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Broadening of coreceptor usage by human immunodeficiency virus type 2 does not correlate with increased pathogenicity in an in vivo model

Department of Virology, Erasmus Medical Centre Rotterdam, Dr Molewaterplein 50, 3015 GE Rotterdam, The Netherlands¹
Department of Internal Medicine, Erasmus Medical Centre Rotterdam, Dr Molewaterplein 40, 3015 GD Rotterdam, The Netherlands²
UMR103 CNRS BioMerieux, ENS Lyon, Lyon, France³
Bernhard Nocht Institut für Tropen Medicin, Körber Labor für AIDS Forsschung, Bernhard Nocht Straße 74, 2000 Hamburg 36, Germany⁴

Author for correspondence: A. D. M. E. Osterhaus. Fax +31 10 408 9485. e-mail osterhaus{at}viro.fgg.eur.nl

The pathogenic properties of four primary human immunodeficiency virus type 2 (HIV-2) isolates and two primary HIV-2 biological clones were studied in an in vivo human-to-mouse chimeric model. The cell-associated viral load and the ability to reduce the severity of the induced graft-versus-host disease symptoms, the CD4/CD8 ratio and the level of repopulation of the mouse tissues by the graft, were determined. All HIV-2 strains, irrespective of their in vitro biological phenotype, replicated to high titres and significantly reduced graft-versus-host disease symptoms as well as the CD4/CD8 ratios. Reduction of graft repopulation caused by infection with the respective HIV-2 strains showed that the in vitro replication rate, syncytium-inducing capacity and ability to infect human macrophages did influence the in vivo pathogenic potential whereas broadening of coreceptor usage did not.

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				M. Schutten, C. A. van Baalen, C. Guillon, R. C. Huisman, P. H. M. Boers, K. Sintnicolaas, R. A. Gruters, and A. D. M. E. Osterhaus Macrophage Tropism of Human Immunodeficiency Virus Type 1 Facilitates In Vivo Escape from Cytotoxic T-Lymphocyte Pressure J. Virol., March 15, 2001; 75(6): 2706 - 2709. [Abstract] [Full Text]