Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A recently developed tetrazolium-based microculture assay was used to screen extracts of cultured cyanobacteria (blue-green algae) for inhibition of the cytopathic effects of the human immunodeficiency virus (HIV-1), which is implicated as a causative agent of AIDS. A number of extracts were found to be remarkably active against the AIDS virus. A new class of HIV-1-inhibitory compounds, the sulfonic acid-containing glycolipids, was discovered through the use of the microculture assay to guide the fractionation and purification process. The pure compounds were active against HIV-1 in cultured human lymphoblastoid CEM, MT-2, LDV-7, and C3-44 cell lines in the tetrazolium assay as well as in p24 viral protein and syncytium formation assays.
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PMID:AIDS-antiviral sulfolipids from cyanobacteria (blue-green algae). 250 35

We examined the structural variability of the external glycoprotein (gp130) of a cloned simian immunodeficiency virus (SIV) in culture. Cloned SIVmac142 was either permanently propagated in HUT-78 cells or sequentially passaged in MT-2 cells. After 12, 24 and 60 passages of permanent or lytic cell-culture systems, virus was harvested, gp130 was isolated and peptide mapped. Comparison of gp130 peptide maps of SIVmac142 by computer graphic analysis revealed a variation in relative spot intensity of up to 20%. No major variability of gp130 was observed in SIVmac142 propagated in HUT-78 cells (i.e. without cytopathic effect induction) in up to 60 passages. However, in MT-2 cells, which are lysed by this virus, gp130 exhibited significant variability and displayed six additional fragments in peptide maps after 24 passages. Peptide map of SIVmac142 gp130 obtained after 60 passages in MT-2 cells was comparable to that after 24 passages. Alterations in the intensity of certain spots indicated changes in the composition of the replicating virus population.
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PMID:Structural variability of the external glycoprotein of simian immunodeficiency virus propagated in cell cultures. 250 10

The in vitro effects of recombinant human interferon-beta ser (rIFN-beta ser) and 3'-azido-3'-deoxythymidine (AZT) alone and in combination on human immunodeficiency virus (HIV) replication were examined. rIFN-beta ser inhibited HIV progeny virus synthesis in cell cultures chronically infected with HIV. When used in combination, suboptimally effective concentrations of rIFN-beta ser and AZT synergistically inhibited HIV-mediated syncytium formation in HeLa T4 cell cultures. Whereas AZT alone reduced HIV replication in human MT-2 cells, addition of low concentrations of rIFN-beta ser reduced by 4- to 1,000-fold the amount of AZT required to maximally block HIV p24 antigen synthesis and HIV-mediated cell lysis. No drug-related cytoxicity was observed when the two agents were used together at and above maximally effective concentrations. These results suggest that a safer, yet effective, therapy for HIV infections may be achieved with reduced doses of AZT in combination with rIFN-beta ser.
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PMID:Recombinant human interferon-beta suppresses the replication of HIV and acts synergistically with AZT. 251 33

The effect of centrifugal inoculation of human immunodeficiency virus (HIV) and human herpesvirus-6 (HHV-6) on the infectivity of the viruses for cell cultures was examined. Three HIV-1 strains, ARV-2, HTLV-IIIb and a local isolate, WA-46c, were tested in peripheral blood lymphocytes, HUT-78, H9 and MT-2 cells. The HHV-6 strain was a local isolate and was studied only in peripheral blood lymphocyte cultures. Centrifugal inoculation of the viruses at a force of 2500 x g for 60 min, enhanced HIV-1 infectivity by a factor of about 10-fold in all cell cultures tested. Infectivity was increased about 100-fold for HHV-6.
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PMID:Centrifugal enhancement of human immunodeficiency virus (HIV) and human herpesvirus type 6 (HHV-6) infection in vitro. 266 17

The antiviral activity of mismatched dsRNA of the form poly(I):poly(C12-U)n (Ampligen) against the human immunodeficiency virus type 1 (HIV-1) was investigated by RNA-RNA and RNA-DNA hybridizations. Mismatched dsRNA delayed the appearance of newly transcribed HIV-1 RNA as detected by liquid dot-blot hybridization in cultures of H9 T-lymphoblastoid cells following virus challenge. The appearance of proviral DNA as detected by Southern hybridization following virus challenge in H9 cells was also delayed. Mismatched dsRNA had no effect in syncytium inhibition assays performed by fusing MT-2 cells with H9/HTLV-IIIB cells. These results suggest that the in vitro anti-HIV-1 activity of mismatched dsRNA occurs, at least in part, at an early stage in the viral replication cycle following initial gp120-CD4 binding.
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PMID:Inhibition of HIV-1 proviral DNA synthesis and RNA accumulation by mismatched dsRNA. 278 55

