Role of APOBEC3G/F-mediated hypermutation in the control of human immunodeficiency virus type 1 in elite suppressors
Role of APOBEC3G/F-mediated hypermutation in the control of human immunodeficiency virus type 1 in elite suppressors
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DOI：
10.1128/jvi.01533-07
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发表时间：
2008-03-01
影响因子：
5.4
通讯作者：
Blankson, Joel N.
中科院分区：
文献类型：
--
作者：
Gandhi, Shiv K.;Siliciano, Janet D.;Blankson, Joel N.
虽然许多研究表明，APOBEC 3家族的胞苷脱氨酶可以抑制人类免疫缺陷病毒1型（HIV-1）的复制，这种宿主防御机制的临床意义尚不清楚。精英抑制者是HIV-1感染者，他们在没有抗逆转录病毒治疗的情况下将病毒载量维持在50拷贝/ml以下。为了确定APOBEC 3G/F蛋白在控制这些患者病毒血症中的作用，我们使用了一种新的测定方法来测量高度突变的前病毒基因组的频率。在大多数精英抑制者中，该频率与在高效抗逆转录病毒治疗患者中观察到的频率没有显著差异。因此，单独增强的APOBEC 3活性不能解释精英抑制因子控制病毒血症的能力。
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.