An AIV replicates primarily in the respiratory system (Sturm-Ramirez et al., 2004), from where it spreads to the brain and lymphoid tissues by way of infection. Such infection induces batteries of receptors and triggers a signaling cascade that ultimately activates the host’s immune response. As part of that process, for example, the endosomal Toll-like receptor (TLR) 3 and sphingosine-1-phosphate-1 receptor (S1PR1) recognize double-stranded viral RNA released during the uncoating of an internalized virus (Barton, 2007; Teijaro et al., 2011). During AIV infection in mammals, the endosomal TLR 7/8, which recognizes single-stranded viral RNA, can prompt the production of interferon (IFN)-α and IFN-β (Diebold et al., 2004). As MacDonald et al. (2008) have shown, when TLR7/8 are activated by AIV infection in host cells, the recognition of viral RNA results in the secretion of proinflammatory cytokines (e.g., IL-1β, IL-6) and antiviral cytokines (e.g., IFNs). By extension, the expression of proinflammatory cytokines and IFNs influences both viral clearance and the manifestation of clinical symptoms. At the same time, since major histocompatibility complex (MHC) classes I and II antigen presentation molecules used for AIV uptake activated cellular immunity and humoral immunity of B cells (i.e., IFN-γ) and T cells (i.e., CD3+, CD4+, CD8+), MHC molecules likely play a role in activating host innate immune response to AIV infection (Gromme and Neefjes, 2002; Williams et al., 2002).