence on susceptibility to perinatal HIV-1 infection among 106 Black infants from New York and San Francisco born to mothers infected with HIV-1. Genes tested by molecular techniques are HLA class II loci DRB1, DPB1 and DQA1; HLA class III loci complement C4A and C4B; alpha and beta interferons; and the constant region of the T-cell receptor beta chain. Of the 106 infants analysed, 54 are infected with HIV and 52 remain uninfected at age 15 months and older. Genotypes in the HLA region appear to influence risk of HIV infection. Specifically, infants with the amino acid sequence -asp-glu-ala-val- at DPB1 positions #84-87 are more likely to be infected (P = 0.001) and infants with the allele DQA1*0102 are less likely to be infected (P = 0.031). Combinations of these two risk factors show a strong dose response (P = 0.0005). HLA DPB1 and DQA1 may play a direct role in immune response associated with HIV-1 infection, or the critical region may be located between these two genes. Characterisation of other class II HLA genes in these infants will allow more precise determination of the role of HLA loci in susceptibility to HIV-1 infection.
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PMID:Genetic risk factors for perinatally acquired HIV-1 infection. 158 23

Depending on the cell line used for virus propagation, human immunodeficiency virus (HIV) particles may possess class II MHC proteins, as demonstrated by FACS analysis. HLA-DR appeared in high amounts at the HIV envelope, if the virus was grown in HLA-DR+ cells, but was absent if the virus had been grown in HLA-DR- cells. No other cellular constituents, including HLA-DQ and HLA-DP, were detected in these virions. The presence of HLA-DR in the virion envelope itself in preparations used for diagnostic purposes may explain some of the false-positive results obtained in earlier serological tests for HIV infection. Possible implications of these virus-associated cellular antigens in the immunopathogenesis of AIDS should be considered.
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PMID:Presence of class II histocompatibility DR proteins on the envelope of human immunodeficiency virus demonstrated by FACS analysis. 160 22

Immunization of AIDS/ARC patients with autologous cells expressing HIV antigens, although providing clinical and biological benefits, fails to restore cellular immunity. The latter result is due partly to the antiproliferative effect of HIV-1 on activated T-cells (immune suppression), which leads to blockade of specific immune reactions. To overcome immune suppression, a new vaccine strategy was designed consisting of an immunization against HIV-1 combined with components of the T-cell-suppressive (antiproliferative) network. This new vaccine treatment proved to be innocuous in mice, monkeys, and two non-HIV-infected humans. A Phase I clinical trial was performed in six patients previously under cellular immunotherapy and still presenting a cellular immune defect. Preliminary results confirmed, after a 1-year follow-up of the patients, the safety of the new vaccine, which also partially restored the cellular immune response, including anti-HIV HLA-restricted cell-mediated cytotoxicity, delayed hypersensitivity to recall antigens, and proliferation of T-cells specifically activated by recall antigens.
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PMID:One-year follow-up of vaccine therapy in HIV-infected immune-deficient individuals: a new strategy. 161 65

Non-Hodgkin's lymphomas (NHL) are part of the spectrum of disease associated with HIV infection. However, there are only occasional reports of NHL of T-cell origin in HIV-infected patients. A previously asymptomatic HIV-infected man, who was seronegative for human T-lymphotropic virus type I antibodies, developed a high-grade peripheral T-cell lymphoma of anaplastic large-cell type which was Ki-1 + (CD30 +), HLA-DR+, epithelial membrane antigen +, CD25 +, CD71 +, CD2 + and CD5 +. Pan-B markers CD19 and CD22 and histiocytic marker CD68 were negative. At diagnosis the patient had 0.3 x 10(9)/l T-helper lymphocytes. The response to chemotherapy was dramatic and the patient is alive and disease-free 18 months after treatment. A review of previously described peripheral T-cell lymphomas in HIV-positive individuals is performed, and we conclude that the spectrum of neoplasms in such cases is probably broader than originally thought.
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PMID:Ki-1+ anaplastic large-cell lymphoma of T-cell origin in an HIV-infected patient. 165 81

Musculoskeletal conditions occurring in individuals with human immunodeficiency virus infection are becoming increasingly well documented. Arthritis with features of Reiter's syndrome or psoriatic arthritis has been further studied; an association with HLA-B27 but not with HLA antigens chemically associated with psoriasis or psoriatic arthritis has been demonstrated. Human immunodeficiency virus has been identified in synovial fluid dendritic cells and in the synovium; immunohistochemical analysis is revealing the nature of the lymphocyte infiltrate in the synovium of affected individuals. Postmortem studies suggest that there may be histologic evidence of premature aging in clinically unaffected joints from patients with acquired immunodeficiency syndrome. Epidemiologic studies are needed to elucidate which rheumatic lesions occur as a direct consequence of human immunodeficiency infection and which may be chance associations.
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PMID:Arthritis in the acquired immunodeficiency syndrome and other viral infections. 165 72

