Hence, we tested the biological relevance of PTPN22 in the lymphocytic choriomeningitis virus clone 13 (LCMV Cl13) viral infection system, where two amino acid substitutions in the virus genome cause persistent infection for more than 3 months, leading to antiviral CD4 and CD8 T cells that are physically deleted or persist in a “non-functional” state and characterized by the inability to produce effector cytokines (exhausted T cells) (13–16). This evidence concerns the gene CD8A and viral infectious disease.