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Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Several viral trans-activators and a tumor promoter were examined for the ability to activate human papillomavirus type 18 (HPV-18) gene expression. A plasmid containing the HPV-18 noncoding region placed upstream of the chloramphenicol acetyltransferase reporter gene was cotransfected with different herpes simplex virus type 1 (HSV-1) genes into several cell lines. Both HSV-1 TIF and ICP0 activated HPV-18 expression; however, activation by TIF was observed only in epithelial cells, while ICP0 stimulated expression in a wide variety of cells. The element activated by both TIF and ICP0 was mapped to a 229-base-pair fragment which also contains an HPV-18 epithelial cell-preferred enhancer. The inclusion of a papillomavirus E2 trans-activator with TIF and ICP0 further increased HPV-18 expression. In contrast, the HSV-1 ICP4 and ICP27 genes, as well as the human T-cell lymphotropic virus type I and human immunodeficiency virus type 1 tat genes, were found to have no effect on HPV-18 expression. In transient assays, the addition of the tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) also activated HPV-18 expression. The region of HPV-18 activated by TPA was localized to a sequence which is homologous to other TPA-responsive elements.
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PMID:Activation of human papillomavirus type 18 gene expression by herpes simplex virus type 1 viral transactivators and a phorbol ester. 253 91

Visna virus is a lentivirus which causes a slow progressive disease involving the immune system and the central nervous system. To determine the role of the viral long terminal repeat (LTR) in targeting the virus to specific host cells and tissues, transgenic mice were constructed which contained the visna virus LTR directing expression of the bacterial gene encoding chloramphenicol acetyltransferase (CAT). Analysis of the transgenic mouse tissues for CAT activity revealed that the viral LTR was responsible, in part, for the tropism of visna virus for macrophages and the central nervous system. Expression of the LTR required the macrophage to be in an activated state both in vivo and in vitro. Thioglycolate activation of peritoneal macrophages in vivo and 12-O-tetradecanoylphorbol 13-acetate treatment in vitro induced expression of the visna virus LTR. Lymphocytes from the spleens of the transgenic mice expressed CAT activity, suggesting that visna virus was able to replicate in lymphocytes, as did human immunodeficiency virus and simian immunodeficiency virus. These studies demonstrated that the lentivirus LTR was responsible, in part, for cell and tissue tropism in vivo.
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PMID:The visna virus long terminal repeat directs expression of a reporter gene in activated macrophages, lymphocytes, and the central nervous systems of transgenic mice. 253 92

Individuals infected with the human immunodeficiency virus (HIV), the etiologic agent of acquired immunodeficiency syndrome (AIDS), often show symptoms associated with reactivation of Epstein-Barr virus (EBV). In this study, we show that exposure of EBV-positive B lymphocytes to HIV-1 in vitro induced the EBV replicative cycle in these cells, as evidenced by an increased proportion of cells expressing EBV early antigens (EA) and capsid antigens (VCA). Reactivation of EBV by HIV-1 appeared to be virus-dose-dependent and required virus penetration and expression in B cells. Although HIV-1 RNA was detected by in situ hybridization in the majority of HIV-1-infected B lymphocytes, induction of EA and VCA was transient and limited to less than 20% of the cell population. The tumor-promoting phorbol ester 12-O-tetradecanoyl-phorbol-13-acetate (TPA) and HIV-1 acted synergistically and had similar kinetics in inducing the expression of EBV. Direct reactivation of EBV by HIV-1 may contribute to the role of EBV as a factor in the genesis of AIDS-related conditions.
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PMID:Induction of Epstein-Barr virus in B-lymphoblastoid cells by human immunodeficiency virus type 1. 254 43