Human immunodeficiency virus (HIV), the etiologic agent of acquired immunodeficiency syndrome (AIDS), was rapidly cytopathic to SKT-1B, a cell line established from a patient with adult T cell leukemia, in vitro. This cytopathic effect was preceded by the expression of HIV antigen, defined with a monoclonal antibody (mAb) specific for the core protein (p24) of HIV. SKT-1B is highly susceptible to HIV as compared with MT-2 and H9 cells. HIV is known to be transmitted via blood products, and thus we examined whether or not currently used procedures for manufacturing blood products are safe by using SKT-1B. Lyophilized HIV was heated at 65 degrees for time periods in the range of 10 min to 48 hr, and the infectivity was examined. The results showed that heating at 65 degrees for less than 2 hr was not sufficient to inactivate HIV, but the virus heated for 48 hr had no effect on SKT-1B. In addition, HIV completely lost its infectivity on sulfonation, which is commonly used to avoid anaphylactic shock on intravenous infusion of human immunoglobulins. These findings indicate that blood products manufactured by currently used procedures are probably safe with respect to HIV infection.
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PMID:Evaluation of the safety of blood products with respect to human immunodeficiency virus infection by using an HTLV-I-infected cell line (SKT-1B). 288 6

The ultrastructural features of early events in human immunodeficiency virus (HIV) infection of HTLV-I-carrying MT-2 lymphocytes were investigated by electron microscopy. Within 10 min after virus inoculation at 37 degrees C, the virus entered the cell in two ways; (1) the virus attached to the lymphocyte membrane and the viral core entered the cell after fusion of the viral envelope with the cell membrane, and (2) part of the cell membrane to which the virus was attached became invaginated, the virus became trapped in a phagosome and the viral core entered after the fusion of viral membrane with the vacuolar membrane. Thereafter, some cells were observed to form syncytia with multiple nuclei. When the proportion of anti-HIV antibody-reactive cells present exceeded 90%, virus production was strongly activated, and budding on the cell membrane was frequently observed.
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PMID:Entry of human immunodeficiency virus (HIV) into MT-2, human T cell leukemia virus carrier cell line. 290 53

Mismatched double-stranded RNA of the form r(I)n.r(C12-U)n (Ampligen) has been shown to be active against human immunodeficiency virus type 1 (HIV-1) using CEM and C3 cells as targets for infection by the highly similar HIV-1 isolates HTLV-IIIB and LAV (Montefiori, D.C. and Mitchell, W.M., 1987, Proc. Natl. Acad. Sci. U.S.A., 84, 2985-2989). The scope of Ampligen's anti-HIV-1 activity was examined in this study using the genetically divergent HIV-1 isolate HTLV-IIIRF, two additional target T-cell lines, H9 and MT-2, and a monocyte/macrophage cell line, U937. As judged by indirect immunofluorescence, reverse transcriptase activity and vital dye uptake, Ampligen was active against HTLV-IIIRF in H9, MT-2, C3 and U937 cells in addition to being active against HTLV-IIIB in U937 cells. A minimum of 1 h preincubation of cells (MT-2) with Ampligen was required for maximum activity. These results suggest that Ampligen's potential clinical efficacy may not be limited by either the highly variable nature or host cell range of HIV-1.
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PMID:Mismatched dsRNA (ampligen) induces protection against genomic variants of the human immunodeficiency virus type 1 (HIV-1) in a multiplicity of target cells. 296 77

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

Both 2',3'-dideoxyadenosine and 2',3'-dideoxyinosine have been shown (Mitsuya, H., and Broder, S. (1987) Nature 325, 773-778) to have in vitro activity against the human immunodeficiency virus-1 (HIV). However, these dideoxynucleosides may be catabolized by human T cells, even when adenosine deaminase is inhibited by deoxycoformycin. To overcome this problem, we have synthesized the 2-fluoro-, 2-chloro-, and 2-bromo-derivatives of 2',3'-dideoxyadenosine. The metabolism and anti-HIV activity of the 2-halo-2',3'-dideoxyadenosine derivatives and of 2',3'-dideoxyadenosine were compared. The 2-halo-2',3'-dideoxyadenosine derivatives were not deaminated significantly by cultured CEM T lymphoblasts. Experiments with 2-chloro-2',3'-dideoxyadenosine showed that the T cells converted the dideoxynucleoside to the 5'-monophosphate, 5'-diphosphate, and 5'-triphosphate metabolites. At concentrations lower than those producing cytotoxicity in uninfected cells (3-10 microM), the 2-halo-2',3-dideoxyadenosine derivatives inhibited the cytopathic effects of HIV toward MT-2 T lymphoblasts, and retarded viral replication in CEM T lymphoblasts. Experiments with a deoxycytidine kinase-deficient mutant CEM T cell line showed that this enzyme was necessary for the phosphorylation and anti-HIV activity of the 2-chloro-2',3'-dideoxyadenosine. In contrast, 2',3'-dideoxyadenosine was phosphorylated by the deoxycytidine kinase-deficient mutant and retained anti-HIV activity in this cell line. Thus, the 2-halo derivatives of 2',3'-dideoxyadenosine, in contrast to 2',3'-dideoxyadenosine itself, are not catabolized by T cells. Their anti-HIV and anti-proliferative activities are manifest only in cells expressing deoxycytidine kinase. The in vivo implications of these results for anti-HIV chemotherapy are discussed.
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PMID:Metabolism and anti-human immunodeficiency virus-1 activity of 2-halo-2',3'-dideoxyadenosine derivatives. 325 2


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