If the shared N termini of V and W proteins act as inhibitors of viral replication, the decreased expression levels of the V and W proteins by the VCT virus (due to less editing) may have led to increased viral replication at later time points during infection (after 12 h, due to relatively more functional P protein), which would correspond with the delayed kinetics observed for its induction of IFN-β, CXCL10, and CCL5. Here, CCL5 is linked to infection.