We discovered that BEV 2C uses a new strategy to promote virus replication: either directly interacting with p65 to block the dimerisation of p65/p50 or inhibiting the activation of NF-κB signalling elicited by viral infection by suppressing the inhibitor of nuclear factor kappa B kinase subunit beta (IKBKB) expression. Here, NFKB1 is linked to viral infectious disease.