| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Previous Article | Next Article ![]()
Journal of Virology, August 2007, p. 8838-8842, Vol. 81, No. 16
0022-538X/07/$08.00+0 doi:10.1128/JVI.02663-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Nienke Vrisekoop,2,
Christine A. Jansen,2
Sigrid A. Otto,2
Hanneke Schuitemaker,3
Frank Miedema,2 and
David Camerini1*
Department of Molecular Biology and Biochemistry, Center for Immunology and Center for Virus Research, University of California, Irvine, California 92697-3900,1 Department of Immunology, University Medical Center, Utrecht, The Netherlands,2 Sanquin Research Landsteiner Lab and Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands3
Received 1 December 2006/ Accepted 20 May 2007
Long-term asymptomatic human immunodeficiency virus (HIV)-infected individuals (LTA) usually have low viral load and low immune activation. To discern whether viral load or immune activation is dominant in determining progression to AIDS, we studied three exceptional LTA with high viral loads. HIV type 1 isolates from these LTA were as pathogenic as viruses from progressors in organ culture. Despite high viral loads, these LTA had low levels of proliferating and activated T cells compared to progressors, like other LTA. In contrast to those in progressors, HIV-specific CD4+ T-cell responses in these LTA were maintained. Thus, low immune activation despite a high viral load preserved HIV-specific T-cell responses and resulted in a long-term asymptomatic phenotype.
Published ahead of print on 30 May 2007.
These authors contributed equally to this study.
This article has been cited by other articles:
Copyright © 2009 by the American Society for Microbiology. For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»