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

The majority of lymphomas in the setting of acquired, iatrogenic, or congenital immunodeficiencies are B-cell lymphoproliferations. We describe a rare T-cell lymphoma in a fulminantly ill patient infected with human immunodeficiency virus type 1 (HIV-1). The T-cell nature of the process was defined genotypically (monoclonal T-cell receptor beta-chain [CT beta] rearrangement) and phenotypically (CD45RO+, CD4+, CD5+, CD25+, CD8-, CD3- and negative for a variety of B-cell and monocyte markers). The CD4+, CD25+ (interleukin-2 receptor [IL-2R]) phenotype with production of IL-2 and IL-2R RNA is analogous to human T-lymphotropic virus type I (HTLV-I)-associated adult T-cell leukemia/lymphoma (ATLL); however, no HTLV-1 could be detected. Southern blot analysis did demonstrate monoclonally integrated HIV-1 within the tumor genome. Furthermore, the tumor cells were producing HIV p24 antigen as shown by immunohistochemistry. This is the first case of acquired immunodeficiency syndrome (AIDS)-associated non-Hodgkin's lymphoma in which HIV-1 infection may have played a central role in the lymphocyte transformation process.
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PMID:Acquired immunodeficiency syndrome-associated T-cell lymphoma: evidence for human immunodeficiency virus type 1-associated T-cell transformation. 137 87

HTLV-I (Human T-cell leukemia virus type I) has been the first human retrovirus identified and then associated with a definite pathological entity, a leukemic syndrome that specifically affects mature T-lymphocytes (ATL, adult T-cell leukemia), expressing CD3+, CD4+, CD8-, CD11- phenotype. This form of leukemia/lymphoma is endemic in southwestern islands of Japan, although at present the number of HTLV-I seropositive individuals has greatly increased, with a worldwide diffusion, following the expansion wave of the AIDS-associated HIV retrovirus. In fact, double seropositivity for both HIV and HTLV is frequently found among intravenous drug users. Although ATL leukemia or lymphoma occurs with a low frequency among HTLV-I seropositive individuals, it is likely that the evolution from a latent phase of infection to acute leukemia could be favoured by depression of immunosurveillance levels in the host. Therefore, special attention is required to prevent the diffusion of this retrovirus in adults, taking into consideration that newborn babies from seropositive mothers have to be considered at high risk for development of HTLV-I associated disease, on the basis of their immature immunocompetence.
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PMID:[Etiopathogenesis and therapeutic trends in adult T-cell leukemia associated with HTLV-I retrovirus]. 137 77

Human immunodeficiency virus type 1(HIV-1) induces extensive immune cell alterations which can be detected by changes both in serum levels of soluble immune activation products and in several lymphoid phenotypic markers. The current studies were conducted in 70 HIV-1 seropositive subjects to determine whether changes among four important serum immune activation markers (neopterin, beta-2 microglobulin, soluble CD8, and soluble IL-2 receptor) and seven lymphoid phenotypic markers (CD38, HLA-DR, CD57, CD11b, CD45RA, leu8, and CD71) reflect similar or disparate aspects of immune pathology. On the basis of correlation coefficient calculation, four groups of related markers (Fig. 1) were identified: Group A, sIL-2R was related to group B where serum neopterin, beta 2M, sCD8 levels, and lymphocyte CD38 antigen expression correlated closely. Loss of CD45RA or Leu 8 antigens in group C correlated with group B and D markers increase. HLA-D in group D was a more distantly related immune activation marker. Phenotypic markers CD57, CD11b, and CD71 did not correlate with the immune activation processes reflected by the serum and phenotypic marker groups A-D. Correlations between serum and certain lymphoid phenotypic markers were generally stronger later in HIV-1 infection when CD4 levels were less than 500/mm3. This study provides information for selecting markers for investigating immune changes in HIV-1 infection and immune-related diseases. Many serum and lymphoid phenotypic markers reflect related aspects of immune dysregulation. However, some markers can indicate different aspects of disease.
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PMID:Immune changes in HIV-1 infection: significant correlations and differences in serum markers and lymphoid phenotypic antigens. 137 54

