At a functional level, it is reasonable to conclude that in MeWos that fail to express the necessary anti-inflammatory mediators in the context of infection, viral latency is the more likely outcome, whereas the rapid increase in expression of MC1-R and other anti-inflammatory molecules in infected Mel1700 cells blocks NF-κB [53, 55–57], which would consequently limit establishment of a latent state and/or result in a greater propensity for Mel1700 cells to support lytic replication. This evidence concerns the gene NFKB1 and infection.