Alternatively, after it enters the cell’s nucleus, the virus may become latent. This is particularly the case in neural tissue. The viral DNA inserts itself into the host DNA, where it lies dormant and hidden from expression until reactivation occurs at some later time. It accomplishes this by specialized folding of the DNA and histone complex so as not to allow for viral gene expression. When the virus is reactivated and ready to produce viral particles, this mechanism of latency is somehow deactivated, allowing for viral reproduction.
Treatment: Therapy and its efficacy are highly dependent on the timing of administration. Antiviral medications work by inhibiting viral synthesis, and they work best when used early in the course of disease. Primary infections should all be treated with one of the antiviral agents in the acyclovir family. These closely related medications include acyclovir, famciclovir, valacyclovir, and topical penciclovir. Recurrent episodes of the disease can be treated at the time of outbreak or with a chronic daily suppressive regimen. Widespread eczema herpeticum, CNS infection, or infection in an immunosuppressed patient is probably best treated with intravenous antiviral medication. The acyclovir family of medications are converted to their active form by viral-specific thymidine kinase. After conversion, this metabolite is a potent inhibitor of viral DNA polymerization. These medications are highly specific for the viral enzymes and have an excellent side effect profile. Acyclovir-resistant HSV has become well recognized and is best treated with foscarnet. Foscarnet does not require modulation by thymidine kinase to become an active inhibitor of HSV replication, thereby bypassing the HSV resistance mechanism. No medication to date has shown activity against latent viral infection.
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