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 cDNA sequence fused to EGFP gene were transfected 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.