Viral infections occurring during the cold season pave the way for subsequent bacterial secondary infection by T-cell mediated release of interferon-γ, which inhibits bacterial phagocytosis by macrophages [9], and increases the expression of adhesion receptors on epithelial cells such as carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1) [10]. This evidence concerns the gene CEACAM1 and viral infectious disease.