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Single-cell Quantitation of mRNA and Surface Protein Expression in Simian Immunodeficiency Virus-infected CD4+ T Cells Isolated from Rhesus macaques
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Short-lived infected cells support virus replication in sooty mangabeys naturally infected with simian

Shari N Gordon1, Richard M Dunham, Jessica C Engram

  • 1University of Pennsylvania School of Medicine, 705 Stellar-Chance Laboratories, 422 Curie Boulevard, Philadelphia, PA 19143, USA.

Journal of Virology
|January 25, 2008
PubMed

Insights

Sooty mangabeys infected with simian immunodeficiency virus (SIV) resist AIDS. Virus replication primarily occurs in short-lived CD4(+) T cells, not long-lived cells, explaining their disease resistance.

Area of Science:

  • Immunology
  • Virology
  • Primatology

Background:

  • Sooty mangabeys (SMs) infected with simian immunodeficiency virus (SIV) resist AIDS despite high viral loads.
  • Mechanisms of this disease resistance are not well understood.

Purpose of the Study:

  • To test if SIV-infected SMs avoid immunodeficiency due to virus replication in longer-lived cells compared to HIV-infected human cells.
  • To investigate the role of infected cell lifespan in SIV pathogenesis.

Main Methods:

  • Six SIV-infected SMs were treated with potent antiretroviral therapy (ART).
  • Plasma viremia decline was measured longitudinally.
  • Mathematical models used for HIV-1 research were applied to SIV-infected SM data.

Main Results:

  • SIV-infected SMs showed a two-phase viremia decay post-ART, similar to HIV-1.
  • 92-99% of virus replication was sustained by short-lived cells (average lifespan 1.06 days).
  • Only 1-8% of virus replication occurred in longer-lived cells; ART had minimal impact on CD4(+) T cells.

Conclusions:

  • Short-lived, activated CD4(+) T cells are the primary source of SIV production in SMs, not macrophages.
  • A short in vivo lifespan of infected cells is characteristic of both pathogenic and nonpathogenic primate lentivirus infections.
  • Direct killing of infected cells is not the main driver of AIDS pathogenesis.

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