Dermatology MCQ - Viral serology - Recurrent oro-facial and cutaneous herpes

A 25-year-old woman presents with a recurrent eruption of grouped vesicles on an erythematous base along the vermilion border of her lip. She reports a prodrome of tingling and burning at the site 24 hours prior to the appearance of the lesions. This is the third such episode in the past year. Which of the following best describes the virologic pathogenesis of this recurrent infection?

A) Reactivation of latent varicella-zoster virus from dorsal root ganglia
B) Reactivation of latent herpes simplex virus from trigeminal ganglia
C) Reinfection with a new strain of herpes simplex virus through skin contact
D) Persistent infection of epidermal keratinocytes by human papillomavirus
E) Autoimmune-mediated inflammation triggered by prior viral exposure

Correct Answer: B) Reactivation of latent herpes simplex virus from trigeminal ganglia

Explanation

This clinical scenario is classic for recurrent herpes labialis (cold sores), the most common manifestation of recurrent HSV-1 infection.

Key Clinical Features:

• Presentation: Grouped vesicles on an erythematous base that rupture, crust, and heal without scarring.

• Location: Predominantly on the vermilion border of the lip (herpes labialis), but can occur on other perioral sites.

• Prodrome: A localized prodrome of pain, burning, or tingling 6-24 hours before lesions appear is highly characteristic.

• Recurrence: Reactivations can be triggered by stress, sunlight, fever, or immunosuppression.

Virologic Pathogenesis:

• Primary Infection: Typically asymptomatic or presents as gingivostomatitis in childhood.

• Latency: After primary infection, HSV-1 (or less commonly HSV-2) establishes lifelong latency in the sensory neuron cell bodies of the trigeminal ganglion.

• Reactivation: Various triggers (e.g., UV exposure, stress) cause reactivation. The virus travels anterograde along the sensory nerve to the original site of infection (e.g., the lip), where it replicates in epidermal cells, causing the characteristic vesicles.

Why Not the Other Options?

• (A) Reactivation of latent varicella-zoster virus (VZV): VZV reactivation causes herpes zoster (shingles), which presents as a painful dermatomal vesicular rash, not recurrent localized lip lesions.

• (C) Reinfection with a new strain: Reinfection with a different HSV strain is theoretically possible but exceedingly rare due to robust humoral and cellular immunity after primary infection. Recurrences are almost always due to reactivation of latent virus.

• (D) Persistent HPV infection: Human papillomavirus causes warts (verrucous papules) or dysplastic changes, not acute vesicular eruptions.

• (E) Autoimmune-mediated inflammation: This describes conditions like pemphigus or lupus, which cause erosions, bullae, or plaques, not recurrent grouped vesicles with a prodrome.

Management:

• Topical antivirals (e.g., penciclovir, acyclovir cream) may reduce healing time if applied during the prodrome.

• Oral antivirals (e.g., valacyclovir) are used for frequent or severe recurrences.

• Sun protection (lip balm with SPF) can prevent sun-induced recurrences.

Prognosis: Recurrences are self-limiting (7-10 days) but can be bothersome. Severe or disseminated disease may occur in immunocompromised patients.