This aligns with higher cellular CXCL10 mRNA expression in LNCaP cells compared to PANC-1 upon rSFV infection, supporting the hypothesis that innate non-conventional cellular pathways, such as NF-kB or IRF3 activation,27,28,29 play a role in SFV-induced CXCL10 expression independent of the JAK-STAT pathway. Here, IRF3 is linked to infection.