When a respiratory virus is inhaled it first binds to nonspecific receptors on the respiratory epithelium, usually glycolipids or glycoproteins. Membrane fusion or endocytosis follows, thus internalizing the virus and enabling subsequent replication, transсrіption, and translation of new viruses which can then be released to infect new cells. Once a cell has been infected, pathogen-associated molecular patterns (PAMPs) on the virus can be recognized by various intracellular innate pathogen recognition receptors (PRRs) such as the toll-like receptors (TLRs), retinoic-acid-inducible gene-I- (RIG-I-) like receptors (RLRs), and nucleotide binding-oligomerization domain (NOD-) like receptors (NLRs) [12]. Pulmonary epithelial cells have been shown to express all of the known human TLRs and RLRs that detect viruses, and ligands for these PRRs activate epithelial cells in order to initiate a rapid immune response against viral invasion [13]. In addition to direct infection of epithelial cells, intraepithelial dendritic cells (DCs) residing just below the respiratory epithelium and tissue-resident macrophages continually sample particles in the airway lumen and can internalize them by phagocytosis and macropinocytosis, thus activating PRRs and initiating an immune response [14, 15]. Features of the induced antiviral state include resistance to viral replication in all cells, induction of apoptotic cell death in infected cells, increased major histocompatibility complex (MHC) class I expression to enhance antigen presentation, activation of dendritic cells (DCs) and macrophages, and stimulation of natural killer (NK) cells to enhance their cytolytic activity [16]. The inflammatory cytokines TNF-α, IL-1β, IL-6, and IL-12 are also produced at an early stage of the innate immune response. These cytokines promote leukocyte extravasation by increasing endothelial expression of adhesion molecules increasing vascular permeability, induce synthesis of acute phase proteins, and contribute to recruitment and activation of cells of the adaptive immune response [12]. Other antimicrobial vitamin D dependent peptides, such as cathelicidins and defensins, are involved in the second barrier.