A further reason for defining the structural rules governing TCR cross-recognition is that similar effects have been found for different epitopes derived from unrelated viruses. Published studies provide evidence for cross-reactive CD8 + T cell responses between influenza A virus and Epstein-Barr virus (EBV) [45] , influenza A virus and Hepatitis C virus (HCV) [46, 47] or lymphocytic choriomeningitis virus (LCMV) and Pichinde virus (PV) [48] . Such heterologous cross-reactive immunity can unintentionally skew TCR recruitment, result in a narrow TCR repertoire and subsequent viral escape [48] as well as influenza disease severity [22] . doi:10.1371/journal.ppat.1001039.g006 [45] . The topic of TCR cross-reactivity in CD8 + T cell responses clearly merits more attention.