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Newport Retro Keen

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Abstract

Infections by herpes simplex virus (HSV) cannot yet be eliminated, but the severity of the disease can be reduced. Two newer drugs with established efficacy for such infections, famciclovir and valacyclovir, were tested in a mouse eye model of HSV infection. Both drugs significantly reduced mortality and titers of virus shed from the eyes of mice infected with an otherwise lethal dose of HSV type 1 (HSV-1). Similar titers of HSV-1 were found in the eyes, ganglia, and brains of treated animals. Although valacyclovir reduced the latent viral DNA load better in these studies than did famciclovir, rates of reactivation by explantation and UV exposure were the same. Thus, in this study, famciclovir and valacyclovir were equally effective in limiting the virulence and spread of HSV-1, despite their biochemical and pharmacologic differences.

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Herpes simplex virus (HSV) types 1 and 2 are important human pathogens that cause orofacial and genital lesions [ 1 ]. During the initial infection, HSV infects neurons, where it remains in a latent state until reactivated by stimuli such as heat and UV light [ 2 , 3 ]. In vivo reactivation of HSV depends on multiple factors, such as the anatomic site of infection [ 4 ], the host's immune status [ 5–7 ], and the quantity of latent viral DNA [ 8 ].

Currently, there is no vaccine or cure for HSV infections; however, treatments are available that diminish the severity of the disease. Valacyclovir and famciclovir, the oral forms of acyclovir and penciclovir, respectively, are guanine analogues that inhibit HSV replication at the level of DNA synthesis [ 9–16 ]. Acyclovir has been the standard for treating herpes infections; however, because of its poor bioavailability (15%–20% vs. 55% for valacyclovir and 75% for famciclovir), it was prudent to develop new compounds. Following their absorption, valacyclovir and famciclovir are rapidly and efficiently metabolized by host enzymes to acyclovir and penciclovir, respectively.

Both acyclovir and penciclovir enter infected and uninfected cells but require viral thymidine kinase for activity [ 9 , 14 , 15 ]. Previous reports showed that penciclovir has a higher affinity than acyclovir for the viral thymidine kinase, a faster rate of phosphorylation, and a longer intracellular half-life [ 10 , 11 ]; however, penciclovir has a lower affinity than acyclovir for the HSV DNA polymerase. The end result is that the penciclovir prodrug, famciclovir, which is effective in humans at doses similar to those for acyclovir, can be given less often. The higher acyclovir blood levels effected by valacyclovir achieve the same end result of reduced dosage frequency. Given these modest differences between valacyclovir and famciclovir, it is noteworthy that a series of animal studies suggested that famciclovir is better than valacyclovir in terminating ganglionic HSV infection and thereby limits subsequent reactivation [ 17–20 ].

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