The nucleoside analogues currently used to treat HSV aren't super effective, and do sometimes carry harmful side-effects.
We may have a more effective treatment in Pritelivir, if this ever gets through clinical trials. It has a different mechanism than acyclovir et al — it is a helicase primase inhibitor.
It may even be true that HSV is more effectively treated when helicase primase inhibitors and nucleoside analogues work in conjunction.
It also wouldn't touch latent virus, only a minority that were actively replicating.
"The bioavailability of orally administered acyclovir is limited to 15 to 30% (23), and the level of passage across the blood-brain barrier has been assumed to be low, probably due to the relatively low lipophilicity of acyclovir (8). It was previously found (14) that upon oral administration the acyclovir concentration in cerebrospinal fluid (CSF) is only 13 to 52% of that found in plasma. When sustained and high concentrations of acyclovir in plasma are desirable, improved bioavailability can be achieved with valacyclovir, the hydrochloride salt of the l-valyl ester of acyclovir." [1]