These cross-reactive T cells, stimulated upon a secondary infection with a different serotype, also displayed quantitative and qualitative differences in their response to the cross-reactive epitope [61], with higher ratios of Tumor Necrosis Factor alpha (TNF-α) to Interferon gamma (IFN-γ)-producing CD4 T cells [62], suboptimal degranulation but high cytokine production [63], or more specifically impaired IFN-γ production [64]. This evidence concerns the gene TNF and infection.