Recently, it has been reported that the substitution of three charged amino acid residues at positions 151, 153, and 154 within C protein conserved among SeV strains dramatically reduced the anti-IFN ability without any alteration of the other functions of C protein in experiments with C protein expressed from cDNA as well as infections of SeV recombinants [10], [11]. The gene discussed is IFNA1; the disease is infection.