After viral infection and endosomal-mediated degradation of viral nucleic acids, macrophages, dendritic cells, NK, and antigen-specific T cells (CD4+ Th1 and CD8+ cytotoxic T lymphocytes) expose viral antigens to toll-like receptors (TLRs), triggering a nonspecific antiviral response, and induce the transcription of hundreds of genes, which are distinct for different IFNs and target cell types [57]. The gene discussed is CD8A; the disease is viral infectious disease.