AAC
Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Other Versions of this Article:
AAC.00736-07v1
51/11/4160    most recent
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 Chou, S.
Right arrow Articles by Weinberg, A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Chou, S.
Right arrow Articles by Weinberg, A.

 Previous Article  |  Next Article 

Antimicrobial Agents and Chemotherapy, November 2007, p. 4160-4162, Vol. 51, No. 11
0066-4804/07/$08.00+0     doi:10.1128/AAC.00736-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Growth and Drug Resistance Phenotypes Resulting from Cytomegalovirus DNA Polymerase Region III Mutations Observed in Clinical Specimens{triangledown}

Sunwen Chou,1,2* Gail I. Marousek,2 Laura C. Van Wechel,1 Shaobing Li,3 and Adriana Weinberg3,4

Division of Infectious Diseases, Oregon Health and Science University,1 VA Medical Center, Portland, Oregon,2 Divisions of Infectious Diseases,3 Pediatric Infectious Diseases, University of Colorado Health Sciences Center, Denver, Colorado4

Received 6 June 2007/ Returned for modification 3 August 2007/ Accepted 10 August 2007

Recombinant phenotyping of cytomegalovirus (CMV) pol region III mutations from clinical specimens showed that T813S and G841A each conferred foscarnet resistance and approximately threefold increased ganciclovir resistance; adding the UL97 mutation C592G increased ganciclovir resistance to approximately sixfold. Bacterial artificial chromosome CMV clones containing pol mutation L845P were nonviable unless repaired with the wild-type sequence.

* Corresponding author. Mailing address: VA Medical Center P3ID, 3710 SW U.S. Veterans Hospital Road, Portland, OR 97239. Phone: (503) 273-5115. Fax: (503) 273-5116. E-mail: chous{at}ohsu.edu

{triangledown} Published ahead of print on 20 August 2007.

Antimicrobial Agents and Chemotherapy, November 2007, p. 4160-4162, Vol. 51, No. 11
0066-4804/07/$08.00+0     doi:10.1128/AAC.00736-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.





Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
Clin. Vaccine Immunol. Clin. Microbiol. Rev.
J. Clin. Microbiol. ALL ASM JOURNALS

Copyright © 2007 by the American Society for Microbiology. All rights reserved.