中文摘要：

腺苷酸脱氨酶（ADAR）1可催化双链RNA的腺嘌呤核苷酸（A）脱氨转化为次黄嘌呤核苷酸（I），该基因参与了很多病毒的复制与进化。在前期研究中对马传染性贫血病毒（EIAv）疫苗株基因组在体外培养细胞传代致弱过程中的变异规律进行了分析，表明与致弱前强毒株相比，EIAV弱毒疫苗株基因组出现高频率的A—I超突变，推测主要由腺苷酸脱氨酶1（ADARl）催化导致，使基因组突变累积后的EIAV体内复制能力降低而弱化。为初步研究ADARl在EIAV致弱中的作用，本研究应用PCR技术首次克隆了马ADARl（eADARll的cDNA。经确认该重组蛋白在293T细胞中的正确表达后，将表达eADARl的质粒与EIAV长末端重复区fLTR）控制的报告基因质粒共同转染马胎皮N（FED）细胞，检测eADARl对LTR启动活性的影响。实验数据表明，该ADARl可以在体外培养的EIAV靶细胞中显著促进LTR启动的荧光素酶表达，显示eADARl可以通过调控LTR促进EIAV的复制。以上结果提示eADARl可以明显影响EIAV复制，但其机制较复杂，尚待深入研究。

英文摘要：

To investigate the equine infectiou anemia virus （EIAV） attenuated mechanism, we compared the genomes of virulent strains and vaccines, and the result showed that high frequency of A to G hypermutation was identified in viral genomes of EIAV during the attenuating process. Base on the published results of others, it is presumed that the adenosine deaminases that Act on RNA 1 （ADAR1） played an important role in the A to G hypermutation. And we speculated the accumulated A to G mutation might reduce the EIAV replication ability which attenuated the virus. In this study, to explore the role of ADAR1, the equine ADAR1 cDNA was cloned and over-expressed in cultivated equine fetal dermal （FED） cells. The results showed that the recombinant ADAR1 significantly enhanced the luciferase activity in a reporter plasmid that promoted by EIAV LTR, suggesting the enhancive potency rather than inhibition of equine ADAR1 on EIAV replication. These results suggest thateADAR1 was able to significantly affect EIAV replication, but the mechanism is more complex, have yet to be explored.