Notably, initial work on the HSV-1 LAT-encoded miRNAs suggested that although hsv1-miR-H2, -H4, -H5, and -H6 were detectable in TGs during latency, these molecules may be dispensable for latent infection: in wild-type mice, LAT promoter mutants that lacked expression of these miRNAs replicated normally and established wild-type levels of latent infection [10]. This evidence concerns the gene LAT and disease arising from reactivation of latent virus.