Nuclear localization of the C1 factor (host cell factor) in sensory neurons correlates with reactivation of herpes simplex virus from latency

After a primary infection, herpes simplex virus is maintained in a latent s tate in neurons of sensory ganglia until complex stimuli reactivate viral l ytic replication. Although the mechanisms governing reactivation from the l atent state remain unknown, the regulated expression of the viral immediate early genes represents a critical point in this process. These genes are c ontrolled by transcription enhancer complexes whose assembly requires and i s coordinated by the cellular C1 factor (host cell factor). In contrast to other tissues, the C1 factor is not detected in the nuclei of sensory neuro ns. Experimental conditions that induce the reactivation of herpes simplex virus in mouse model systems result in rapid nuclear localization of the pr otein, indicating that the C1 factor is sequestered in these cells until re activation signals induce a redistribution of the protein. The regulated lo calization suggests that C1 is a critical switch determinant of the viral l ytic-latent cycle.