Human Herpes Virus (HHV)
– basic definition and overview
→ Human herpes virus is a DNA virus of the Herpesviridae family that infects humans and establishes lifelong latency
Causes / transmission
→ Direct contact with infected saliva, genital secretions, or lesions
→ Vertical transmission to neonate during birth (especially HHV‑2)
Types (two main variants)
→ HHV‑1 (Herpes simplex virus type 1) – mainly oral‑facial infection
→ HHV‑2 (Herpes simplex virus type 2) – mainly genital infection
Morphology (Robbins, Harsh Mohan)
→ Enveloped virus with icosahedral capsid
→ Linear double‑stranded DNA genome (~152 kb)
→ Tegument layer containing viral enzymes
Pathogenesis – step‑wise sequence
- Virus attaches to heparan‑sulfate receptors on epithelial cells →
- Fusion of viral envelope with cell membrane → entry of capsid into cytoplasm →
- Capsid transports to nucleus, releases DNA → replication of viral genome →
- Assembly of nucleocapsids in nucleus → budding through nuclear membrane → acquisition of envelope →
- Anterograde transport along sensory neurons to peripheral epithelium →
- Lytic replication in epithelial cells → formation of vesicular lesions →
- Some virions travel retrograde to sensory ganglia → establish latency in neuronal nuclei →
- Reactivation (stress, immunosuppression) → travel back to periphery → recurrent lesions
Clinical features – HHV‑1
→ Primary infection (often in childhood) → fever, malaise, painful vesicles on lips, gums, oral mucosa (cold sores)
→ Herpetic gingivostomatitis in infants/young children → ulceration, drooling, lymphadenopathy
→ Recurrent oral lesions triggered by sunlight, fever, stress
Clinical features – HHV‑2
→ Primary genital infection → painful grouped vesicles on penis, vulva, perianal area, accompanied by dysuria and tender lymphadenopathy
→ May be asymptomatic or present as mild ulceration → later recurrences at same site
→ Can cause aseptic meningitis (especially in young adults) → headache, neck stiffness, photophobia
→ Neonatal herpes (vertical transmission) → disseminated disease, skin‑eye‑mouth lesions, CNS involvement, high mortality
Complications (essential NCH points)
→ Secondary bacterial infection of lesions → impetigo, cellulitis
→ Herpetic encephalitis (rare, high mortality)
→ Aseptic meningitis (more common with HHV‑2)
→ Neonatal disseminated infection → organ failure, long‑term neuro deficits
Diagnosis (Harsh Mohan, Ananthanarayan)
→ Clinical appearance of typical vesicles
→ Tzanck smear – multinucleated giant cells (non‑specific)
→ Viral culture from lesion swab (gold standard)
→ PCR for HSV DNA – rapid, highly sensitive
→ Serology – IgM for recent infection, IgG for past exposure
Management (Chatterjee, MUHS guidelines)
→ Acyclovir 400 mg PO five times daily for 7‑10 days (primary genital) or 5 days (oral)
→ Valacyclovir or famciclovir – convenient dosing, similar efficacy
→ Topical acyclovir for mild oral lesions (5% cream)
→ Analgesics (paracetamol, NSAIDs) for pain relief
→ Adequate hydration, soft diet for gingivostomatitis
→ Counsel on avoiding contact during active lesions, condom use, and suppressive therapy for frequent recurrences
Life cycle – simplified numbered steps
- Attachment → virus binds to cell‑surface heparan‑sulfate
- Entry → envelope fuses, capsid enters cytoplasm
- Nuclear transport → capsid delivers DNA to nucleus
- Replication → viral DNA synthesis and protein production
- Assembly → nucleocapsids form in nucleus
- Egress → budding through nuclear and Golgi membranes, acquiring envelope
- Anterograde transport → moves along axon to epithelial surface
- Release → lytic destruction of cells, vesicle formation
- Latency → some virions travel retrograde to sensory ganglion, remain dormant
- Reactivation → stress/immunosuppression triggers repeat of steps 7‑8
Memory trick for life cycle (rhyming)
“Attach, hatch, pack, stack, burst, thrust, rest, test” –
Attach (bind), hatch (enter), pack (DNA to nucleus), stack (replicate), burst (assemble), thrust (travel out), rest (latency), test (reactivate)
Key exam points to remember (MUHS + NCH)
→ Two variants: HHV‑1 (oral), HHV‑2 (genital)
→ Enveloped dsDNA, icosahedral capsid, tegument
→ Primary infection → vesicular lesions; latency in sensory ganglia; reactivation → recurrent lesions
→ Diagnosis: clinical + Tzanck + PCR
→ Treatment: acyclovir/valacyclovir, analgesics, suppressive therapy, neonatal prophylaxis
→ Complications: bacterial superinfection, encephalitis, meningitis, neonatal disease
(End of notes – all points are in simple, handwritten‑style language, point‑wise, with arrows and numbered steps as required.)