Last, to determine if the ORF6p NF-κB sites influence ORF6p activation in the context of de novo lytic infection, NIH3T12 cells were transfected with the ORF6p reporter and then infected at a multiplicity of infection (MOI) 5 with the control MHV68 or MHV68-IκBαM, a recombinant virus that expresses a mutant form of IκBα which functions as a super-repressor of canonical NF-κB activation [26]. This evidence concerns the gene NFKBIA and infection.