Gandhi Shiv K, Siliciano Janet D, Bailey Justin R, Siliciano Robert F, Blankson Joel N
Broadway Research Bldg., Rm. 880, Johns Hopkins University School of Medicine, 733 N. Broadway, Baltimore, MD 21205, USA.
J Virol. 2008 Mar;82(6):3125-30. doi: 10.1128/JVI.01533-07. Epub 2007 Dec 12.
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.
虽然许多研究表明，胞苷脱氨酶的载脂蛋白B mRNA编辑酶催化多肽样3（APOBEC3）家族可抑制1型人类免疫缺陷病毒（HIV-1）复制，但这种宿主防御机制的临床意义尚不清楚。精英抑制者是指在未接受抗逆转录病毒治疗的情况下，病毒载量维持在每毫升50拷贝以下的HIV-1感染者。为了确定APOBEC3G/F蛋白在控制这些患者病毒血症中的作用，我们采用了一种新的检测方法来测量高突变前病毒基因组的频率。在大多数精英抑制者中，该频率与接受高效抗逆转录病毒治疗的患者中观察到的频率没有显著差异。因此，仅增强的APOBEC3活性不能解释精英抑制者控制病毒血症的能力。
