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

The rate of multinucleated giant cell formation by the fusion of HIV chronically infected human T-cells (MOLT-4/HIV) and HIV uninfected MOLT-4 cells was examined under various pH conditions. The number of giant cells formed under the different pH conditions was quantitatively monitored by "MULTISIZER". The rate of giant cell formation was significantly less at the pH lower than 6 but not influenced at higher pH. Plaque assay under various pH conditions revealed that inhibition of giant-cell formation at lower pH was not due to the influence over the recognition between gp120 of HIV and CD4 molecules.
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PMID:Effect of pH on giant cell formation induced by human immunodeficiency virus ( HIV ). 253 42

The processing and maturation of envelope glycoproteins of human immunodeficiency virus type 1 (HIV-1) were studied in infected cells treated with inhibitors of oligosaccharide processing. In MOLT-3 cells chronically infected with HIV-1 (strain HTLV-IIIB), tunicamycin severely inhibited the glycosylation of envelope proteins. Deoxynojirimycin, an inhibitor of glucosidase I in the rough endoplasmic reticulum, inhibited the proteolytic processing of gp160, whereas no such effect was noted with either deoxymannojirimycin or swainsonine, inhibitors of mannosidase I and II, respectively, in the Golgi complex. The processed gp120 and gp41 synthesized in the presence of deoxymannojirimycin were found to contain mannose-rich oligosaccharide cores as evidenced by their susceptibility to endoglycosidase H digestion. The formation of syncytia normally observed when CEM cells are cocultured with HIV-1-infected cells was markedly inhibited in the presence of deoxynojirimycin, but such inhibition was not observed in cells treated with deoxymannojirimycin or swainsonine. The infectivity of virions released from MOLT-3/HTLV-IIIB cells treated with deoxynojirimycin or deoxymannojirimycin was significantly lower than the infectivity of virions released from untreated cells. On the other hand, treatment with swainsonine did not affect the infectivity of the progeny virus. These results suggest that the proteolytic processing of gp160 takes place in infected cells when the glycoprotein has mannose-rich oligosaccharide structures. Trimming of glucose residues and the primary trimming of mannose residues are necessary for the release of infectious virus.
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PMID:Role of oligosaccharides in the processing and maturation of envelope glycoproteins of human immunodeficiency virus type 1. 254 46

Defective HIV-producing T-cell lines were subcloned from MT-4/HIVHTLV-IIIB' MOLT-4/HIVHTLV-IIIB, and H9/HIVHTLV-IIIB cell lines chronically infected with HIV. The NY-M10 cell line derived from MOLT-4/HIVHTLV-IIIB and the NY-H6 cell line derived from H9/HIVHTLV-IIIB produce defective HIV, which lacks the ability to infect human T-cell lines. NY-M10 cells retain the capacity to form multinucleated giant cells in cocultivation with HIV-uninfected CD4-positive cells. However, NY-H6 cells failed to fuse with CD4-positive cells. Electron microscopic analysis indicated that the defective HIV produced from NY-M10, like those reported previously, lacked the structure of the nucleocapsid, and the virion released from NY-H6 was indistinguishable from those of authentic HIV particles. Southern and Northern blotting analyses of NY-M10 and NY-H6 cleared that the genome of those defective viruses was not significantly deleted, suggesting minor mutation(s) should take place on the viral genome.
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PMID:Characterization of human T-cell lines harboring defective human immunodeficiency virus type 1. 255 41

Soybean saponins isolated from soybean seeds were investigated for their antiviral activity on HIV in vitro, using an HTLV-I-carrying cell line, MT-4. Saponin B1 completely inhibited HIV-induced cytopathic effects and virus-specific antigen expression 6 days after infection at concentrations greater than 0.5 mg/ml. Saponin B2 also inhibited HIV infection, although less potently. Both saponin B1 and B2 had no direct effect on the reverse transcriptase activity of HIV. Saponin B1 also inhibited HIV-induced cell fusion in the MOLT-4 cell system. The results of this study suggest that soybean saponins, especially saponin B1, have inhibitory activity against HIV infection.
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PMID:Inhibitory effect of glycosides like saponin from soybean on the infectivity of HIV in vitro. 257 82

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

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

An extract of culture medium of Lentinus edodes mycelia (LEM) was prepared. This was further fractionated by 50% ethanol precipitation and both the resulting product, E-P-LEM, and LEM were studied to evaluate their effect on the activity of human immunodeficiency virus (HIV) in vitro. The experiments were performed using either a cell-free infection system with MT-4 cells, or a cell-to-cell infection system with MOLT-4 cells, which induces multinucleated giant cells very efficiently. E-P-LEM almost completely blocked both the cytopathic effect of giant cell formation and specific antigen expression due to HIV, whereas LEM before ethanol precipitation blocked the expression of HIV antigen in MT-4 cells only at a high concentration. Pretreatment of the virus with E-P-LEM before infection blocked HIV infection in the target cells. Thus, the inhibitory effect of LEM and E-P-LEM on HIV could be due to a blocking of the initial stages of HIV infection. Moreover, reverse transcriptase activity of avian myeloblastosis virus was inhibited.
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PMID:Inhibition (in vitro) of replication and of the cytopathic effect of human immunodeficiency virus by an extract of the culture medium of Lentinus edodes mycelia. 317 37

The synthesis and processing of structural proteins of human immunodeficiency virus type 1 (HIV-1) were studied in infected cells treated with monensin and cerulenin. In MOLT-3 cells chronically infected with HTLV-IIIB, monensin inhibited the proteolytic cleavage of the env-coded polyprotein gp160 to gp120, leading to the accumulation of the precursor gp160. The formation of syncytia normally observed when CEM cells are cocultivated with HIV-1-infected MOLT-3 cells was significantly inhibited in the presence of monensin. The effect of the ionophore on the culture was reversible, as withdrawal of monensin from the medium restored the ability of the cells to form syncytia with CEM cells and led to the resumption of the processing of gp160 to gp120. Monensin did not affect the synthesis and processing of gag-coded proteins and regulatory proteins. Cerulenin, an inhibitor of de novo fatty acid biosynthesis, inhibited the myristoylation and the proteolytic cleavage of the gag-coded polyprotein Pr53gag to p24 but did not affect the processing of gp160. However, use for monensin and cerulenin as antiviral agents for treatment of HIV-1 infection cannot be foreseen because of the pronounced in vitro toxicity observed.
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PMID:Processing of the structural proteins of human immunodeficiency virus type 1 in the presence of monensin and cerulenin. 319 24


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