Antiviral therapy for genital herpes (HSV-2): Which drug inhibits viral DNA synthesis?

Introduction / Context: Genital herpes is most commonly caused by herpes simplex virus type 2 (HSV-2) and sometimes HSV-1. The cornerstone of therapy targets viral DNA replication, shortening symptom duration and reducing shedding.

Given Data / Assumptions:

• We need an agent active against HSV that interferes with viral DNA production.
• The clinical context is genital herpes.

Concept / Approach: Acyclovir is a guanosine analog that requires phosphorylation by viral thymidine kinase (TK) to the monophosphate form, then cellular kinases to the triphosphate, which competitively inhibits viral DNA polymerase and causes chain termination. This selectivity spares uninfected cells lacking viral TK.

Step-by-Step Solution: Match mechanism: acyclovir → viral DNA polymerase inhibition/chain termination in HSV-infected cells. Exclude antibacterial agents (erythromycin, vancomycin). Exclude amantadine (influenza A M2 inhibitor) and oseltamivir (influenza neuraminidase inhibitor). Choose acyclovir as the correct antiviral.

Verification / Alternative check: Clinical guidelines endorse acyclovir/valacyclovir/famciclovir for HSV; all rely on similar DNA polymerase–targeting mechanisms.

Why Other Options Are Wrong: They target bacteria or different viruses (influenza), not HSV DNA replication.

Common Pitfalls: Confusing HSV therapy with anti-influenza drugs; overlooking the need for viral TK activation and implications for TK-negative resistance.

Final Answer: Acyclovir.