Viral burden and disease progression in rhesus monkeys infected with chimeric simian-human immunodeficiency viruses

Keith A. Reimann, Andrew Watson, Peter J. Dailey, Wenyu Lin, Carol I. Lord, Tavis D. Steenbeke, Robert A. Parker, Michael Axthelm, Gunilla B. Karlsson

    Research output: Contribution to journalArticle

    48 Citations (Scopus)

    Abstract

    To determine the role of viral burden in simian-human immunodeficiency virus (SHIV)-induced disease, cellular provirus and plasma viral RNA levels were measured after inoculation of rhesus monkeys with four different SHIVs. These SHIVs included SHIV-HXBc2 and SHIV-89.6, constructed with env, tat, rev, and vpu derived from either cell line-passaged or primary patient isolates of human immunodeficiency virus type 1; the viral quasispecies SHIV- 89.6P derived after in vivo passage of SHIV-89.6; and a molecular clone, SHIV-KB9, derived from SHIV-89.6P. SHIV-HXBc2 and SHIV-89.6 are nonpathogenic in rhesus monkeys; SHIV-89.6P and SHIV-KB9 cause rapid CD4+ T cell depletion and an immunodeficiency syndrome. Relative SHIV provirus levels were highest during primary infection in monkeys infected with SHIV-89.6P, the virus that caused the most rapid and dramatic CD4+ T cell depletion. However, by 10 weeks postinoculation, provirus levels were similar in monkeys infected with the pathogenic and nonpathogenic chimeric viruses. The virus infections that resulted in the highest peak and chronic viral RNA levels were the pathogenic viruses SHIV-89.6P and SHIV-KB9. SHIV-89.6P uniformly caused rapid and profound CD4+ T cell depletion and immunodeficiency. Infection with the SHIV-KB9 resulted in very low CD4+ T cell counts without seroconversion in some monkeys and a substantial but less profound CD4+ T cell depletion and rapid seroconversion in others. Surprisingly, the level of plasma viremia did not differ between SHIV-KB9-infected animals exhibiting these contrasting outcomes, suggesting that host factors may play an important role in AIDS virus pathogenesis.

    Original languageEnglish (US)
    Pages (from-to)15-21
    Number of pages7
    JournalVirology
    Volume256
    Issue number1
    DOIs
    StatePublished - Mar 30 1999

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    Simian Immunodeficiency Virus
    Virus Diseases
    Macaca mulatta
    Viral Load
    Disease Progression
    HIV
    Proviruses
    T-Lymphocytes
    Haplorhini
    Viral RNA
    Viruses

    ASJC Scopus subject areas

    • Virology
    • Infectious Diseases

    Cite this

    Reimann, K. A., Watson, A., Dailey, P. J., Lin, W., Lord, C. I., Steenbeke, T. D., ... Karlsson, G. B. (1999). Viral burden and disease progression in rhesus monkeys infected with chimeric simian-human immunodeficiency viruses. Virology, 256(1), 15-21. https://doi.org/10.1006/viro.1999.9632

    Viral burden and disease progression in rhesus monkeys infected with chimeric simian-human immunodeficiency viruses. / Reimann, Keith A.; Watson, Andrew; Dailey, Peter J.; Lin, Wenyu; Lord, Carol I.; Steenbeke, Tavis D.; Parker, Robert A.; Axthelm, Michael; Karlsson, Gunilla B.

    In: Virology, Vol. 256, No. 1, 30.03.1999, p. 15-21.

    Research output: Contribution to journalArticle

    Reimann, KA, Watson, A, Dailey, PJ, Lin, W, Lord, CI, Steenbeke, TD, Parker, RA, Axthelm, M & Karlsson, GB 1999, 'Viral burden and disease progression in rhesus monkeys infected with chimeric simian-human immunodeficiency viruses', Virology, vol. 256, no. 1, pp. 15-21. https://doi.org/10.1006/viro.1999.9632
    Reimann, Keith A. ; Watson, Andrew ; Dailey, Peter J. ; Lin, Wenyu ; Lord, Carol I. ; Steenbeke, Tavis D. ; Parker, Robert A. ; Axthelm, Michael ; Karlsson, Gunilla B. / Viral burden and disease progression in rhesus monkeys infected with chimeric simian-human immunodeficiency viruses. In: Virology. 1999 ; Vol. 256, No. 1. pp. 15-21.
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    abstract = "To determine the role of viral burden in simian-human immunodeficiency virus (SHIV)-induced disease, cellular provirus and plasma viral RNA levels were measured after inoculation of rhesus monkeys with four different SHIVs. These SHIVs included SHIV-HXBc2 and SHIV-89.6, constructed with env, tat, rev, and vpu derived from either cell line-passaged or primary patient isolates of human immunodeficiency virus type 1; the viral quasispecies SHIV- 89.6P derived after in vivo passage of SHIV-89.6; and a molecular clone, SHIV-KB9, derived from SHIV-89.6P. SHIV-HXBc2 and SHIV-89.6 are nonpathogenic in rhesus monkeys; SHIV-89.6P and SHIV-KB9 cause rapid CD4+ T cell depletion and an immunodeficiency syndrome. Relative SHIV provirus levels were highest during primary infection in monkeys infected with SHIV-89.6P, the virus that caused the most rapid and dramatic CD4+ T cell depletion. However, by 10 weeks postinoculation, provirus levels were similar in monkeys infected with the pathogenic and nonpathogenic chimeric viruses. The virus infections that resulted in the highest peak and chronic viral RNA levels were the pathogenic viruses SHIV-89.6P and SHIV-KB9. SHIV-89.6P uniformly caused rapid and profound CD4+ T cell depletion and immunodeficiency. Infection with the SHIV-KB9 resulted in very low CD4+ T cell counts without seroconversion in some monkeys and a substantial but less profound CD4+ T cell depletion and rapid seroconversion in others. Surprisingly, the level of plasma viremia did not differ between SHIV-KB9-infected animals exhibiting these contrasting outcomes, suggesting that host factors may play an important role in AIDS virus pathogenesis.",
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