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Journal of Virology, July 2005, p. 8979-8990, Vol. 79, No. 14
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.14.8979-8990.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

The Replicative Fitness of Primary Human Immunodeficiency Virus Type 1 (HIV-1) Group M, HIV-1 Group O, and HIV-2 Isolates{dagger}

Kevin K. Ariën,1,2 Awet Abraha,2 Miguel E. Quiñones-Mateu,3 Luc Kestens,4 Guido Vanham,1,4,5 and Eric J. Arts2*

Department of Microbiology, HIV Virology Research Unit, Institute of Tropical Medicine, Nationalestraat 155, B-2000 Antwerp, Belgium,1 Division of Infectious Diseases, Department of Medicine, Case Western Reserve University, 2109 Adelbert Rd., Cleveland, Ohio 44106,2 Department of Virology, Lerner Research Institute, The Cleveland Clinic Foundation, 9500 Euclid Ave., Cleveland, Ohio 44106,3 Department of Microbiology, Laboratory of Immunology, Institute of Tropical Medicine, Nationalestraat 155, B-2000 Antwerp, Belgium,4 Department of Biomedical Sciences, University of Antwerp, Universiteitsplein 1, B-2610 Wilrijk, Belgium5

Received 19 December 2004/ Accepted 14 March 2005

The main (M) group of human immunodeficiency virus type 1 (HIV-1) is responsible for the global AIDS epidemic while HIV-1 group O (outlier) and HIV type 2 are endemic only in west and central Africa. The failure of HIV-2 and especially HIV-1 group O to spread following the initial zoonotic jumps is not well understood. This study was designed to examine the relative replicative capacities between these human lentiviruses. A pairwise competition experiment was performed with peripheral blood mononuclear cells with eight HIV-2 isolates, 6 group O viruses, and 15 group M viruses of subtype A (2 viruses), B (5 viruses), C (4 viruses), D (2 viruses) and CRF01_AE (2 viruses). HIV-1 group M isolates of any subtype were typically 100-fold-more fit than group O or HIV-2 strains when competed in peripheral blood mononuclear cells from various humans. This order in replicative fitness was also observed when virus pairs were added to human dendritic cells and then cocultured with primary, quiescent T cells, which is the model for HIV-1 transmission. These results suggest that reduced replicative and transmission fitness may be contributing to the low prevalence and limited geographical spread of HIV-2 and group O HIV-1 in the human population.

* Corresponding author. Mailing address: Division of Infectious Diseases, BRB 1034, Case Western Reserve University, 10900 Euclid Ave., Cleveland, OH 44106. Phone: (216) 368-8904. Fax: (216) 368- 2034. E-mail: eja3{at}po.cwru.edu.

{dagger} Supplemental material for this article may be found at http://jvi.asm.org/.

Journal of Virology, July 2005, p. 8979-8990, Vol. 79, No. 14
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.14.8979-8990.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



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