Although HO-1 stimulation with CoPP has been reported to upregulate the transcription factor Nrf-2 (nuclear factor erythroid 2-related factor 2) [28], which relates to the downregulation of NF-κB signaling, which in turn is required for events leading to DC profiles that induce Th17 phenotypes in CD4+ T cells [56,57,58], the fact that HSV significantly modulates NF-κB activation during infection could relate to a pro-Th17 T cell phenotype elicited in CD4+ T cells by HSV-infected DCs, despite HO-1 expression [4]. This evidence concerns the gene NFKB1 and infection.