The results show that point mutations in the aforementioned proline residues individually affected replication of the virus somewhat without G-A hypermutation, but a Vif P21 A/P24 A mutant replicated considerably slower than a wild type virus with significant increase in G-A mutations, and the triple mutant Vif P21 A/P24 A/P192 A was even more attenuated, showing about the same amount of APOBEC 3 activity as a MVV mutant unable to bind the ubiquitin ligase complex (SLQ-AAA).
Einnig var tíðni G-A stökkbreytinga í P21 A/P24 A veirunni hækkuð. Veiru afbrigði sem inniheldur allar stökkbreytingarnar P21 A/P24 A/P192 A eftirmyndast á svipuðum hraða og veira sem ekki getur bundið ubiquitin lígasann (SLQ-AAA) og er fjöldi APOBEC 3 stökkbreytinga einnig sambærilegur.