Herpes Simplex and Varicella-Zoster Virus Infections

Herpesvirus Family Trait: LATENCY

HSV+VZV = Herpesviridae. Enveloped dsDNA. KEY shared trait: LATENCY — retreats to sensory ganglia (transcriptionally silent) after primary infection, reactivates with weakened local control (stress, UV, immunosuppression, fever, aging for VZV). All clinical patterns trace to this.

HSV (HSV-1, HSV-2)

Historically: HSV-1=oral/facial, HSV-2=genital. BLURRED now (oral-genital contact transmits either to either site) — site no longer reliably predicts serotype. Transmission: direct contact + ASYMPTOMATIC SHEDDING (major spread route, unwitnessed).

Pathogenesis: primary infection at entry site → retrograde travel via sensory axon → dorsal root ganglion (trigeminal=oral HSV-1, sacral=genital HSV-2) → LATENCY. Reactivation → back down SAME nerve → SAME dermatomal location each time (unlike fresh infection).

Clinical:

• Primary orolabial (usually HSV-1, childhood): asymptomatic or gingivostomatitis (painful oral ulcers+fever)
• Recurrent orolabial: “cold sore,” milder, prodromal tingling
• Genital HSV (usually HSV-2): primary = painful vesicles/ulcers+fever+dysuria+inguinal LAD. Recurrence = milder/shorter. ASYMPTOMATIC SHEDDING between outbreaks = major transmission route (underappreciated)
• Neonatal HSV: EMERGENCY. Vaginal delivery through shedding maternal tract. Localized (skin/eye/mouth) to disseminated/encephalitis. Substantial mortality/morbidity even treated. → C-section if active lesions at term.
• HSV encephalitis: MOST FEARED complication beyond neonatal period. TEMPORAL LOBE localization. High untreated mortality, acyclovir dramatically reduces if prompt.
• Eczema herpeticum: severe disseminated cutaneous HSV in skin-barrier-defect patients (classic: atopic dermatitis).

Diagnosis: PCR (vesicle fluid/swab) = DOC, more sensitive than culture, standard for CSF in suspected encephalitis. Tzanck smear: multinucleated giant cells, rapid/cheap, CANNOT distinguish HSV from VZV (same cytopathic effect). Serology (type-specific): identifies carriers/past infection, NOT useful for acute lesion diagnosis.

Treatment: Acyclovir (or valacyclovir/famciclovir, better bioavailability) — primary, recurrent, suppressive therapy (↓transmission too). IV acyclovir: neonatal HSV, encephalitis, disseminated/severe.

VZV — Two Diseases, One Virus

Varicella (chickenpox) = primary infection. Herpes zoster (shingles) = reactivation. Single continuous story.

Varicella

Respiratory transmission (HIGHLY contagious) or vesicle contact. 2wk incubation. Rash: SUCCESSIVE CROPS — different stages (macule/papule/vesicle/crust) SIMULTANEOUSLY visible = distinctive (contrast smallpox’s synchronous single-crop, see Poxvirus topic). Fever+malaise. Complications (adults/neonates/immunocompromised): bacterial superinfection, varicella pneumonia, rare encephalitis/cerebellar ataxia. Congenital varicella syndrome: early pregnancy maternal infection → limb hypoplasia, skin scarring, eye/CNS abnormalities.

Herpes Zoster

Reactivation (dorsal root/cranial nerve ganglion) → painful vesicular rash, STRICTLY SINGLE DERMATOME (unilateral, sharp midline respect — distinguishes from nearly every other vesicular rash). Risk ↑ with age + immunosuppression (↓VZV-specific CMI). Post-herpetic neuralgia: COMMONEST/most disabling complication, persistent pain post-rash-healing, ↑ with age. Ophthalmic zoster: V1 trigeminal, nasal-tip lesion (Hutchinson’s sign) predicts eye involvement — urgent ophthalmology. Ramsay Hunt syndrome: geniculate ganglion — facial palsy + ear vesicles + vestibulocochlear symptoms.

Diagnosis: mostly CLINICAL (distinctive rash). PCR for atypical/severe. Tzanck = same as HSV (indistinguishable).

