It is also required for TNFR-1-initiated neuronal apoptosis following in vitro infection with virus as an essential component of the antiviral response (Zhu et al., 2001; Michallet et al., 2007; Arnd, 2008; Vivek et al., 2010; Bai-Liang et al., 2012; Gaud et al., 2013). Here, TNFRSF1A is linked to infection.