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

We have developed a flow cytometric method for demonstrating cell fusion between human immunodeficiency virus type 1 (HIV-1)- or HIV-2-infected HUT-78 cells and uninfected CD4-bearing MOLT-4 cells. Syncytium formation due to an interaction between the gp120 glycoprotein expressed on HIV-infected HUT-78 cells and the CD4 receptor present on MOLT-4 cells, resulted in an immediate decrease in the number of MOLT-4 cells; after a 24 h incubation period almost all MOLT-4 cells had disappeared from the culture. To show that the target MOLT-4 cells and not the aggressor HUT-78 cells were destroyed, specific monoclonal antibodies (MAbs) that reacted with antigens expressed on either MOLT-4 or HUT-78 cells were used. The formation of giant cells and the concomitant disappearance of MOLT-4 cells was blocked by MAbs specific for OKT4A and Leu3a, and, to a much lower level, by the MAbs specific of OKT4 and gp120. MAbs specific for OKT3, Leu2a, HLA-DR, Leu18 and LeuM3 did not prevent the disappearance of MOLT-4 cells. Sera from two AIDS patients containing antibodies to the HIV envelope glycoproteins did not protect MOLT-4 cells against the destructive effect of the HIV-infected HUT-78 cells. The fusion index, the percentage fusion inhibition and the 50% fusion inhibitory concentration of the MAbs can be accurately determined with the flow cytometric assay. The method can be readily implemented to evaluate any therapeutic treatment by examining its capacity to block cell-to-cell fusion, and hence destruction of the target bystander cells. Five anti-HIV compounds which have been previously shown to interfere with HIV binding to cells (namely pentosan polysulphate, heparin, suramin, aurintricarboxylic acid and Evans Blue) were further evaluated by this new method. With the exception of heparin, all of these compounds were found to inhibit cell-to-cell fusion and the concomitant destruction of the target bystander cells. Azidothymidine failed to inhibit fusion or bystander T cell destruction.
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PMID:Syncytium formation and destruction of bystander CD4+ cells cocultured with T cells persistently infected with human immunodeficiency virus as demonstrated by flow cytometry. 278 68

The capacity of human immunodeficiency virus (HIV) antibody-positive sera from homosexually active men without acquired immune deficiency syndrome to lyse the HIV-infected T cell lines MOLT-4f and CCRF-CEM (CEM) in cooperation with lymphocytes from normal donors was investigated. Twenty-seven HIV antibody-positive sera, most of which enhanced the killing of HIV-infected MOLT-4f and CEM target cells by normal mononuclear cells were studied in detail. HIV antibody-positive sera resulted in lysis at dilutions as high as 1/10,000. HIV antibody-negative sera did not augment lysis of infected target cells. In addition, lysis of uninfected targets was not enhanced in the presence of HIV antibody-positive sera. Because fractionation of the HIV antibody-positive sera on a protein A affinity column resulted in recovery of the activity from the IgG fraction, the extra cytotoxic activity mediated by nonimmune cells in the presence of immune sera appears to be antibody-dependent. Furthermore, the cytotoxic effector cells were in the nonrosetting fraction of lymphocytes and expressed Leu-11 (cluster designation (CD)15) antigens, which is characteristic of cells participating in antibody-dependent cellular cytotoxicity reactions. The antibody specificity of the sera, determined by radioimmunoprecipitation, provides evidence that antibody-dependent cellular cytotoxicity can occur even when there are no detectable antibodies directed against gag proteins. Sera which lacked detectable antibodies to the envelope protein gp120 by radioimmunoprecipitation did not mediate antibody-dependent cellular cytotoxicity.
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PMID:Antibodies to human immunodeficiency virus in human sera induce cell-mediated lysis of human immunodeficiency virus-infected cells. 282 Nov 15

PSK, a biological response modifier (BRM), was studied to determine its anti-viral activity on human immunodeficiency virus (HIV) in vitro. Either a novel infection system using human T-cell lymphotropic virus type I (HTLV-I)-carrying MT-4 cells or a coculture system using MOLT-4 cells and its virus-producing cells MOLT-4/HIVHTLV-IIIB which induces multinucleated giant cells very efficiently was used. PSK almost completely blocked the cytopathic effect such as giant cell formation and HIV-specific antigen expression both in MT-4 cells and MOLT-4 cells at a concentration of 0.4 and 0.8 mg/ml, respectively. Pretreatment of the virus with PSK may specifically interfere with early stages of HIV infection by modifying the viral receptor.
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PMID:A biological response modifier, PSK, inhibits human immunodeficiency virus infection in vitro. 282 69

Persistently HIV-infected cell lines were isolated from surviving and proliferating cells after infection of HTLV-I-carrying MT-4 cells with cell-free human immunodeficiency virus (HIV); HTLV-IIIB and LAV. The media of the cloned cell cultures did not cause HIV infection of MT-4, MOLT-4, TALL-1, or HL-60 cells. Most of the constituents of the virus in the media were env proteins and many defective doughnut-shaped particles released from the cells were identified by electron microscopy.
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PMID:Defective human immunodeficiency virus (HIV) particles produced by cloned cells of HTLV-I-carrying MT-4 cells persistently infected with HIV. 289 63

