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  • 1
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    Expanded HIV-1 cellular tropism by phenotypic mixing with murine endogenous retroviruses (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-02-16
    Description: In view of the current interest in in vivo murine models for acquired immunodeficiency syndrome (AIDS), the interaction between human immunodeficiency virus type 1 (HIV-1) and endogenous murine leukemia virus (MuLV)-related retroviruses was investigated with a human leukemic T cell line (PF-382x) that acquired xenotropic MuLV (X-MuLV) after in vivo passage in immunosuppressed mice. Despite similar levels of membrane CD4 expression and HIV-1 125I-labeled gp 120 binding, a dramatic acceleration in the time course of HIV-1 infection was observed in PF-382x compared to its X-MuLV-negative counterpart (PF-382). Moreover, PF-382 cells coinfected by X-MuLV and HIV-1 generated a progeny of phenotypically mixed viral particles, enabling HIV-1 to productively infect a panel of CD4- human cells, including B lymphoid cells and purified normal peripheral blood CD4-/CD8+ T lymphocytes. Mixed viral phenotypes were also produced by human CD4+ T cells coinfected with an amphotropic MuLV-related retrovirus (A-MuLV) and HIV-1. These data show that endogenous MuLV acquired by human cells transplanted into mice can significantly interact with HIV-1, thereby inducing important alterations of HIV-1 biological properties.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lusso, P -- di Marzo Veronese, F -- Ensoli, B -- Franchini, G -- Jemma, C -- DeRocco, S E -- Kalyanaraman, V S -- Gallo, R C -- New York, N.Y. -- Science. 1990 Feb 16;247(4944):848-52.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Tumor Cell Biology, National Cancer Institute, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2305256" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/immunology ; Animals ; Antibodies, Monoclonal ; Antigens, CD4/analysis ; Cell Line ; Cell Transformation, Viral ; Disease Models, Animal ; HIV-1/*genetics/physiology ; Hematopoietic Stem Cells/cytology/microbiology ; Humans ; Mice ; Phenotype ; Retroviridae/*genetics ; Viral Proteins/analysis ; Virus Replication
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Hydroxyurea as an inhibitor of human immunodeficiency virus-type 1 replication (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-11-04
    Description: Hydroxyurea, a drug widely used in therapy of several human diseases, inhibits deoxynucleotide synthesis--and, consequently, DNA synthesis--by blocking the cellular enzyme ribonucleotide reductase. Hydroxyurea inhibits human immunodeficiency virus-type 1 (HIV-1) DNA synthesis in activated peripheral blood lymphocytes by decreasing the amount of intracellular deoxynucleotides, thus suggesting that this drug has an antiviral effect. Hydroxyurea has now been shown to block HIV-1 replication in acutely infected primary human lymphocytes (quiescent and activated) and macrophages, as well as in blood cells infected in vivo obtained from individuals with acquired immunodeficiency syndrome (AIDS). The antiviral effect was achieved at nontoxic doses of hydroxyurea, lower than those currently used in human therapy. Combination of hydroxyurea with the nucleoside analog didanosine (2',3'-dideoxyinosine, or ddl) generated a synergistic inhibitory effect without increasing toxicity. In some instances, inhibition of HIV-1 by hydroxyurea was irreversible, even several weeks after suspension of drug treatment. The indirect inhibition of HIV-1 by hydroxyurea is not expected to generate high rates of escape mutants. Hydroxyurea therefore appears to be a possible candidate for AIDS therapy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lori, F -- Malykh, A -- Cara, A -- Sun, D -- Weinstein, J N -- Lisziewicz, J -- Gallo, R C -- New York, N.Y. -- Science. 1994 Nov 4;266(5186):801-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Tumor Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892-4255.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973634" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/drug therapy/immunology/virology ; Cell Survival/drug effects ; DNA Replication/drug effects ; DNA, Viral/analysis/biosynthesis ; Didanosine/pharmacology ; Dose-Response Relationship, Drug ; Drug Synergism ; HIV Core Protein p24/analysis ; HIV-1/*drug effects/physiology ; Humans ; Hydroxyurea/*pharmacology ; Leukocytes, Mononuclear/drug effects/*virology ; Lymphocyte Activation ; Macrophage Activation ; Macrophages/drug effects/*virology ; Virus Replication/*drug effects ; Zidovudine/pharmacology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 3
