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Author Notes:

Address correspondence to Jason M. Brenchley, jbrenchl@niaid.nih.gov.

We acknowledge Richard Herbert and all the veterinary staff at the NIH Animal Center.

We thank Alicia Buckler-White, Ronald Plishka, Ranjini Iyengar, and all the staff of the NIAID LMM Core for assistance with viral loads and sequencing.

We thank Vanessa Hirsch and Que Dang for providing SIVmac239 for inoculation in PTM.

We thank the Cleveland Immunopathogenesis Consortium (BBC/CLIC) for advice and helpful discussions.

The content of this publication does not necessarily reflect the views or policies of the Department of Health and Human Services, nor does mention of trade names, commercial products, or organizations imply endorsement by the U.S. Government.

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Research Funding:

These studies were supported by the intramural program of the National Institute of Allergy and Infectious Diseases, U.S. National Institutes of Health, and in part by NIH grants R01-AI90797; to G. Silvestri and AI054292 to L. Picker as well as ONPRC Core grant RR00163.

Keywords:

  • Science & Technology
  • Life Sciences & Biomedicine
  • Virology
  • VIROLOGY
  • PIG-TAILED MACAQUES
  • CD4(+) T-CELLS
  • ACUTE SIV INFECTION
  • MACACA-NEMESTRINA
  • IMMUNE ACTIVATION
  • HIV-1 INFECTION
  • IN-VIVO
  • AFRICAN INDIVIDUALS
  • TYPE-1 INFECTION
  • MOLECULAR CLONES

Dynamics of Simian Immunodeficiency Virus SIVmac239 Infection in Pigtail Macaques

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Journal Title:

Journal of Virology

Volume:

Volume 86, Number 2

Publisher:

, Pages 1203-1213

Type of Work:

Article | Final Publisher PDF

Abstract:

Pigtail macaques (PTM) are an excellent model for HIV research; however, the dynamics of simian immunodeficiency virus (SIV) SIVmac239 infection in PTM have not been fully evaluated. We studied nine PTM prior to infection, during acute and chronic SIVmac239 infections, until progression to AIDS. We found PTM manifest clinical AIDS more rapidly than rhesus macaques (RM), as AIDS-defining events occurred at an average of 42.17 weeks after infection in PTM compared to 69.56 weeks in RM (P=0.0018). However, increased SIV progression was not associated with increased viremia, as both peak and set-point plasma viremias were similar between PTM and RM (P=0.7953 and P=0.1006, respectively). Moreover, this increased disease progression was not associated with rapid CD4 + T cell depletion, as CD4 + T cell decline resembled other SIV/human immunodeficiency virus (HIV) models. Since immune activation is the best predictor of disease progression during HIV infection, we analyzed immune activation by turnover of T cells by BrdU decay and Ki67 expression. We found increased levels of turnover prior to SIV infection of PTM compared to that observed with RM, which may contribute to their increased disease progression rate. These data evaluate the kinetics of SIVmac239-induced disease progression and highlight PTM as a model for HIV infection and the importance of immune activation in SIV disease progression.

Copyright information:

© 2012, American Society for Microbiology. All Rights Reserved.

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