In our experiments, when type I IFN signaling was blocked with MAR1-5A3 prior to infection with an attenuated WNV strain, we observed at day 9 paradoxically enhanced numbers of antigen-specific effector CD8+ T cell responses that had deficits in IFN-γ or TNF-α production, results that are consistent with prior infection experiments [52]. This evidence concerns the gene TNF and infection.