Endogenous 4-1BB/4-1BBL interactions have been shown to participate in priming of virus-specific CD8 T cells during infection with influenza virus (Bertram et al., 2002, 2004), LCMV (Tan et al., 1999, 2000) and HSV (Seo et al., 2003), and correspondingly targeting 4-1BB with an agonist antibody, or incorporation of 4-1BBL into a vaccine vector, allowed enhanced CD8 responses to these viruses (Halstead et al., 2002; Kim et al., 2005; Zhang et al., 2007; Moraes et al., 2011; Vezys et al., 2011). This evidence concerns the gene TNFRSF9 and infection.