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). The gene discussed is IFNAR1; the disease is HIV infectious disease.