Importantly, we have identified two cell lines that displayed dichotomous properties with respect to their ability to support the KSHV latency program and mapped these cytologic attributes to (a) differences in the state of virus-induced NF-κB activation immediately following primary infection and upon establishment of latency, (b) expression of unique LANA isoforms associated with lytic replication, and (c) susceptibility of persistently infected cells to viral impairment of key components of the endogenous anti-inflammatory response pathways. This evidence concerns the gene NFKB1 and infection.