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Blood, 15 April 2006, Vol. 107, No. 8, pp. 3258-3264.
Prepublished online as a Blood First Edition Paper on December 22, 2005; DOI 10.1182/blood-2005-11-4374.
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Submitted November 7, 2005
Accepted December 9, 2005
Impact of vaccine-induced mucosal high avidity CD8+ CTL in delay of AIDS-viral dissemination from mucosa
Igor M Belyakov*, Vladimir A Kuznetsov, Brian Kelsall, Dennis Klinman, Marcin Moniuszko, Michael Lemon, Phillip D Markham, Ranajit Pal, John D Clements, Mark G Lewis, Warren Strober, Genoveffa Franchini, and Jay A Berzofsky
Vaccine Branch, National Cancer Institute, Bethesda, MD, USA
Division of Information and Mathematical Sciences, Genome Institute of Singapore, Singapore, Singapore
Laboratory Of Clinical Investigation, NIAID, NIH, Bethesda, MD, USA
Center for Biologics Evaluation and Research, Food and Drug Administration, Bethesda, MD, USA
Advanced BioScience Laboratories, Inc., Kensington, MD, USA
Department of Microbiology and Immunology, Tulane University School of Medicine, New Orleans, LA, USA
Southern Research Institute, Frederick, MD, USA
* Corresponding author; email: belyakov{at}mail.nih.gov.
Natural HIV transmission occurs through mucosa, but it is debated whether mucosal cytotoxic T lymphocytes (CTL) can prevent or reduce dissemination from the initial mucosal site to the systemic circulation. Also, the role of CTL avidity in mucosal AIDS viral transmission is unknown. To address these questions, we used delay in acute-phase peak viremia after intrarectal challenge as an indicator of systemic dissemination. We find that a peptide-prime/poxviral boost vaccine inducing high levels of high avidity mucosal CTL can impact dissemination of intrarectally administered pathogenic SHIV-ku2 in macaques, and that such protection correlates better with mucosal than with systemic CTL and particularly with levels of high avidity mucosal CTL.
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