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

The effect of culture supernatant of MT-2 cells on human immunodeficiency virus (HIV)-producing cells, MOLT-4/HIVHTLV-IIIB cells, was examined. As compared to the effect on MOLT-4 cells, parent cells not infected with HIV, a selective cytotoxic/cytostatic effect on MOLT-4/HIVHTLV-IIIB cells was observed 4 days after treatment with up to 640-fold-diluted MT-2 supernatant. Furthermore, under similar conditions, a 2- to 6-fold increase in the number of HIV particles was detected in the culture of MOLT-4/HIVHTLV-IIIB cells 6 hr after treatment. Complete blocking of these effects by anti-lymphotoxin monoclonal antibody, but not by anti-tumor necrosis factor antibody, indicates that these effects of MT-2 supernatant on MOLT-4/HIVHTLV-IIIB cells are attributable to a lymphotoxin-related cytotoxic factor.
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PMID:Effect of culture supernatant of MT-2 cells on human immunodeficiency virus-producing cells, MOLT-4/HIVHTLV-IIIB cells. 313 Mar 48

Simian immunodeficiency virus (SIV) was isolated from the total peripheral blood mononuclear cell population and the monocyte-macrophage adherent cell population of three seropositive green monkeys originating from Kenya. SIV from these African green monkeys (SIVagm) was isolated and continuously produced with the MOLT-4 clone 8 (M4C18) cell line but not with a variety of other cells including HUT-78, H9, CEM, MT-4, U937, and uncloned MOLT-4 cells. Once isolated, these SIVagm isolates were found to replicate efficiently in M4C18, SupT1, MT-4, U937, and Jurkat-T cells but much less efficiently if at all in HUT-78, H9, CEM, and MOLT-4 cells. The range of CD4+ cells fully permissive for replication of these SIVagm isolates thus differs markedly from that of previous SIV isolates from macaques (SIVmac). These SIVagm isolates had a morphogenesis and morphology like that of human immunodeficiency virus (HIV) and other SIV isolates. Antigens of SIVagm and SIVmac cross-reacted by comparative enzyme-linked immunosorbent assay only with reduced efficiency, and optimal results were obtained when homologous antibody and antigen were used. Western blotting (immunoblotting) of purified preparations of SIVagm isolate 385 (SIVagm385) revealed major viral proteins of 120, 27, and 16 kilodaltons (kDa). The presumed major core protein of 27 kDa cross-reacted antigenically with the corresponding proteins of SIVmac (28 kDa) and HIV-1 (24 kDa) by Western blotting. Hirt supernatant replicative-intermediate DNA prepared from cells freshly infected with SIVagm hybridized to SIVmac and HIV-2 DNA probes. Detection of cross-hybridizing DNA sequences, however, required very low stringency, and the restriction endonuclease fragmentation patterns of SIVagm were not similar to those of SIVmac and HIV-2. The nucleotide sequence of a portion of the pol gene of SIVagm385 revealed amino acid identities of 65% with SIVmac142, 64% with HIV-2ROD, and 56% with HIV-1BRU; SIVagm385 is thus related to but distinct from previously described primate lentiviruses SIVmac, HIV-1, and HIV-2. Precise information on the genetic makeup of these and other SIV isolates will possibly lead to better understanding of the history and evolution of these viruses and may provide insight into the origin of viruses that cause acquired immunodeficiency syndrome in humans.
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PMID:Simian immunodeficiency virus from African green monkeys. 317 40

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

Glycyrrhizin (GL) achieved a dose-dependent inhibition of the replication of human immunodeficiency virus type 1 (HIV-1) in MOLT-4 (clone No. 8) cells within the concentration range of 0.075 to 0.6 mM. Within this concentration range, GL also effected a dose-dependent reduction in the protein kinase C (PKC) activity of MOLT-4 (clone No. 8) cells. A well-known PKC inhibitor, 1-(5-isoquinolinesulfonyl)-2-methylpiperazine dihydrochloride (H-7), also proved inhibitory to HIV-1 replication in MOLT-4 (clone No. 8) cells. PKC inhibition may thus be considered as one of the mechanisms by which GL inhibits HIV-1 replication. In addition, GL may also owe its anti-HIV-1 activity, at least in part, to an interference with virus-cell binding, since the compound at 1.2 mM partially inhibited the adsorption of radiolabeled HIV-1 particles to MT-4 cells. At this concentration GL also suppressed giant cell formation induced by co-culturing MOLT-4 (clone No. 8) cells with MOLT-4/HTLV-IIIB cells, whereas the PKC inhibitor H-7 failed to do so.
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PMID:Mechanism of inhibitory effect of glycyrrhizin on replication of human immunodeficiency virus (HIV). 325 Mar 33

The effect of natural lymphotoxin (n-LT) on CD4+ MOLT-4 cells and those cells producing human immunodeficiency virus (HIV), MOLT-4/HIVHTLV-IIIB cells, was studied. Four days after treatment with n-LT, a significant cytotoxic/cytostatic effect was observed predominantly on MOLT-4/HIVHTLV-IIIB cells. Furthermore, with regard to the production of HIV, an almost 3- to 5-fold increase of viral particles was observed in MOLT-4/HIVHTLV-IIIB cells 6 h after treatment with n-LT. These data indicate the possibility that this cytotoxic factor is one of the responsible molecules in the pathogenesis of the acquired immunodeficiency syndrome (AIDS).
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PMID:Enhancement of human immunodeficiency virus production by natural lymphotoxin. 326 93

