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 Google Scholar
Google Scholar
Right arrow Articles by Johnston, E.
Right arrow Articles by Shafer, R. W.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Johnston, E.
Right arrow Articles by Shafer, R. W.

 Previous Article  |  Next Article 

Antimicrobial Agents and Chemotherapy, December 2004, p. 4864-4868, Vol. 48, No. 12
0066-4804/04/$08.00+0     DOI: 10.1128/AAC.48.12.4864-4868.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Association of a Novel Human Immunodeficiency Virus Type 1 Protease Substrate Cleft Mutation, L23I, with Protease Inhibitor Therapy and In Vitro Drug Resistance

Elizabeth Johnston,1 Mark A. Winters,1 Soo-Yon Rhee,1 Thomas C. Merigan,1 Celia A. Schiffer,2 and Robert W. Shafer1*

Division of Infectious Diseases, Department of Medicine, Stanford University, Stanford, California,1 Department of Biochemistry and Molecular Pharmacology, University of Massachusetts Medical School, Worcester, Massachusetts2

Received 26 April 2004/ Returned for modification 14 July 2004/ Accepted 17 August 2004

We observed a previously uncharacterized mutation in the protease substrate cleft, L23I, in 31 of 4,303 persons undergoing human immunodeficiency virus type 1 genotypic resistance testing. In combination with V82I, L23I was associated with a sevenfold reduction in nelfinavir susceptibility and a decrease in replication capacity. In combination with other drug resistance mutations, L23I was associated with multidrug resistance and a compensatory increase in replication capacity.

* Corresponding author. Mailing address: Division of Infectious Diseases, Room S-169, Stanford University, Stanford, CA 94305. Phone: (650) 725-2946. Fax: (650) 725-2088. E-mail: rshafer{at}stanford.edu.

Antimicrobial Agents and Chemotherapy, December 2004, p. 4864-4868, Vol. 48, No. 12
0066-4804/04/$08.00+0     DOI: 10.1128/AAC.48.12.4864-4868.2004
Copyright © 2004, 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»