This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Lin, Y.-L.
Right arrow Articles by Corbeau, P.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Lin, Y.-L.
Right arrow Articles by Corbeau, P.

 Previous Article  |  Next Article 

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.

G-Protein Signaling Triggered by R5 Human Immunodeficiency Virus Type 1 Increases Virus Replication Efficiency in Primary T Lymphocytes

Yea-Lih Lin,1 Clément Mettling,1 Pierre Portalès,2 Brigitte Réant,1,2 Jacques Clot,2 and Pierre Corbeau1,2*

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.


* Corresponding author. Mailing address: Laboratoire d'Immunologie, Hopital Saint Eloi, 80 avenue Augustin Fliche, 34295 Montpellier Cedex 5, France. Phone: 33-4-67-33-71-35. Fax: 33-4-67-33-71-29. E-mail: pierre.corbeau{at}igh.cnrs.fr.


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.




This article has been cited by other articles:

  • Heredia, A., Gilliam, B., Latinovic, O., Le, N., Bamba, D., DeVico, A., Melikyan, G. B., Gallo, R. C., Redfield, R. R. (2007). Rapamycin Reduces CCR5 Density Levels on CD4 T Cells, and This Effect Results in Potentiation of Enfuvirtide (T-20) against R5 Strains of Human Immunodeficiency Virus Type 1 In Vitro. Antimicrob. Agents Chemother. 51: 2489-2496 [Abstract] [Full Text]