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    EPA dioxin reassessment (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-12-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bradfield, C A -- Gallo, M A -- Gasiewicz, T A -- Greenberg, R S -- Greenlee, W F -- Margolick, J -- Mattison, D R -- Munson, P -- Neal, R A -- Okey, A B -- New York, N.Y. -- Science. 1994 Dec 9;266(5191):1628-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7992038" target="_blank"〉PubMed〈/a〉
    Keywords: *Carcinogens ; Dioxins/*adverse effects ; Humans ; Risk Assessment ; United States ; United States Environmental Protection Agency
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 4
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    Identification of a major growth factor for AIDS-Kaposi's sarcoma cells as oncostatin M (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-03-13
    Description: Conditioned medium from human T cell leukemia virus type 2 (HTLV-II)-infected T cells supports the growth and long-term culture of cells derived from acquired immunodeficiency syndrome (AIDS)-associated Kaposi's sarcoma lesions (AIDS-KS cells). A protein of 30 kilodaltons was purified from conditioned medium that supports the growth of AIDS-KS cells. The amino-terminal sequence of this protein was identical to the amino-terminal sequence of Oncostatin M, a glycoprotein that inhibits the growth of a variety of cancer cells. Oncostatin M from conditioned medium stimulated a twofold increase in the growth of AIDS-KS cells at a concentration of less than 1 nanogram of the protein per milliliter of medium.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nair, B C -- DeVico, A L -- Nakamura, S -- Copeland, T D -- Chen, Y -- Patel, A -- O'Neil, T -- Oroszlan, S -- Gallo, R C -- Sarngadharan, M G -- N01-CO-74101/CO/NCI NIH HHS/ -- N01-CP-73723/CP/NCI NIH HHS/ -- New York, N.Y. -- Science. 1992 Mar 13;255(5050):1430-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, Advanced BioScience Laboratories, Inc., Kensington, MD.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1542792" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/*complications ; Amino Acid Sequence ; Culture Media/chemistry ; Growth Substances/isolation & purification/*physiology ; Humans ; Molecular Sequence Data ; Oncostatin M ; Peptides/isolation & purification/*physiology ; Sarcoma, Kaposi/etiology/*pathology ; Tumor Cells, Cultured
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    Inhibition of development of Kaposi's sarcoma-related lesions by a bacterial cell wall complex (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-03-13
    Description: In vitro and in vivo model systems for the study of human immunodeficiency virus (HIV)-associated Kaposi's sarcoma (KS) were used to evaluate compounds for their potential as therapeutic agents. A sulfated polysaccharide-peptidoglycan compound (SP-PG) produced by bacteria controlled the in vitro growth of acquired immunodeficiency syndrome (AIDS)-associated, KS-derived spindle-shaped cells (AIDS-KS cells) at noncytotoxic concentrations. Angiogenesis induced by AIDS-KS cells in the chicken chorioallantoic membrane assay was blocked by SP-PG, which also inhibited the vascular hyperpermeability response and the angiogenesis associated with the induction of KS-like lesions that develop after subcutaneous inoculation of AIDS-KS cells into nude mice. Suramin, pentosan polysulfate, and interferon alpha, which are currently in use for therapy of KS, were either less effective than SP-PG or much more cytotoxic, or both.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nakamura, S -- Sakurada, S -- Salahuddin, S Z -- Osada, Y -- Tanaka, N G -- Sakamoto, N -- Sekiguchi, M -- Gallo, R C -- New York, N.Y. -- Science. 1992 Mar 13;255(5050):1437-40.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Internal Medicine, University of Southern California, Los Angeles 90033.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1371891" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/complications ; Animals ; Arthrobacter ; Arylsulfatases ; Capillary Permeability/drug effects ; Cell Division/drug effects ; Cells, Cultured ; Endothelium, Vascular/cytology/drug effects ; Fibroblasts/drug effects ; Humans ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Neoplasm Transplantation ; Neovascularization, Pathologic/*prevention & control ; *Peptidoglycan ; Polysaccharides/*pharmacology ; Sarcoma, Kaposi/etiology/*pathology ; Tumor Cells, Cultured
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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