Many viruses have evolved surprising strategies to interfere with the MHC class I antigen presentation pathway . After the initial NK response , the host will produce adaptive CD8 + T and CD4 + T(36) cellular responses. Viral MHC class I molecules allow evasion of NK cell effector responses in the body and contribute to immune evasion . Many studies have shown that MHC class I virus proteins interfere with infected cells recognizing, antigen processing, and presentation . The specific recognition of MHC by inhibitory KIR provides excellent protection against a decoy molecule of virus evolution . The diversity of the receptor system may be the result of this specific interaction between MHC and KIR molecules. However, NK cells in severely ill patients with COVID-19 are severely depleted. The protective function of inhibitory KIR shows signs of failure. It shows that some regions of human MHC have an irreplaceable role. The MHC-like structures of the virus were precisely in these areas. If a mutation site was in the MHC-like domain, the mutation enhanced the MHC decoy function. In other words, the human immune system hard to neutralize these MHC-like sites by producing antibodies. Otherwise, the antibodies could also bind to MHC proteins. Then the antibodies would affect normal MHC antigen presentation function, causing autoimmune diseases.