The transactivator protein, tat, encoded by the human immunodeficiency virus is a key regulator of viral transcription. Activation by the tat protein requires sequences downstream of the transcription initiation site called the transactivating region (TAR). RNA derived from the TAR is capable of forming a stable stem-loop structure and the maintenance of both the stem structure and the loop sequences located between +19 and +44 is required for complete in vivo activation by tat. Gel retardation assays with RNA from both wild-type and mutant TAR constructs generated in vitro with SP6 polymerase indicated specific binding of HeLa nuclear proteins to the TAR. To characterize this RNA-protein interaction, a method of chemical "imprinting" has been developed using photoactivated uranyl acetate as the nucleolytic agent. This reagent nicks RNA under physiological conditions at all four nucleotides in a reaction that is independent of sequence and secondary structure. Specific interaction of cellular proteins with TAR RNA could be detected by enhanced cleavages or imprints surrounding the loop region. Mutations that either disrupted stem base-pairing or extensively changed the primary sequence resulted in alterations in the cleavage pattern of the TAR RNA. Structural features of the TAR RNA stem-loop essential for tat activation are also required for specific binding of the HeLa cell nuclear protein.
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PMID:Specific binding of a HeLa cell nuclear protein to RNA sequences in the human immunodeficiency virus transactivating region. 254 77

The trans activator (p40tax) of human T-cell leukemia virus type I (HTLV-I) is a transcriptional factor that activates the long terminal repeat (LTR) of HTLV-I and interleukin-2 receptor alpha. We examined the HTLV-I enhancer responsible for tax-mediated trans activation and identified (A/T)(G/C)(G/C)CNNTGACG(T/A) as a plausible tax-responsive element (TRE). The putative TRE in the LTR was found to be different from the elements required for activation by cycle AMP and 12-O-tetradecanoylphorbol-13-acetate, although these elements overlapped each other. The TRE was also different from a binding site of an NF-kappa B-like factor that was identified in the interleukin-2 receptor alpha promoter and human immunodeficiency virus LTR as a TRE. The latter result was further demonstrated by the failure of the NF-kappa B sequence to compete with the TRE of the LTR in a protein-binding assay. These findings indicate that tax function and its cascade can modulate activities of various enhancer sequences, which are probably regulated by distinct DNA-binding factors.
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PMID:A unique enhancer element for the trans activator (p40tax) of human T-cell leukemia virus type I that is distinct from cyclic AMP- and 12-O-tetradecanoylphorbol-13-acetate-responsive elements. 254 1

A rapidly proliferating T-cell line, HCD8, was derived from the peripheral blood lymphocytes of an apparently healthy individual during the course of a T-cell cloning experiment. This T-cell line expressed a very unusual phenotype: CD1+, CD2-, CD3+ (cytoplasmic), CD4-, CD5+, CD7+, CD8-, interleukin-2 receptor (IL-2 R) (p55)-, and T-cell antigen receptor (TCAR) alpha beta-. Assays for reverse transcriptase activity and for human T-lymphotropic retroviral sequences in the cellular DNA were negative, indicating that the cells were not transformed by human T-lymphotropic virus (HTLV)-I, HTLV-II, or human immunodeficiency virus (HIV)-I. Culturing the cells in the differentiation inducing agent 12-O-tetradecanoyl phorbol 13-acetate induced an increased expression of CD3 but no other significant changes in T-cell markers. A small population of CD4-negative and CD8-negative T-lymphocytes exist in human peripheral blood and they exhibit natural killer (NK) and antibody-dependent cell-mediated cytotoxic (ADCC) activity. However, the authors' cell line failed to demonstrate such cytotoxic function. The TCAR gene rearrangement studies showed that both T gamma genes were rearranged while the T beta genes were in the germ line configuration and the T delta genes were deleted. HCD8 strongly expressed the antigens Leu M1 and Ki-1, markers detected only rarely on normal unstimulated human T-cells, but quite consistently found on Reed-Sternberg cells and cells of some large pleomorphic T-cell lymphomas. HCD8 may be used to study the control of Leu M1 and Ki-1 expression in T-cells and it may provide some insight into the cellular origin of the above-mentioned lymphomas.
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PMID:A T-cell line with an unusual phenotype. 255 76

