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      Sulphated Polymers are Potent and Selective Inhibitors of Various Enveloped Viruses, Including Herpes Simplex Virus, Cytomegalovirus, Vesicular Stomatitis Virus, Respiratory Syncytial Virus, and Toga-, Arena- and Retroviruses

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          Rapid and automated tetrazolium-based colorimetric assay for the detection of anti-HIV compounds.

          A rapid, sensitive and automated assay procedure was developed for the in vitro evaluation of anti-HIV agents. An HTLV-I transformed T4-cell line, MT-4, which was previously shown by Koyanagi et al. (1985) to be highly susceptible to, and permissive for, HIV infection, served as the target cell line. Inhibition of the HIV-induced cytopathic effect was used as the end point. The viability of both HIV- and mock-infected cells was assessed spectrophotometrically via the in situ reduction of 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT). The procedure was optimized as to make optimal use of multichannel pipettes, microprocessor-controlled dispensing and optical density reading. The absorbance ratio of the mock-infected control to the HIV-infected samples was about 20. This allowed an accurate determination of the 50% effective doses, as demonstrated for 3'-azido-2',3'-dideoxythymidine (AZT), 2',3'-dideoxycytidine (ddCyd), dextran sulfate and heparin. The technique significantly reduced labor time as compared to the trypan blue exclusion method, and permits the evaluation of large numbers of compounds for their anti-HIV activity.
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            Mechanism of inhibitory effect of dextran sulfate and heparin on replication of human immunodeficiency virus in vitro.

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              Role of the HTLV-III/LAV envelope in syncytium formation and cytopathicity.

              Acquired immune deficiency syndrome (AIDS) is characterized by marked depletion of the T4+ helper subset of T cells. The aetiological agent of the disease, the human T-lymphotropic virus type III (HTLV-III)/lymphadenopathy-associated virus (LAV), specifically kills T4+ cells in vitro. Part of this specificity for the T4+ population residues in the relative efficiency with which HTLV-III infects these cells, as a result of a specific interaction between the T4 molecule and the virus envelope glycoprotein. In addition, the cytotoxic consequences of HTLV-III replication are dependent on cell type, as certain lymphoid and myeloid cells can be productively infected without notable cytopathic effect. Here we investigate the basis for the specific cytotoxicity of the virus, and report that high-level expression of the HTLV-III envelope gene induces syncytia and concomitant cell death in T4+ cell lines but not in a B-lymphocyte line. Syncytium formation depends on the interaction of envelope-expressing cells with neighbouring cells bearing surface T4 molecules. These results explain, at least in part, the specific cytopathic effect of HTLV-III infections.
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                Author and article information

                Journal
                Antiviral Chemistry and Chemotherapy
                Antivir Chem Chemother
                SAGE Publications
                0956-3202
                2040-2066
                June 24 2016
                August 1990
                June 24 2016
                August 1990
                : 1
                : 4
                : 233-240
                Affiliations
                [1 ] Department of Colloid Science, Eötvös Loránd University, Budapest, Hungary
                [2 ] 2nd Institute of Biochemistry, Semmelweis University Medical School, Budapest, Hungary
                [3 ] Chemical Works of Gedeon Richter Ltd, Budapest, Hungary
                Article
                10.1177/095632029000100402
                3f693bd0-5f82-4d2c-ac2b-5b5563bb9ad9
                © 1990

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