To the Editor-Thackray and Field [1] raise 4 points that they believe explain why our recent study [2] failed to document the virologic superiority of famciclovir over valacyclovir that they described in several reports and numerous abstracts.First, the route of infection did differ, as we acknowledged in our Discussion section [2].They argue, however, that infection of the cornea (as opposed to the ear pinna in their model system) would favor direct uptake of virus into the axons, eliminating the opportunity a drug started 24 h later might have to limit viral amplification in the ganglia.We believe that any such aspect of our model system is overstated.In our studies, virus titers in tissues continued to rise for some days after the start of treatment (figure 3 in [2]).Thus, there remained ample opportunity for viral replication to be affected by the drugs.Nonetheless, we failed to observe any differential benefit of famciclovir.Moreover, Thackray and colleagues [3][4][5] reported experiments in which they delayed treatment even further and still observed superiority of famciclovir.Second, Thackray and Field [1] are concerned about the virus inoculum that we used, because it was associated with universal mortality in the absence of treatment.It is true that no positive controls remained with which to compare the effects of treatment on latency and reactivation; however, untreated animals survived long enough for us to observe that famciclovir and valacyclovir were equivalent in virologic outcome measures of the acute infection.Third, with regard to a rebound of virus titers, we disagree that there is a "variance with the results published" [1].It has been our experience that the time points chosen are more than sufficient to track the spread of herpes simplex virus (HSV) from the eye to the trigeminal ganglia and into the brain.With the chosen time points, we saw the spread of virus through these tissues.Moreover, we detected no differences in the effect of either drug during the testing period.Obviously, for a true rebound to occur, the initial infection first must be cleared.Clearance was beginning to occur by the final time point, postinfection day 11.In an immunosuppression model, Field et al.[3] tested ear and brain samples on intermittent days and still detected a rebound of virus titers.Fourth, we claimed equivalence of both drugs in "terminat-ing ganglionic infection" [2], by which we meant the presence of infectious virus in the tissue.Despite their claim to the contrary, Thackray and Field [4, 5] reported that famciclovir was superior in reducing the amount of both infectious and latent virus in ganglia and in "preventing the establishment of latency" (Discussion in [4]; Introduction and Discussion in [5]).We agree that each animal model has its own advantages and disadvantages.We believe, from our own data, that famciclovir and valacyclovir are equivalent for the acute treatment of HSV infections and will continue to believe so until a welldesigned clinical trial proves otherwise.