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
Google Scholar
Right arrow Articles by Vermeire, K.
Right arrow Articles by Schols, D.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Vermeire, K.
Right arrow Articles by Schols, D.

 Previous Article  |  Next Article 

Journal of Virology, September 2009, p. 9577-9583, Vol. 83, No. 18
0022-538X/09/$08.00+0     doi:10.1128/JVI.00648-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Human Immunodeficiency Virus Type 1 Escape from Cyclotriazadisulfonamide-Induced CD4-Targeted Entry Inhibition Is Associated with Increased Neutralizing Antibody Susceptibility{triangledown}

Kurt Vermeire,1* Kristel Van Laethem,1 Wouter Janssens,2 Thomas W. Bell,3 and Dominique Schols1

Rega Institute for Medical Research, Katholieke Universiteit Leuven, Leuven, Belgium,1 Institute of Tropical Medicine, Antwerp, Belgium,2 Department of Chemistry, University of Nevada, Reno, Nevada3

Received 30 March 2009/ Accepted 21 June 2009

Continuous specific downmodulation of CD4 receptor expression in T lymphocytes by the small molecule cyclotriazadisulfonamide (CADA) selected for the CADA-resistant human immunodeficiency virus type 1 (HIV-1) NL4.3 virus containing unique mutations in the C4 and V5 regions of gp120, likely stabilizing the CD4-binding conformation. The amino acid changes in Env were associated with decreased susceptibility to anti-CD4 monoclonal antibody treatment of the cells and with higher susceptibility of the virus to soluble CD4. In addition, the acquired ability of a CADA-resistant virus to infect cells with low CD4 expression was associated with an increased susceptibility of the virus to neutralizing antibodies from sera of several HIV-1-infected patients.

* Corresponding author. Mailing address: Rega Institute for Medical Research, Katholieke Universiteit Leuven, Minderbroedersstraat 10, B-3000 Leuven, Belgium. Phone: 32-16-337341. Fax: 32-16-337340. E-mail: kurt.vermeire{at}rega.kuleuven.be

{triangledown} Published ahead of print on 1 July 2009.

Journal of Virology, September 2009, p. 9577-9583, Vol. 83, No. 18
0022-538X/09/$08.00+0     doi:10.1128/JVI.00648-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»