期刊
JOURNAL OF VIROLOGY
卷 82, 期 6, 页码 3125-3130出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.01533-07
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- NIAID NIH HHS [R56 AI73185-01A1, K08 AI51191, R56 AI073185, K08 AI051191] Funding Source: Medline
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 anti-retroviral 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.
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