Upon viral infection, its genetic material that enters the cell will trigger the type I interferon production through the endosomal toll-like receptor or RIG-like receptor pathway.[1] Initially, this interferon is synthesized by infected cells and dendritic cells and is essential to inhibit viral replication. Further, natural killer cells will kill virus-infected cells before adaptive immunity response to fight the virus is developed. Several viruses can shut off MHC class I-antigen presentation, thus escaping recognition by cytotoxic T lymphocytes (CTL). Antibodies are effective against the virus only during the virus's extracellular stage, mainly by neutralizing the virus. The primary antibody contributing to this process is secretory IgA that neutralizes viral particles in the respiratory or intestinal mucosal. In the adaptive immune system, CTL is the main cell to eliminate virus infection. This cell recognized the endogenous viral peptide presented by MHC class I and directly showed its antiviral activity by killing the infected cells.