Taken together, our results to date show that 1) certain populations of trigeminal ganglion neurons are more likely to support productive infection in an HSV-serotype-specific manner, which results in the establishment of HSV latent infection in a serotype-specific manner [1]–[4]; 2) there is a viral function that regulates this set of phenotypes and it appears to map to the LAT region of the viral genome [2], [3]; and 3) this function is not mediated in trans by factors produced by the 2.8 kb region of the HSV-1 and HSV-2 LAT regions investigated in these studies. This evidence concerns the gene LAT and infection.