A 29-year-old man with HIV and a recent CD4 count of 36 cells/mm3 is seen in clinic for evaluation of persistent painful ulcers in the perianal region despite taking a 14-day course of valacyclovir 1,000 mg twice daily. In the past 2 years he has intermittently taken valacyclovir for recurrent episodes of genital herpes. A sample of the perianal region is obtained for viral culture; subsequently, the culture is positive for herpes simplex virus-2 (HSV-2), and acyclovir susceptibility testing shows resistance to acyclovir.
Which one of the following would be the next best step in the management of this acyclovir-resistant herpes lesion?
Figure 1. Acyclovir Mechanism of Action
As acyclovir enters cells infected with HSV, it is initially activated by the viral thymidine kinase (TK); the second and third phosphorylation steps occur through cellular kinases. The active drug acyclovir triphosphate then inhibits HSV DNA replication.
Illustration by David H. Spach, MD
Figure 2. Acyclovir-Resistant HSV
Most acyclovir-resistance HSV occurs via the mechanism of decreased or absent production of thymidine kinase (TK) by HSV. The strains are referred to as HSV TK- mutants. With inadequate production of TK, acyclovir does not undergo the mandatory initial phosphorylation step and HSV replication proceeds uninhibited.
Illustration by David H. Spach, MD
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Question Last Updated
February 4th, 2025
February 4th, 2025
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