DR8.1 | Common Viral Skin Infection Foundations — Summary & Reflection

KEY TAKEAWAYS

Cutaneous viral infections are caused by a small set of DNA virus families, each with a distinct biology and a recognisable morphological signature. The Herpesviridae — HSV (perioral HSV-1, genital HSV-2) and VZV (varicella then herpes zoster) — establish ganglion latency and reactivate, produce grouped vesicles on an erythematous base, and show multinucleate giant cells on Tzanck smear (which confirms the family but not the specific virus); they respond to aciclovir/valaciclovir. The Papillomaviridae — HPV — infect keratinocytes to produce verrucous warts with thrombosed capillaries and koilocytes on histology; they have no systemic antiviral and are treated by destruction or resolve as immunity develops. The Poxviridae — molluscum contagiosum virus — replicate in the cytoplasm to produce pearly umbilicated papules containing Henderson-Paterson bodies, are often self-limiting, and become extensive in immunosuppression. Reading lesion type plus distribution first, then choosing a confirmatory test and deciding whether an antiviral helps, is the framework that carries through into the focused recognition SDLs on each entity.

REFLECT

Think back to a viral skin infection you have seen on a ward round or in an outpatient clinic — a cold sore, shingles, a wart, or a cluster of umbilicated papules. At the time, did you recognise it by its morphological signature, or did you rely on someone else's label? Now that you have the family-level framework, which feature would you read first the next time you see it — the lesion type, the grouping, or the distribution — and what single confirmatory test, if any, would you choose? Anchoring this framework to a real patient you remember is what turns it from a list into a clinical reflex you will use throughout your career.