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Journal of Virology, March 2008, p. 3125-3130, Vol. 82, No. 6
0022-538X/08/$08.00+0     doi:10.1128/JVI.01533-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Role of APOBEC3G/F-Mediated Hypermutation in the Control of Human Immunodeficiency Virus Type 1 in Elite Suppressors{triangledown}

Shiv K. Gandhi,1 Janet D. Siliciano,1 Justin R. Bailey,1 Robert F. Siliciano,1,2 and Joel N. Blankson1*

Department of Medicine, Johns Hopkins University School of Medicine,1 Howard Hughes Medical Institute, Baltimore, Maryland 212052

Received 12 July 2007/ Accepted 5 December 2007

While many studies show that the APOBEC3 family of cytidine deaminases can inhibit human immunodeficiency virus type 1 (HIV-1) replication, the clinical significance of this host defense mechanism is unclear. Elite suppressors are HIV-1-infected individuals who maintain viral loads below 50 copies/ml without antiretroviral therapy. To determine the role of APOBEC3G/F proteins in the control of viremia in these patients, we used a novel assay to measure the frequency of hypermutated proviral genomes. In most elite suppressors, the frequency was not significantly different than that observed in patients on highly active antiretroviral therapy. Thus, enhanced APOBEC3 activity alone cannot explain the ability of elite suppressors to control viremia.

* Corresponding author. Mailing address: Broadway Research Bldg., Rm. 880, Johns Hopkins University School of Medicine, 733 N. Broadway, Baltimore, MD 21205. Phone: (410) 955-7757. Fax: (443) 287-6218. E-mail: jblanks{at}jhmi.edu

{triangledown} Published ahead of print on 12 December 2007.

Journal of Virology, March 2008, p. 3125-3130, Vol. 82, No. 6
0022-538X/08/$08.00+0     doi:10.1128/JVI.01533-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.



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