Tumor necrosis factor-alpha is an inducer of acute-phase protein synthesis in liver cells. The mechanism by which tumor necrosis factor-alpha alters gene expression in these cells is largely unknown. In this study, we demonstrate that tumor necrosis factor-alpha stimulates human immunodeficiency virus-1 long terminal repeat-promoted gene expression in the human hepatoblastoma HepG2 cell line and increased binding of trans-activating factors to kappa B (kappa B) DNA sequences. In contrast to lymphocytic cells where the nuclear factors recognizing the kappa B sequences are activated by both tumor necrosis factor-alpha and phorbol-12-myristate-13-acetate through a posttranslational mechanism, in HepG2 cells phorbol-12-myristate-13-acetate does not activate these factor(s), and de novo protein synthesis seems to be required in HepG2 cells for gene activation by tumor necrosis factor-alpha.
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PMID:Tumor necrosis factor-alpha induces a kappa B sequence-specific DNA-binding protein in human hepatoblastoma HepG2 cells. 255 96

The pathogenesis of cellular immune deficiency following human immunodeficiency virus (HIV) infection could result from quantitative and/or qualitative dysfunction of the CD4+ lymphocyte population. To better characterize the T-cell response to soluble antigen with HIV infection, we have isolated peripheral blood lymphocytes and purified populations of CD4+ lymphocytes from healthy HIV antibody-positive subjects, patients with acquired immunodeficiency syndrome (AIDS)-related complex (ARC), and healthy HIV antibody-negative controls. T-lymphocyte function was determined by proliferative response to lectin (phytohemagglutinin), phorbol 12-myristate 13-acetate (PMA), calcium ionophore, purified recombinant HIV envelope gp120, tetanus toxoid antigen, and tetanus toxoid antigen in the presence of recombinant gp120 or purified recombinant soluble CD4. PBLs and CD4+ lymphocytes from asymptomatic HIV-infected subjects responded equally well to lectin, PMA, and/or calcium ionophore and to tetanus toxoid as cells from uninfected control subjects. The cells that proliferated in response to a soluble antigenic stimulus did not respond to gp120. Cells from subjects with ARC had a selective antigen recognition defect independent of the number of CD4+ lymphocytes. Recombinant gp120 inhibited CD4+ lymphocyte proliferation to antigenic stimulus by 30-40%. Recombinant soluble CD4, a proposed therapeutic for HIV, had no effect on T-cell response to antigen. A selective antigen recognition response was not compromised early in HIV infection but was compromised in subjects with ARC. Inhibition of proliferation to tetanus toxoid by gp120 suggests that HIV may affect major histocompatibility complex II restricted antigen recognition independent of CD4+ cell loss.
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PMID:CD4+ lymphocyte function with early human immunodeficiency virus infection. 256 77

Phenotypes of the tumor cells of malignant histiocytosis (MH) were studied by using monoclonal and polyclonal antibodies in 18 autopsy cases. The tumor cells expressed different antigens in various degrees. Almost all tumor cells showed positive reaction for alpha 1-ACT; partially for alpha 1-AT, LCA and a few for lysozyme as well as LeuM1. It was most likely that the tumor cells of MH originated from the mononuclear phagocytic system (MPS). In order to reveal the relationship between MH and immunodeficiency, morphological changes of the lympho-reticular system in 18 cases of MH were studied. It was found that the lymphoid tissues, including lymph nodes, thymus, tonsil, spleen, bone marrow, lymphoid tissues of GI tract and lung etc showed severe depletion. These findings indicate that MH usually combine with immunodeficiency which is also closely related to the pathogenesis and pathological changes of MH.
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PMID:[Malignant histiocytosis and immunodeficiency]. 258 56

The CD4 molecule functions as a receptor for the binding and infectivity of the human immunodeficiency virus (HIV). It is of interest, therefore, to develop procedures for its down-regulation. In the present study, the effect of 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) on the expression of cell surface antigens of the HL-60 promyelocytic leukemia cell line was analyzed. Exposure of HL-60 cells to 1,25(OH)2D3 resulted in down-regulation of CD4 as assessed by their staining with the Leu-3a monoclonal antibody (MoAb). This treatment increased the staining of HL-60 cells with the monocyte-specific 63D3 MoAb. In contrast to the rapid elimination of cell surface CD4 by exposure of HL-60 to phorbol myristate acetate (PMA), the maximal reduction of CD4 by 1,25(OH)2D3 was attained within 48 h after the beginning of the exposure.
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PMID:Modulation of the expression of CD4 on HL-60 cells by exposure to 1,25-dihydroxyvitamin D3. 269 87


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