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Journal of Virology, June 2005, p. 7938-7941, Vol. 79, No. 12
0022-538X/05/$08.00+0 doi:10.1128/JVI.79.12.7938-7941.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.
Institut de Génétique Humaine, CNRS UPR1142,1 Laboratoire d'Immunologie, Hôpital Saint Eloi, Montpellier, France2
Received 15 March 2004/ Accepted 18 February 2005
The binding of R5 envelope to CCR5 during human immunodeficiency virus type 1 (HIV-1) entry provokes cell activation, which has so far been considered to have no effect on virus replication, since signaling-defective CCR5 molecules have been shown to function normally as HIV-1 coreceptors on transformed cells or mitogen-stimulated T lymphocytes. As the background state of activation of these cells might have biased the results, we performed experiments using the same approach but with nonactivated primary T lymphocytes. We now report that the single R126N mutation in the DRY motif, involved in G-protein coupling, results in a signaling-defective CCR5 coreceptor with a drastically impaired capacity to support HIV-1 infection.
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