Role of APOBEC3G/F-mediated hypermutation in the control of human immunodeficiency virus type 1 in elite suppressors.
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.
Gandhi
Shiv K
SK
Broadway Research Bldg., Rm. 880, Johns Hopkins University School of Medicine, 733 N. Broadway, Baltimore, MD 21205, USA.
Siliciano
Janet D
JD
Bailey
Justin R
JR
Siliciano
Robert F
RF
Blankson
Joel N
JN
D000071480:APOBEC-3G Deaminase; D023241:Antiretroviral Therapy, Highly Active; D001483:Base Sequence; D003564:Cytidine Deaminase / Q000502:physiology*; D043525:Cytosine Deaminase / Q000502:physiology*; D004279:DNA, Viral; D015658:HIV Infections / Q000188:drug therapy / Q000821:virology*; D015497:HIV-1 / Q000502:physiology*; D006801:Humans; D009154:Mutation
D004279:DNA, Viral; C492906:APOBEC3F protein, human; D043525:Cytosine Deaminase; D000071480:APOBEC-3G Deaminase; C464924:APOBEC3G protein, human; D003564:Cytidine Deaminase