Treatment: Varicella — healthy child = self-limited/symptomatic. Oral acyclovir (adults/adolescents/high-risk). IV acyclovir (severe/immunocompromised). Zoster — oral antivirals (acyclovir/valacyclovir/famciclovir), START EARLY (<72hr rash onset) → ↓severity + ↓PHN risk.

Prevention: Live attenuated varicella vaccine (childhood primary prevention). Zoster vaccine (recombinant subunit NOW PREFERRED over old live form) — older adults, prevents reactivation+PHN. VZIG: post-exposure passive protection, high-risk contacts (immunosuppressed, susceptible pregnant, exposed neonates) who can’t get live vaccine.

The Herpesvirus Family Trait: Latency

Herpes simplex virus (HSV) and varicella-zoster virus (VZV) both belong to the Herpesviridae — large, enveloped, double-stranded DNA viruses whose single defining shared behaviour, more than any other feature, is latency: after primary infection, the virus retreats into sensory neuron ganglia in a transcriptionally near-silent state, invisible to immune clearance, and can reactivate intermittently throughout life whenever local immune control weakens — stress, sunlight (UV exposure), immunosuppression, fever, or, for VZV specifically, simply ageing. Every clinical pattern described below traces back to this one shared property.

Herpes Simplex Virus (HSV-1 and HSV-2)

Virology and Transmission

Two serotypes exist, historically associated with different anatomical sites — HSV-1 classically oral/facial, HSV-2 classically genital — though this distinction has blurred considerably with changing sexual practices (oral-genital contact readily transmits either type to either site), so site alone no longer reliably predicts serotype. Transmission is by direct contact with active lesions or, importantly, asymptomatic viral shedding from mucosal surfaces even without visible lesions — a major reason HSV, especially HSV-2, spreads so persistently despite most transmission events being unwitnessed by either partner.

Pathogenesis

Primary infection occurs at a mucocutaneous entry site, with local replication producing the primary lesion; the virus then travels retrograde along sensory nerve axons to the corresponding dorsal root ganglion (trigeminal ganglion for oral HSV-1, sacral ganglia for genital HSV-2), establishing lifelong latency there. Reactivation sends virus back down the same nerve to the original dermatomal skin/mucosal territory, producing a recurrent lesion — which is why recurrences characteristically appear in the same anatomical location each time, unlike a fresh, unrelated infection.

Clinical Manifestations

Primary orolabial HSV (usually HSV-1, often in childhood) can be asymptomatic or present as gingivostomatitis (painful oral ulcers, fever, in a young child); recurrent orolabial HSV presents as the familiar “cold sore”/fever blister at the lip margin, typically milder than the primary episode and preceded by a prodromal tingling.

Genital HSV (usually HSV-2, though HSV-1 genital infection is rising) presents as painful genital vesicles/ulcers, often with fever, dysuria, and inguinal lymphadenopathy in a first (primary) episode; recurrences are typically milder and shorter, and — critically for public health messaging — asymptomatic shedding between recognized outbreaks is a major, underappreciated route of ongoing transmission.

Neonatal HSV is a genuine emergency, acquired most often during vaginal delivery through an actively shedding maternal genital tract, ranging from localized skin/eye/mouth disease to disseminated infection or encephalitis, with mortality and long-term neurological morbidity substantial even with treatment — which is exactly why a mother with active genital lesions at term is typically delivered by caesarean section.

HSV encephalitis (see also Infections of the Central Nervous System) is the most feared HSV complication in any age group beyond the neonatal period, classically localizing to the temporal lobe, with a high untreated mortality that acyclovir dramatically reduces if started promptly.

Eczema herpeticum is a severe, disseminated cutaneous HSV infection specifically in patients with an underlying skin barrier defect (classically atopic dermatitis), where HSV spreads widely across already-compromised skin rather than staying localized.

