This discrepancy may result from differences in innate signals induced by L. monocytogenes vs MuPyV infection, in acutely vs persistently infecting pathogens, the dominant Kb/SIINFEKL OT-1 epitope vs the weak subdominant Db/TagV TCR-V epitope, and/or in the TCR stimulation strength of the analogue epitope ligands used in these infection models. This evidence concerns the gene OXT and infection.