The effect of tumor necrosis factor (TNF) on the replication of human immunodeficiency virus type 1 (HIV-1) was investigated in several T4 lymphocyte cell lines. TNF markedly enhanced the cytopathogenicity of HIV-1, virion-associated reverse transcriptase (RT) activity in the cell culture supernatant, and viral antigen expression in MOLT-4 cells as early as 3 days after HIV-1 infection. A slight increase in RT activity was also observed in the supernatant of H9 cell cultures exposed to TNF. However, TNF did not increase either RT activity in MT-4 cell supernatants or viral antigen expression in HUT-78 cells. Thus, TNF is able to stimulate the replication of HIV-1 in de novo infected T4 cells although not all T4 cells seem to be sensitive to this stimulatory effect.
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PMID:Tumor necrosis factor enhances replication of human immunodeficiency virus (HIV) in vitro. 291 52

Large plaque-inducing clones were obtained from small plaque-inducing parental clones of human immunodeficiency virus (HIV) by the plaque-cloning method. The cloned HIVs that formed large and small plaques were studied as follows: 1) infectivity was determined by the ratio of plaque-forming units (PFU) to reverse transcriptase (RT) activity; 2) viral growth was assessed by the amount (RT activity) of virus after infection; and 3) HIV long terminal repeat (LTR)-linked gene expression of the viruses was measured by chloramphenicol acetyltransferase (CAT) assay using persistently infected MOLT-4 cells. Results showed that clones producing large plaques showed similar or slightly lower infectivity but higher virus production, faster viral growth, and higher gene expression activity than clones producing small plaques. These analyses revealed that clones producing large plaques could replicate more rapidly than those producing small plaques. Restriction enzyme map analysis of these cloned viruses showed that they were also genetically different. These results suggest that the changes in the biological features observed here might be due to mutation during the cloning procedure.
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PMID:Emergence of large plaque-producing clones of human immunodeficiency virus (HIV) in vitro. 292 4

The effect of 3'-azido-3'-deoxythymidine (AZT) on replication of human immunodeficiency virus (HIV) in various hematopoietic cell lines was investigated. The concentration of AZT required to block HIV replication varied depending on the cell line used. U-937 cells required as little as 0.01 microM AZT to block HIV replication, a concentration almost 100 times lower than that required for MT-4 or MOLT-4 cells. However, 467 and TALL-1 cells required concentrations of AZT higher than 5 microM. It was clear that AZT was ineffective once the viral gene was integrated into chromosomal DNA; removal of AZT from culture fluids at that stage allowed the full expression of HIV. The effect of the potent immunostimulator lentinan was also examined, and it was shown that lentinan enhanced the effect of AZT.
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PMID:Suppression of human immunodeficiency virus replication by 3'-azido-3'-deoxythymidine in various human hematopoietic cell lines in vitro: augmentation of the effect by lentinan. 311 74

The amount of infectious virus released into the culture fluid from human immunodeficiency virus (HIV)-producing MOLT-4 cells (MOLT-4/HIV HTLV-III) was measured as a function of the culture conditions and cell density. After 3 days, the daily yield of infectious virus per cell in the fluid of non-growing cells cultured at high cell density was about 15 times higher than the accumulated yield from growing cells cultured at low cell density. SDS-PAGE analysis also showed a similar difference in the amounts of major gag protein p24.
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PMID:Amplification of human immuno-deficiency virus production from a virus-producing cell line in culture at high cell density. 311 93

Biosynthesis was examined of sialophorin (formerly called gpL115) which is altered in the inherited immunodeficiency Wiskott-Aldrich syndrome. Sialophorin is greater than 50% carbohydrate, primarily O-linked units of sialic acid, galactose, and galactosamine. Pulse-labeling with [35S]methionine and chase incubation established that sialophorin is synthesized in CEM lymphoblastoid cells as an Mr 62,000 precursor which is converted within 45 min to mature glycosylated sialophorin, a long-lived molecule. Experiments with tunicamycin and endoglycosidase H demonstrated that sialophorin contains N-linked carbohydrate (approximately two units per molecule) and is therefore an N,O-glycoprotein. Pulse-labeling of tunicamycin-treated CEM cells together with immunoprecipitation provided the means to isolate the [35S]-methionine-labeled polypeptide core of sialophorin and determine its molecular weight (58,000). This datum allowed us to express the previously established composition on a "per molecule" basis and determine that sialophorin molecules contain approximately 520 amino acid residues and greater than or equal to 100 O-linked carbohydrate units. A recent study showed that various blood cells express sialophorin and that there are two molecular forms: lymphocyte/monocyte sialophorin and platelet/neutrophil sialophorin. Biosynthesis of the two forms was compared by using sialophorin of CEM cells and sialophorin of MOLT-4 cells (another lymphoblastoid line) as models for lymphocyte/monocyte sialophorin and platelet/neutrophil sialophorin, respectively. The time course of biosynthesis and the content of N units were found to be identical for the two sialophorin species. [35S]Methionine-labeled polypeptide cores of CEM sialophorin and MOLT sialophorin were isolated and compared by electrophoresis, isoelectrofocusing, and a newly developed peptide mapping technique.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Biosynthesis of human sialophorins and analysis of the polypeptide core. 311 91

Liposomes containing fragment A of diphtheria toxin killed human immunodeficiency virus (HIV)-producing MOLT-4 or TALL-1 cells, and HTLV-I-carrying MT-4 cells infected with HIV, but did not kill these cells when they were not infected with HIV. This killing was not affected by the presence of HIV antibodies. These results show that liposomes containing fragment A of diphtheria toxin selectively killed cells expressing HIV antigens or producing the virus in vitro.
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PMID:Selective killing of human immunodeficiency virus-infected and -producing cells by liposomes containing diphtheria toxin fragment A. 312 51


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