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Virus subtype-specific features of natural simian immunodeficiency virus SIVsmm infection in sooty mangabeys

Cristian Apetrei1, Rajeev Gautam, Beth Sumpter

  • 1Division of Microbiology and Immunology, Tulane National Primate Research Center, 18703 Three Rivers Road, Covington, LA 70433, USA. capetrei@tulane.edu

Journal of Virology
|May 18, 2007
PubMed

Insights

Simian immunodeficiency virus (SIV) subtypes show varying pathogenicity in sooty mangabeys (SMs). Certain SIV subtypes, particularly subtype 5, are linked to CD4+ T-cell depletion, indicating distinct disease courses in natural hosts.

Area of Science:

  • Virology
  • Immunology
  • Primate Health

Background:

  • Simian immunodeficiency virus (SIV) infects sooty mangabeys (SMs) and is the progenitor of HIV-2.
  • Previous research identified nine SIV subtypes in SMs, with genetic distances comparable to HIV-1 group M subtypes.
  • SIV infection in SMs is typically nonpathogenic.

Purpose of the Study:

  • To investigate the cocirculation and pathogenicity of SIV subtypes within a SM colony.
  • To identify specific immunologic features associated with different SIV subtypes.
  • To determine if SIV subtype influences disease progression and CD4+ T-cell counts.

Main Methods:

  • Phylogenetic analysis of SIV strains from SMs at Yerkes National Primate Research Center.
  • Monitoring of CD4+ T-cell counts and immunologic markers in infected SMs.
  • Comparison of viral replication levels across different SIV subtypes.

Main Results:

  • At least four SIV subtypes cocirculate in the studied SM colony, with subtypes 1, 2, and 3 being most common.
  • Subtypes 1, 2, and 3 are associated with a benign infection course and preserved CD4+ T-cell counts.
  • Three out of four SMs infected with SIV subtype 5 exhibited significant CD4+ T-cell depletion, despite similar viral replication levels.

Conclusions:

  • SIV subtypes exhibit distinct pathogenic potentials in their natural SM hosts.
  • SIV subtype 5 is associated with CD4+ T-cell depletion, suggesting mechanisms beyond direct viral killing.
  • Understanding subtype-specific pathogenicity is crucial for SIV research and potential therapeutic strategies.

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