Changes in human immunodeficiency virus type 1 envelope glycoproteins responsible for the pathogenicity of a multiply passaged simian-human immunodeficiency virus (SHIV-HXBc2)

Mark Cayabyab, Gunilla B. Karlsson, Bijan A. Etemad-Moghadam, Wolfgang Hofmann, Tavis Steenbeke, Matilda Halloran, John W. Fanton, Michael Axthelm, Norman L. Letvin, Joseph G. Sodroski

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    Abstract

    In vivo passage of a poorly replicating, nonpathogenic simian-human immunodeficiency virus (SHIV-HXBc2) generated an efficiently replicating virus, KU-1, that caused rapid CD4+ T-lymphocyte depletion and AIDS-like illness in monkeys (S. V. Joag, Z. Li, L. Foresman, E. B. Stephens, L.-J. Zhao, I. Adany, D. M. Pinson, H. M. McClure, and O. Narayan, J. Virol. 70:3189-3197, 1996). The env gene of the KU-1 virus was used to create a molecularly cloned virus, SHIV-HXBc2P 3.2, that differed from a nonpathogenic SHIV-HXBc2 virus in only 12 envelope glycoprotein residues. SHIV-HXBc2P 3.2 replicated efficiently and caused rapid and persistent CD4+ T-lymphocyte depletion in inoculated rhesus macaques. Compared with the envelope glycoproteins of the parental SHIV-HXBc2, the SHIV-HXBc2P 3.2 envelope glycoproteins supported more efficient infection of rhesus monkey peripheral blood mononuclear cells. Both the parental SHIV-HXBc2 and the pathogenic SHIV-HXBc2P 3.2 used CXCR4 but none of the other seven transmembrane segment receptors tested as a second receptor. Compared with the parental virus, viruses with the SHIV-HXBc2P 3.2 envelope glycoproteins were more resistant to neutralization by soluble CD4 and antibodies. Thus, changes in the envelope glycoproteins account for the ability of the passaged virus to deplete CD4+ T lymphocytes rapidly and specify increased replicative capacity and resistance to neutralization.

    Original languageEnglish (US)
    Pages (from-to)976-984
    Number of pages9
    JournalJournal of Virology
    Volume73
    Issue number2
    StatePublished - 1999

    Fingerprint

    Simian Immunodeficiency Virus
    Human immunodeficiency virus
    Human immunodeficiency virus 1
    Virulence
    HIV-1
    glycoproteins
    Glycoproteins
    pathogenicity
    HIV
    Viruses
    viruses
    Lymphocyte Depletion
    T-lymphocytes
    Macaca mulatta
    T-Lymphocytes
    neutralization
    env Genes
    receptors
    mononuclear leukocytes
    Haplorhini

    ASJC Scopus subject areas

    • Immunology

    Cite this

    Cayabyab, M., Karlsson, G. B., Etemad-Moghadam, B. A., Hofmann, W., Steenbeke, T., Halloran, M., ... Sodroski, J. G. (1999). Changes in human immunodeficiency virus type 1 envelope glycoproteins responsible for the pathogenicity of a multiply passaged simian-human immunodeficiency virus (SHIV-HXBc2). Journal of Virology, 73(2), 976-984.

    Changes in human immunodeficiency virus type 1 envelope glycoproteins responsible for the pathogenicity of a multiply passaged simian-human immunodeficiency virus (SHIV-HXBc2). / Cayabyab, Mark; Karlsson, Gunilla B.; Etemad-Moghadam, Bijan A.; Hofmann, Wolfgang; Steenbeke, Tavis; Halloran, Matilda; Fanton, John W.; Axthelm, Michael; Letvin, Norman L.; Sodroski, Joseph G.

    In: Journal of Virology, Vol. 73, No. 2, 1999, p. 976-984.

    Research output: Contribution to journalArticle

    Cayabyab, M, Karlsson, GB, Etemad-Moghadam, BA, Hofmann, W, Steenbeke, T, Halloran, M, Fanton, JW, Axthelm, M, Letvin, NL & Sodroski, JG 1999, 'Changes in human immunodeficiency virus type 1 envelope glycoproteins responsible for the pathogenicity of a multiply passaged simian-human immunodeficiency virus (SHIV-HXBc2)', Journal of Virology, vol. 73, no. 2, pp. 976-984.
    Cayabyab, Mark ; Karlsson, Gunilla B. ; Etemad-Moghadam, Bijan A. ; Hofmann, Wolfgang ; Steenbeke, Tavis ; Halloran, Matilda ; Fanton, John W. ; Axthelm, Michael ; Letvin, Norman L. ; Sodroski, Joseph G. / Changes in human immunodeficiency virus type 1 envelope glycoproteins responsible for the pathogenicity of a multiply passaged simian-human immunodeficiency virus (SHIV-HXBc2). In: Journal of Virology. 1999 ; Vol. 73, No. 2. pp. 976-984.
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    abstract = "In vivo passage of a poorly replicating, nonpathogenic simian-human immunodeficiency virus (SHIV-HXBc2) generated an efficiently replicating virus, KU-1, that caused rapid CD4+ T-lymphocyte depletion and AIDS-like illness in monkeys (S. V. Joag, Z. Li, L. Foresman, E. B. Stephens, L.-J. Zhao, I. Adany, D. M. Pinson, H. M. McClure, and O. Narayan, J. Virol. 70:3189-3197, 1996). The env gene of the KU-1 virus was used to create a molecularly cloned virus, SHIV-HXBc2P 3.2, that differed from a nonpathogenic SHIV-HXBc2 virus in only 12 envelope glycoprotein residues. SHIV-HXBc2P 3.2 replicated efficiently and caused rapid and persistent CD4+ T-lymphocyte depletion in inoculated rhesus macaques. Compared with the envelope glycoproteins of the parental SHIV-HXBc2, the SHIV-HXBc2P 3.2 envelope glycoproteins supported more efficient infection of rhesus monkey peripheral blood mononuclear cells. Both the parental SHIV-HXBc2 and the pathogenic SHIV-HXBc2P 3.2 used CXCR4 but none of the other seven transmembrane segment receptors tested as a second receptor. Compared with the parental virus, viruses with the SHIV-HXBc2P 3.2 envelope glycoproteins were more resistant to neutralization by soluble CD4 and antibodies. Thus, changes in the envelope glycoproteins account for the ability of the passaged virus to deplete CD4+ T lymphocytes rapidly and specify increased replicative capacity and resistance to neutralization.",
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    AU - Etemad-Moghadam, Bijan A.

    AU - Hofmann, Wolfgang

    AU - Steenbeke, Tavis

    AU - Halloran, Matilda

    AU - Fanton, John W.

    AU - Axthelm, Michael

    AU - Letvin, Norman L.

    AU - Sodroski, Joseph G.

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