It is unclear whether the residual levels of latency observed in mice infected with the IκBαM expressing viruses represent the infection of a population of cells that do not require NF-κB activation for establishment of γHV68 latency or whether they arise from latently infected cells in which the levels of expression of IκBαM were not sufficient to block NF-κB activation. Here, NFKB1 is linked to infection.