We reported previously that TPA facilitates the replication of human immunodeficiency virus (HIV) and has a selective lethal effect on HIV-infected cells by a cytopathic effect induced by HIV. We have now studied the cytopathic effects of TPA-type tumor promoters (teleocidin, aplysiatoxin, and TPA) and the non-TPA type tumor promoters (palytoxin and thapsigargin) on MOLT-4/HIVHTLV-IIIB cells. All TPA-type and non-TPA type tumor promoters tested except palytoxin stimulated in HIV production three- to sevenfold, and caused more lysis of MOLT-4/HIVHTLV-IIIB cells than of the parental MOLT-4 cells. Fifty percent of the MOLT-4/HIVHTLV-IIIB cells were killed by teleocidin, aplysiatoxin, TPA and thapsigargin at concentrations of 2.0, 2.0, 1.0 and 10 ng/ml respectively, and by palytoxin at the very low concentration of 2.0 pg/ml. Moreover, combinations of one TPA-type tumor promoter and one non-TPA type tumor promoter--but not the combination of two TPA-type tumor promoters--had additive lethal effects, supporting the idea that TPA-type and non-TPA type tumor promoters exert their cytolytic effects by different mechanisms. These latter effects may be due to production of prostaglandin E2, which is commonly induced by both types of tumor promoters.
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PMID:Lysis of human immunodeficiency virus infected cells by TPA-type and non-TPA type tumor promoters. 336 59

Immunoglobulin samples (HIV-Ig) were prepared by cold ethanol fractionation of human plasma containing antibody against human immunodeficiency virus (HIV). The ability to prevent viral spreading was studied using either human T-cell leukemia virus type I (HTLV-I)-carrying MT-4 cells or in a coculture system using MOLT-4 cells and virus-producing MOLT-4/HIV HTLV-IIIB cells. Treatment of HIV-infected MT-4 cells with HIV-Ig effectively blocked the appearance of antigens of HIV and the virus-induced cytopathic effect. HIV-Ig blocked multinucleated giant cell formation in the MOLT-4 and MOLT-4/HIV HTLV-IIIB coculture system.
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PMID:Efficacy of an immunoglobulin preparation from HIV carriers in preventing HIV replication in vitro. 336 35

Cocultivation of MOLT-4 and MOLT-4/HIVHTLV-IIIB cells induces syncytium formation very efficiently and is an appropriate model for evaluation of various substances which might inhibit human immunodeficiency virus (HIV)-induced multinucleated giant cell formation in vitro. We attempted here to quantify the grade of the syncytium formation by using a cell multisizer. The size distribution pattern of the cocultivated cells in the presence of glycyrrhizin sulfate, polysaccharide Krestin, dextran sulfate, ribofuranan sulfate, and lentinan sulfate was indistinguishable from that of cocultured cells grown in the absence of inhibitors. However, the pattern of cocultured cells without an inhibitor was quite different from that of MOLT-4 or MOLT-4/HIVHTLV-IIIB cells alone. Moreover, the size distribution pattern of cocultured cells after treatment with two nucleoside analogs, 3'-azido-2',3'-dideoxythymidine and 2',3'-didehydro-2',3'-dideoxythymidine, which were known to inhibit cell-free but not cell-to-cell infection, was similar to that of cocultured cells without an inhibitor. These data are well correlated with the fusion index which was reported previously. Application of the cell multisizer is very quantitative for evaluating the syncytium formation induced by HIV and providing a simple and rapid screening for anti-HIV substances, especially for virus-induced cell fusion.
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PMID:Rapid screening method with a cell multisizer for inhibitors of human immunodeficiency virus-induced cell fusion in vitro. 338 35

HIVYU-6 and HIVYU-7 were isolated from an acquired immune deficiency syndrome patient (MK) and his asymptomatic sexual partner (MM), respectively. YU-6 readily infected not only peripheral lymphocytes from normal individuals but also human T-cell lines such as H9, HUT-78, MOLT-4 and MT-4; YU-7, on the other hand, could not infect H9 and MT-4 cells. Furthermore, although autologous serum failed to neutralize YU-6, it was neutralized by the heterologous serum from the partner. Restriction endonuclease analysis of YU-6 demonstrated that it was a mixture of viruses. We have isolated two clones from YU-6 (YU-6-a and YU-6-b) by a plaque assay method and showed that YU-6-a had one more KpnI site than YU-6-b. It was also evident that YU-7 derived from YU-6-a, but had already shifted genetically from YU-6-a. Transmission of human immunodeficiency virus through heterosexual contact and a possible genetic shift of YU-6-a, b and YU-7 from a common progenitor virus in vivo is discussed.
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PMID:Transmission and genetic shift of human immunodeficiency virus (HIV) in vivo. 350 21


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