Vulnerability to secondary bacterial infection peaks at approximately one-week post-influenza infection; influenza virus infection facilitates secondary bacterial infection through phagocyte function (macrophage and neutrophil) or phagocyte-independent mechanisms, regulation of antimicrobial peptide, expression of IFN, immune cells (Th17 cells, NK cells, Treg cells, iLCs), and genetic susceptibility [94]. Here, IFNA1 is linked to bacterial infectious disease.