Laboratory Diagnosis

PCR of vesicle fluid or a lesion swab is now the diagnostic method of choice — more sensitive than viral culture and increasingly the standard for CSF testing in suspected HSV encephalitis specifically, where prompt, accurate diagnosis directly changes management. Tzanck smear (cytology of scraped vesicle base, showing multinucleated giant cells) is a rapid, low-cost bedside test but cannot distinguish HSV from VZV, since both herpesviruses produce the identical cytopathic effect. Viral culture and direct fluorescent antibody testing remain available alternatives where PCR access is limited. Serology (type-specific HSV-1/HSV-2 antibody) has a role in identifying asymptomatic carriers or confirming past infection, but is not useful for diagnosing an acute lesion.

Treatment

Acyclovir (or the better-bioavailability oral prodrugs valacyclovir/famciclovir) is standard for both primary and recurrent episodes, and for suppressive therapy in patients with frequent recurrences (which, alongside symptom control, meaningfully reduces transmission risk to partners). IV acyclovir is used for neonatal HSV, HSV encephalitis, and disseminated/severe disease.

Varicella-Zoster Virus (VZV)

Two Diseases, One Virus

VZV causes two entirely distinct clinical syndromes at different points in the same infection’s natural history — varicella (chickenpox) on primary infection, and herpes zoster (shingles) on reactivation — a pattern worth understanding as a single continuous story rather than two unrelated diseases.

Varicella (Chickenpox)

Primary infection, transmitted by the respiratory route (highly contagious — among the most transmissible of all human viral infections) or direct vesicle contact. After a 2-week incubation, a generalized vesicular rash erupts in successive crops, so that lesions at different stages (macule, papule, vesicle, crust) are visible simultaneously on the same patient at the same time — a genuinely distinctive diagnostic feature, in contrast to smallpox’s more synchronous, single-crop eruption (a distinction covered further under Poxvirus Infections). Fever and malaise accompany the rash. Complications, more likely in adults, neonates, and the immunocompromised, include bacterial superinfection of skin lesions, varicella pneumonia, and, rarely, encephalitis/cerebellar ataxia. Congenital varicella syndrome follows maternal infection in early pregnancy, causing limb hypoplasia, skin scarring, and eye/CNS abnormalities in the fetus.

Herpes Zoster (Shingles)

Reactivation of latent VZV from a dorsal root or cranial nerve ganglion, producing a painful vesicular rash strictly confined to the corresponding single dermatome (unilateral, respecting the midline sharply — a distinguishing clinical feature from nearly every other vesicular rash) — direct proof of the underlying single-nerve-root reactivation mechanism. Risk rises sharply with age and with any cause of immunosuppression, since both reflect declining VZV-specific cell-mediated immunity’s ability to keep the latent virus suppressed. Post-herpetic neuralgia — persistent, sometimes severe, pain in the affected dermatome lasting long after the rash has healed — is the commonest and most disabling complication, more likely with increasing age. Ophthalmic zoster (trigeminal V1 division involvement, with a nasal-tip lesion — Hutchinson’s sign — predicting eye involvement) risks serious ocular complications and needs urgent ophthalmology involvement. Ramsay Hunt syndrome (geniculate ganglion reactivation) causes facial palsy plus ear vesicles plus vestibulocochlear symptoms.

Laboratory Diagnosis

Largely clinical for both varicella and zoster, given their distinctive rash patterns; PCR of vesicle fluid confirms in atypical or severe presentations, and Tzanck smear again shows multinucleated giant cells indistinguishable from HSV.

Treatment and Prevention

Varicella in an otherwise healthy child is typically self-limited and managed symptomatically; oral acyclovir is used for adults, adolescents, and higher-risk patients, and IV acyclovir for severe/complicated disease or the immunocompromised. Herpes zoster is treated with oral antivirals (acyclovir, valacyclovir, or famciclovir) started as early as possible, ideally within 72 hours of rash onset, to reduce both acute severity and post-herpetic neuralgia risk. Prevention: live attenuated varicella vaccine for primary prevention in childhood; a separate, higher-antigen-dose zoster vaccine (recombinant subunit vaccine now preferred over the older live formulation) for older adults, specifically to prevent reactivation disease and post-herpetic neuralgia. VZIG (varicella-zoster immunoglobulin) provides post-exposure passive protection for high-risk contacts (immunosuppressed individuals, susceptible pregnant women, exposed neonates) who cannot safely receive the live vaccine.

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