The MA (p15) and p12 Regions of the gag Gene Are Sufficient for the Pathogenicity of the Murine AIDS Virus

J.M. Pozsgay, Manfred Beilharz, B.D. Wines, A.D. Hess, P.M. Pitha

    Research output: Contribution to journalArticle

    25 Citations (Scopus)

    Abstract

    Inoculation of the replication-defective retrovirus DEF27 (BM5d), packaged as an amphotropic virus pseudotype, into C57BL/6J mice leads to development of murine AIDS. Disease development showed a long incubation period (20 to 24 weeks), was associated with amplification of the BM5d provirus in splenocytes and lymph nodes, and was independent of the presence of exogenous or endogenous replication-competent helper viruses. However, both the onset of disease and amplification of the defective provirus were significantly enhanced by coinfection with the replication-competent B-cell-tropic ecotropic helper virus BM5e. The part of the BM5d viral genome that was essential for the pathogenicity was determined by making precisely engineered alterations in the reading frame of the gag and pol genes of BM5d proviral DNA and examining the ability of the altered amphotropic BM5d pseudotypes to induce the disease in C57BL/6J mice. The results show that expression of the MA (p15) and p12 regions of the gag gene is sufficient for pathogenicity of the BM5d retrovirus.
    Original languageEnglish
    Pages (from-to)5989-5999
    JournalJournal of Virology
    Volume67
    Issue number10
    Publication statusPublished - 1993

    Fingerprint

    Murine Acquired Immunodeficiency Syndrome
    gag Genes
    Retroviridae
    Helper Viruses
    proviruses
    Virulence
    Proviruses
    pathogenicity
    HIV
    Inbred C57BL Mouse
    viruses
    mice
    pol Genes
    Reading Frames
    genes
    Viral Genome
    splenocytes
    Coinfection
    mixed infection
    B-lymphocytes

    Cite this

    Pozsgay, J.M. ; Beilharz, Manfred ; Wines, B.D. ; Hess, A.D. ; Pitha, P.M. / The MA (p15) and p12 Regions of the gag Gene Are Sufficient for the Pathogenicity of the Murine AIDS Virus. In: Journal of Virology. 1993 ; Vol. 67, No. 10. pp. 5989-5999.
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    abstract = "Inoculation of the replication-defective retrovirus DEF27 (BM5d), packaged as an amphotropic virus pseudotype, into C57BL/6J mice leads to development of murine AIDS. Disease development showed a long incubation period (20 to 24 weeks), was associated with amplification of the BM5d provirus in splenocytes and lymph nodes, and was independent of the presence of exogenous or endogenous replication-competent helper viruses. However, both the onset of disease and amplification of the defective provirus were significantly enhanced by coinfection with the replication-competent B-cell-tropic ecotropic helper virus BM5e. The part of the BM5d viral genome that was essential for the pathogenicity was determined by making precisely engineered alterations in the reading frame of the gag and pol genes of BM5d proviral DNA and examining the ability of the altered amphotropic BM5d pseudotypes to induce the disease in C57BL/6J mice. The results show that expression of the MA (p15) and p12 regions of the gag gene is sufficient for pathogenicity of the BM5d retrovirus.",
    author = "J.M. Pozsgay and Manfred Beilharz and B.D. Wines and A.D. Hess and P.M. Pitha",
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    The MA (p15) and p12 Regions of the gag Gene Are Sufficient for the Pathogenicity of the Murine AIDS Virus. / Pozsgay, J.M.; Beilharz, Manfred; Wines, B.D.; Hess, A.D.; Pitha, P.M.

    In: Journal of Virology, Vol. 67, No. 10, 1993, p. 5989-5999.

    Research output: Contribution to journalArticle

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    T1 - The MA (p15) and p12 Regions of the gag Gene Are Sufficient for the Pathogenicity of the Murine AIDS Virus

    AU - Pozsgay, J.M.

    AU - Beilharz, Manfred

    AU - Wines, B.D.

    AU - Hess, A.D.

    AU - Pitha, P.M.

    PY - 1993

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    N2 - Inoculation of the replication-defective retrovirus DEF27 (BM5d), packaged as an amphotropic virus pseudotype, into C57BL/6J mice leads to development of murine AIDS. Disease development showed a long incubation period (20 to 24 weeks), was associated with amplification of the BM5d provirus in splenocytes and lymph nodes, and was independent of the presence of exogenous or endogenous replication-competent helper viruses. However, both the onset of disease and amplification of the defective provirus were significantly enhanced by coinfection with the replication-competent B-cell-tropic ecotropic helper virus BM5e. The part of the BM5d viral genome that was essential for the pathogenicity was determined by making precisely engineered alterations in the reading frame of the gag and pol genes of BM5d proviral DNA and examining the ability of the altered amphotropic BM5d pseudotypes to induce the disease in C57BL/6J mice. The results show that expression of the MA (p15) and p12 regions of the gag gene is sufficient for pathogenicity of the BM5d retrovirus.

    AB - Inoculation of the replication-defective retrovirus DEF27 (BM5d), packaged as an amphotropic virus pseudotype, into C57BL/6J mice leads to development of murine AIDS. Disease development showed a long incubation period (20 to 24 weeks), was associated with amplification of the BM5d provirus in splenocytes and lymph nodes, and was independent of the presence of exogenous or endogenous replication-competent helper viruses. However, both the onset of disease and amplification of the defective provirus were significantly enhanced by coinfection with the replication-competent B-cell-tropic ecotropic helper virus BM5e. The part of the BM5d viral genome that was essential for the pathogenicity was determined by making precisely engineered alterations in the reading frame of the gag and pol genes of BM5d proviral DNA and examining the ability of the altered amphotropic BM5d pseudotypes to induce the disease in C57BL/6J mice. The results show that expression of the MA (p15) and p12 regions of the gag gene is sufficient for pathogenicity of the BM5d retrovirus.

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