Individuals infected with HIV frequently develop cytopenias and suppressed hematopoiesis. The role of direct HIV infection of hematopoietic progenitor cells in this process has not been defined. In this study, purified CD34+ bone marrow progenitor cells from 74 Zairian and American patients were studied by both coculture viral isolation and polymerase chain reaction for evidence of HIV infection. A total of 36.5% of Zairian and 14% of American patients had HIV infection of the CD34+ cell subset, with as many as 1 in 500 CD34+ cells infected. Most of the Zairian patients in this study had advanced HIV infection and markedly decreased CD4/CD8 T lymphocyte ratios (mean 0.160 +/- 0.08), and no laboratory value predicted the presence of infection in the CD34+ subset of a given Zairian individual. In contrast, American patients with CD34+ cell infection had total CD4 cells less than 20/mm3 and a greater decrease of the CD4/CD8 T lymphocyte ratio compared to seropositive Americans without CD34+ cell infection (p = 0.003). Hematopoiesis, studied by methylcellulose colony assays, was depressed in all seropositive patients studied with no significant further suppression when CD34+ cells were infected. Thus, CD34+ bone marrow progenitor cells are infected in vivo in a subset of seropositive individuals and may serve as an additional reservoir of virus in HIV-infected individuals.
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PMID:CD34+ bone marrow cells are infected with HIV in a subset of seropositive individuals. 137 76

CTL lines specific for two different proteins derived from the human pathogens, Plasmodium falciparum (malaria) circumsporozoite protein and HIV-1 reverse transcriptase, were obtained by immunizing mice with protein-pulsed syngeneic spleen cells. The lysis of the target cells was dependent on a class I MHC molecule and the accessory molecule CD8. Immunodominant epitopic peptides were identified previously in the two proteins using murine CTL derived after immunization with recombinant virus or sporozoites, or using CTL from HIV-1-infected patients. These peptides were also recognized by the CTL lines obtained after protein-pulsed spleen-cell immunization. A new CTL antigenic determinant was localized in HIV-1 reverse transcriptase to residues 514 to 528, a sequence that, if folded as an alpha-helix, would be strongly amphipathic. The determinant was tentatively narrowed, using overlapping peptides, to a core of at least nine residues, 515 to 523. This site was also recognized by CTL obtained by the two different methods of immunization. Therefore, extracellular proteins incubated with spleen cells can be processed and presented in vivo in the same way as intracellular proteins, resulting in recognition of the same epitopes in association with the same class I MHC molecules. The potential implications for vaccine development and for the understanding of class I-restricted Ag presentation are discussed.
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PMID:Immunization with soluble protein-pulsed spleen cells induces class I-restricted cytotoxic T lymphocytes that recognize immunodominant epitopic peptides from Plasmodium falciparum and HIV-1. 138 39

EDTA-anticoagulated blood samples from 19 HIV-1-positive subjects and 13 healthy laboratory worker controls were analysed for three lymphocyte subpopulations (CD3, CD4, CD8 T cells) (lysed whole blood method, Becton Dickinson FACScan flow cytometer) at 0, 24, 48, 72 and 96 h after venesection, having been stored at either 4 degrees C, 12 degrees C, 16 degrees C or 21 degrees C. In samples stored at 4 degrees C and 12 degrees C there was a significant fall in both %CD3 and %CD 4, and a significant rise in %CD8. At 16 degrees C the %CD8 remained stable, while there were marginal rises in %CD3 and %CD4. At 21 degrees C, the %CD8 again remained stable, while %CD3 and %CD4 rose significantly with time. These trends were independent of HIV-1 status. At each temperature studied, the rates of change of lymphocyte subpopulations were independent of each other. These results suggest that a temperature range of 14-16 degrees C may be optimal for sample storage prior to measurement of T cell subsets. They emphasise the importance of strict control on conditions if samples are to be kept for any length of time before analysis.
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PMID:The effect of the temperature and duration of sample storage on the measurement of lymphocyte subpopulations from HIV-1-positive and control subjects. 138 25

The severe complications of the acquired immunodeficiency syndrome represent the final phase of a prolonged course of immune system destruction during the infection by human immunodeficiency virus (HIV). Many of these complications can be predicted by measuring the depletion of CD4 positive lymphocytes. The CD4 positive lymphocyte counts are now widely accepted as a surrogate marker to assess the stage of disease and to determine immune response in major clinical trials. Other lymphocyte subsets are candidate surrogate markers for antiretroviral therapy. Our laboratory has utilized flow cytometry to perform lymphocyte subset testing, including CD4, CD8, CD4/CD8 ratio, and others for more than three years on persons with suspected immune deficiency. Results from our laboratory are presented to illustrate the use of these procedures in an urban, predominantly inner city population. The role of flow cytometry in monitoring patients with HIV infection is discussed.
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PMID:Lymphocyte subset changes in persons infected with human immunodeficiency virus. 138 8

