These data suggested that the viral infection of dendritic cells in C57BL/6 mice led to the inhibition of crucial immune regulators and inflammatory factors required to activate immune responses in epithelial tissue while increasing the transcription of molecules that act in the negative feedback regulation that maintains the stability of the innate immune system, which is probably beneficial for viral proliferation in tissue, in comparison to what happened in HVEM−/− mice. This evidence concerns the gene TNFRSF14 and viral infectious disease.