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Journal of Virology, October 2004, p. 11405-11410, Vol. 78, No. 20
0022-538X/04/$08.00+0 DOI: 10.1128/JVI.78.20.11405-11410.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.
EMI-0013 Institut National de la Santé et de la Recherche Médicale, Université Paris 7, and Laboratoire d'Immunologie Cellulaire et Immunopathologie de l'Ecole Pratique des Hautes Etudes, Institut Universitaire d'Hématologie, Hôpital Saint-Louis,1 CNRS UPR9051, Institut Universitaire d'Hématologie, Hôpital Saint-Louis, Paris,4 Institut de Biologie Moléculaire des PlantesCNRS, Département de Virologie 12, Strasbourg, France,2 Laboratoire de Biochimie and JFR 3012 Associée à l'Agence Universitaire Francophone (AUPELF-UREF), Faculté des Sciences, Rabat, Morocco3
Received 27 April 2004/ Accepted 25 May 2004
We report that human T cells persistently infected with primate foamy virus type 1 (PFV-1) display an increased capacity to bind human immunodeficiency virus type 1 (HIV-1), resulting in increased cell permissiveness to HIV-1 infection and enhanced cell-to-cell virus transmission. This phenomenon is independent of HIV-1 receptor, CD4, and it is not related to PFV-1 Bet protein expression. Increased virus attachment is specifically inhibited by heparin, indicating that it should be mediated by interactions with heparan sulfate glycosaminoglycans expressed on the target cells. Given that both viruses infect similar animal species, the issue of whether coinfection with primate foamy viruses interferes with the natural course of lentivirus infections in nonhuman primates should be considered.
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