According to the infections of TZM-bl cells (Fig. 3), IFNα2-EIFK, in which IFNAR1 binding sites were introduced from IFNα14, as well as the combination of mutated residues at the IFNAR1 binding sites, putative tunable anchor region, and mutations outside of these defined motifs significantly reduced HIV infection in PBMCs compared with IFNα2 (Fig. 4C and E). Here, IFNA14 is linked to HIV infectious disease.