Defective in vitro T helper cell (Th) function can occur in asymptomatic human immunodeficiency virus (HIV)-seropositive (HIV+) individuals. A characteristic, early finding is the loss of an in vitro response to recall antigens, such as influenza A virus (FLU), despite an intact Th response to alloantigen (ALLO). To determine whether suppressor cells and/or inhibitory factors could contribute to this HIV-associated Th immunodeficiency, coculture studies were performed using peripheral blood leukocytes (PBLs) from monozygotic twins, one of whom was HIV-infected (HIV+) and one of whom was uninfected (HIV-seronegative, HIV-). In vitro Th function was measured as interleukin 2 production or proliferation to FLU and ALLO. Two pairs of twins were repetitively studied. A single HIV+ individual with multiple samples of cryopreserved PBLs over 6 years (including a HIV- specimen) was also studied. PBLs from the HIV+, but not from the HIV-, individuals demonstrated defective in vitro Th function in response to FLU but not to ALLO. PBLs from HIV+ individuals could induce a similar defect in the Th function of syngeneic or autologous HIV- PBLs. This suppression was generated by CD4-depleted, but not by CD8-depleted, PBLs. A suppressive factor from CD8+ cells of HIV+ donors was generated by 24-hr unstimulated cultures of HIV+ PBLs. This factor inhibited FLU but not ALLO responses of autologous, syngeneic, or allogeneic HIV- PBLs. This suppressive effect could not be explained by HIV infection or replication during the culture period. These results demonstrate that selective abrogation of Th function to recall antigens in HIV+ individuals is associated with an inhibitory factor produced by CD8+ T cells.
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PMID:A factor from CD8 cells of human immunodeficiency virus-infected patients suppresses HLA self-restricted T helper cell responses. 138 69

We compared the serum concentrations of soluble CD8 with the immune activation markers neopterin, interferon-gamma, tumour necrosis factor-alpha, soluble CD4, and with CD4+ and CD8+ T-cell counts in patients with human immunodeficiency virus (HIV) infection. The majority of patients had increased concentrations of soluble CD8, interferon-gamma and neopterin, and various significant correlations existed between them. Our results support the view that enhanced soluble CD8 levels indicate activated CD8+ T cells in patients with HIV infection.
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PMID:Association between serum-soluble CD8 levels and parameters of immune activation in patients with human immunodeficiency virus infection. 139 41

In the early 1990s, HIV seroprevalence in the rural community in Casamance, Senegal was .8% (age range from 24 to 68 years). 25 people had HIV-2 infection and 2 had HIV-1 infection. Health workers evaluated 22 of the HIV-2 positive adults and compared them with 64 matched controls. The HIV-2 positive adults were 7.25 times more likely to suffer from ill health than the controls (50% vs. 12.5%). Clinical signs of HIV-2 positive status were more common among HIV-2 positive adults than controls (40.9% vs. 7.8%; odds ration [OR] = 8.2), especially chronic cough (OR - 18.5). Presence of diarrhea was insignificant (22% vs. 40%). HIV-2 positive adults had much higher levels of CD8 cells (p = .03), IgG (p = .0001), and beta 2 macroglobulin (p =.001) than the controls. Their CD4/CD8 ratio levels were much lower than those of the HIV-2 negative individuals (1.1 vs. 1.9; p = .0001). Among HIV-2 positive adults, symptomatic adults had significantly lower levels of red blood cells (p = .02), white blood cells (p = .02), lymphocytes (p = .01), T cells (p = .01), and CD4 cells (p = .002) than the healthy adults. Their beta 2 macroglobulin levels were much greater than controls (4.6 mg/vs. 2.9 mg/l, p = .03). 5 HIV-2 cases (22.7%) researchers suffered from immunosuppression (500 CD4 cells/mcl) compared with only 1 control (1.6%) (OR = 18.5). Clinical symptoms were more likely to be present in immunodepressed people than in non immunodepressed people (35.7% of 14 sick adults vs. 1.4% of healthy adults). 1 person who had AIDS as defined by WHO (weight loss, persistent cough, and diarrhea) had 429 CD4 cells/mcl. 1 person suffered from bronchopneumonia (326 CD4 cells/mcl). Another person had chronic diarrhea and bronchopneumonia (350 CD4 cells/mcl). The mean age of HIV-2 infected people who had a respiratory condition was 51 years (42-68 years) while it was 41 years (26-68 years) for asymptomatic HIV-2 infected people indicating a rather long incubation period. These results suggested that HIV-2 can be significant public health problems.
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PMID:HIV-2 infections in a rural Senegalese community. 140 31


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