Endsley Aaron N, Ho Rodney J Y
Department of Pharmaceutics, University of Washington, Seattle, WA 98195, USA.
J Med Primatol. 2012 Feb;41(1):52-9. doi: 10.1111/j.1600-0684.2011.00518.x. Epub 2011 Oct 24.
Although the interactions of cellular cytidine deaminase A3G and viral infection factor (vif) of human immunodeficiency virus (HIV) were reported, regulation of A3G after in vivo HIV infection and disease progression is not known.
Time courses of plasma virus, CD4(+) T lymphocyte Macaca levels, and concentrations of A3G and vif transcripts were determined in infant macaques infected with HIV-2(287) . These in vivo results were compared with those collected in vitro in HIV-2-infected T cells.
Human immunodeficiency virus-infected macaques exhibited plasma viremia (≥10(8) copies/ml) followed by a precipitous CD4(+) T-cell (from 40-70 to ≤5%) decline. An initial increase in A3G transcripts coincides with early increases in virus and vif RNA. As virus load continues to increase, A3G RNA decreases but recovers at a later phase as virus level stabilizes. Pearson correlation analysis revealed strong interactions of A3G-CD4, vif-CD4, and A3G-vif.
There is a time-dependent A3G and vif RNA interaction throughout the course of HIV infection.
尽管已有报道称细胞胞苷脱氨酶A3G与人类免疫缺陷病毒（HIV）的病毒感染因子（Vif）之间存在相互作用，但体内HIV感染和疾病进展后A3G的调节情况尚不清楚。
测定感染HIV-2(287)的幼猴血浆病毒、CD4(+)T淋巴细胞水平以及A3G和Vif转录本浓度的时间进程。将这些体内结果与在HIV-2感染的T细胞中体外收集的结果进行比较。
感染人类免疫缺陷病毒的猕猴出现血浆病毒血症（≥10(8)拷贝/毫升），随后CD4(+)T细胞急剧下降（从40 - 70降至≤5%）。A3G转录本最初的增加与病毒和Vif RNA的早期增加同时出现。随着病毒载量持续增加，A3G RNA减少，但在后期随着病毒水平稳定而恢复。Pearson相关性分析显示A3G与CD4、Vif与CD4以及A3G与Vif之间存在强烈的相互作用。
在HIV感染过程中，A3G和Vif RNA存在时间依赖性相互作用。
