The role of APOBEC3G/F-mediated hypermutation in the control of HIV-1 in Elite Suppressors

Department of Medicine, Johns Hopkins University School of Medicine, and Howard Hughes Medical Institute, Baltimore, MD 21205

^* To whom correspondence should be addressed. Email: jblanks{at}jhmi.edu.

	Abstract

While many studies show that the APOBEC3 family of cytidine deaminases can inhibit 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 HAART. Thus, enhanced APOBEC3 activity alone cannot explain the ability of elite suppressors to control viremia.