We present a patient with haemophilia A showing human immunodeficiency virus type 1 (HIV-1) infection and factor VIII inhibitor in whom a novel T-cell subpopulation, double-negative (CD4-CD8-) T cells bearing T-cell receptor (TCR)-alpha beta, proliferated polyclonally in the peripheral blood. An interleukin-2-dependent T-cell line with a CD4-CD8-TCR-alpha beta+ phenotype was established from the peripheral blood lymphocytes of the patient, and its biological functions were studied. It was found that the CD4-CD8-TCR-alpha beta+ T cells possessed both HLA-unrestricted cytotoxicity and helper function for immunoglobulin production by B cells. In addition, these T cells were found to produce interferon-gamma and interleukin-2 following activation via CD3-TCR complexes. These data demonstrating the multifunction of these newly defined CD4-CD8-TCR-alpha beta+ T cells thus suggest that these cells play an important role in protection against HIV infection. The mechanism of production of factor VIII inhibitor in the present case is also discussed focusing on the CD4-CD8-TCR-alpha beta+ T cells.
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PMID:Proliferation of double-negative (CD4-CD8-) T cells bearing T-cell receptor-alpha beta in a haemophiliac with human immunodeficiency virus type 1 infection and factor VIII inhibitor: functional properties of double-negative T-cell receptor-alpha beta+ T cells. 166 Nov 24

The APC/stimulating cell (APC/SC) potential of PBMC from Walter Reed stage 1 and 2 patients and patients with AIDS was tested by using these PBMC as stimulators in an allogeneic MLR. The responding cells were PBMC from unrelated, HIV- donors that were either unfractionated or depleted of APC by plastic and nylon wool adherence. Using this approach, we observed no defect in the APC/SC potential of PBMC from Walter Reed stage 1 and 2 patients. However, PBMC from AIDS patients used as allogeneic stimulators exhibited three different patterns of APC/SC function: 1) no defect in alloantigen (ALLO) APC/SC potential; 2) a defect in ALLO APC/SC function that was detected only if the responder cells were depleted of APC (presenting cell defect); and 3) a defect in ALLO APC/SC function, irrespective of whether the responder cells were depleted of APC (stimulating cell defect). These results indicate that in addition to Th cell defects associated with AIDS, the PBMC from AIDS patients can also exhibit a defect in APC/SC function. This study provides an approach that permits the testing of Ag-presenting function in all AIDS patients, and is therefore not limited to testing patients for whom HIV-, HLA-identical T cells and APC are available.
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PMID:Multiple patterns of alloantigen presenting/stimulating cell dysfunction in patients with AIDS. 167 47

T lymphocytes expressing the CD8 surface antigen block HIV replication in CD4+ peripheral blood cells from HIV-infected individuals. We report here that CD4+ cells from HIV seronegative donors, when infected in vitro with HIV, also do not replicate virus when cocultured with CD8+ T cells from HIV-infected individuals. CD8+ cells from HIV-uninfected donors did not show this effect on virus replication. HLA-restriction of the antiviral response was not observed, and virus-containing cells were not eliminated from culture. The antiviral activity was broadly cross-reactive, as CD8+ cells from individuals infected only with HIV-1 suppressed the replication of diverse strains of HIV-1 and HIV-2, as well as the simian immunodeficiency virus. This ability of CD8+ cells to control HIV replication could play an important role in the maintenance of an asymptomatic state in HIV-infected individuals.
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PMID:CD8+ T cells from HIV-1-infected individuals inhibit acute infection by human and primate immunodeficiency viruses. 168 28

Although changes in function of monocytes from AIDS patients have previously been reported, the functional deficits that could occur in monocytes from asymptomatic HIV-seropositive individuals has not been extensively investigated. The goal of this study was to evaluate the oxidative burst response and cell surface marker expression of monocytes from this group. Both the oxidative burst, as measured by 2',7'-dichlorofluorescin diacetate oxidation, and cell surface markers were evaluated on CD14+ (Leu-M3) monocytes by two-color flow cytometry. A significantly lower oxidative burst capacity was observed in asymptomatic, seropositives after phorbol myristate acetate and calcium ionophore stimulation when compared to seronegative controls. However, differences in oxidative burst between the two groups were not observed after stimulation with heat-aggregated IgG. The oxidative burst of monocytes from seropositive HIV antigen+ or antigen- subjects was not significantly different. The most significant difference in monocyte surface markers between seropositive and seronegative controls was a decrease in the proportion of complement receptor 3+ (CD11b+) cells while slightly decreased numbers of CD13+ and CD33+ monocytes were observed. The decreased expression of CD11b+ cells in seropositives was found entirely within the seropositive, HIV antigen+ group. Similarly, when monocytes from seropositive HIV antigen+ and antigen- were compared, significantly lower numbers of CD4+ and HLA-DR+ cells were noted. These results indicate that significant changes in monocyte function and surface markers occur early during the course of HIV infection and are associated with the expression of serum HIV antigen.
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PMID:Decreased oxidative burst activity of monocytes from asymptomatic HIV-infected individuals. 168 21

Epitope mapping of a MHC class I-restricted cytotoxic T cell response to nef, a regulatory protein of HIV, was performed with fresh PBMC from HIV-seropositive donors and target cells pulsed with a panel of overlapping peptides of the nef protein. These nef-specific CTL recognized a synthetic peptide of 10 residues derived from a nonamphipathic, highly conserved region of the nef protein in association with the HLA A3.1 molecule. Using human cell transfectants expressing mutations of the A3 molecule, we demonstrated that the amino acid at position 152 of the A3.1 molecule appears to be critical for detection of this response. Thus, rapid analysis of the epitopes of HIV proteins stimulating CTL responses can be achieved using a combination of fresh donor PBMC and target cells pulsed with synthesized peptides.
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PMID:Mapping the fine specificity of a cytolytic T cell response to HIV-1 nef protein. 169 1


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