罗猴猕猴的主要 histocompatibility 建筑群一级等位基因 Mamu-B *17 是猿的免疫不全的一个精英控制器病毒(SIV ) 感染而 Mamu-B *01 没在 SIV 复制上有禁止的效果。机制仍然是逃犯的。在这研究,在 Mamu-B *1703 等位基因的领先的肽顺序的所谓的错过 G 人工地回来通过 PCR 扩大被插入,并且新顺序作为 Mamu-B *1703 (+G ) 被重命名。怀有 Mamu-B *1703, Mamu-B *1703 (+G ) 和熔化到 EGFP 基因的 Mamu-B *0101 cDNA 顺序的 plasmids 分别地是进 K562 和 Cos-7 房间的 transfected。我们的数据证明这些 plasmids 在 K562 房间,而是建筑群,它是稍微由领先的肽长度的人工的变化影响了的 Mamu-B *1703 的表面密度有类似的 transfection 效率和表示潜力,比 Mamu-B *0101 分子的高得多。这些结果可能部分在罗猴猕猴在 SIV 复制上说明 Mamu-B *17 和 Mamu-B *01 等位基因的微分效果。
The major histocompatibility complex class I allele Mamu-B*17 of rhesus macaques is an elite controller of simian immunodeficiency virus (SIV) infection whereas Mamu-B*01 has no inhibitory effect on SIV replication. The mechanism is still elusive. In this study, the so-called 'missing G' in the leading peptide sequence of Mamu- B'1703 allele was artificially inserted back through PCR amplification, and the new sequence was renamed as Mamu-B*1703(+G). The plasmids harboring Mamu- B*1703, Mamu-B*1703(+G) and Mamu-B*0101 eDNA sequence fused to EGFP gene were transfeeted into K562 and Cos-7 cells, respectively. Our data showed that these plasmids had similar transfection efficiencies and expression potentials in K562 cells, but the surface density of Mamu-B*1703 complexes, which was slightly influenced by the artificial change of the leading peptide length, was much higher than that of Mamu-B*0101 molecules. These results might partially account for the differential effects of Mamu-B*17 and Mamu-B*01 alleles on SIV replication in rhesus macaques.