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Evolution of a simian immunodeficiency virus pathogen

P Edmonson1, M Murphey-Corb, L N Martin

  • 1Department of Pathology, University of Washington, Seattle 98195-7740, USA.

Journal of Virology
|January 7, 1998
PubMed
Summary
This summary is machine-generated.

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Simian immunodeficiency virus (SIV) strains BK28 and BK44 were initially non-pathogenic in macaques. In vivo passage of BK28 created a highly pathogenic SIV strain, demonstrating that viral evolution drives disease progression.

Area of Science:

  • Virology
  • Immunodeficiency Viruses
  • Primate Models

Background:

  • Early simian immunodeficiency virus (SIV) studies lacked molecularly defined pathogenic strains.
  • Initial SIVmacBK28 and SIVmacBK44 clones did not induce disease in macaques within one year.

Purpose of the Study:

  • To investigate the natural history of SIVmacBK28 and SIVmacBK44 infection in rhesus macaques.
  • To enhance the pathogenicity of SIVmacBK28 through genetic modification and in vivo passage.
  • To identify genetic changes responsible for increased SIV pathogenicity.

Main Methods:

  • Inoculation of rhesus macaques with SIVmacBK28 and SIVmacBK44.
  • Genetic manipulation of SIVmacBK28 (TM elongation, LTR modification).
  • In vivo passage of SIVmacBK28 in macaques.

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  • Generation of a chimeric molecular clone (BK28/H824).

    • Main Results:

    • SIVmacBK44 did not induce disease in over 7 years; SIVmacBK28 induced disease in less than half of animals.
    • In vivo passage of SIVmacBK28 generated a highly pathogenic strain with a 50% survival time of 1.3 years.
    • The chimeric clone BK28/H824 mimicked the pathogenicity of the in vivo-passaged strain.
    • Genetic alterations included mutations in TM, Nef, splice sites, TATA box, Sp1 sites, V2 region, and glycosylation sites.

    Conclusions:

    • SIV pathogenicity in macaques can be significantly enhanced through in vivo evolution.
    • Multiple genetic changes, including mutations in coding and regulatory regions, contribute to increased SIV virulence.
    • The evolved pathogenic strain provides a valuable model for studying SIV-induced immunodeficiency.