RIPK3 and Zika virus infectious disease: Unlike our previous findings using a model of WNV encephalitis [16], the RIPK3-dependent transcriptional activation of antiviral effector genes, including ISGs, was required for cell-intrinsic restriction of LGTV replication in neurons, a phenotype more similar to our findings with ZIKV [17], although we did not observe evidence for a regional specification of this response during ZIKV infection.