The glycosylation of the influenza strain can disturb its host specificity, virulence, and contagious nature either directly by changing the biological activity of surface proteins (Schulze, 1997), or indirectly by 1) attenuating receptor-binding sites (Gao et al., 2009), 2) masking antigenic sections of the protein (Abe et al., 2004), 3) obstructing the HA protein precursor via its cleavage into the disulfide-linked subunits HA1 and HA2 (Ohuchi et al., 1989), and 4) regulating the catalytic activity or preventing proteolytic cleavage of the stalk of NA (Matsuoka et al., 2009). This evidence concerns the gene XK and influenza.