HSV
Summary
Herpes Simplex Virus (HSV) is a double-stranded DNA virus of the Herpesviridae family with two main types: HSV-1 (classically oral/orolabial lesions, gingivostomatitis, herpes labialis) and HSV-2 (classically genital herpes), though both can cause either site due to oral-genital contact. HSV establishes lifelong latency in sensory ganglia (HSV-1 in trigeminal ganglion, HSV-2 in sacral ganglia) with potential for reactivation triggered by stress, UV light, illness, or immunosuppression.
Detail
HSV-1 and HSV-2 are enveloped, double-stranded DNA viruses that replicate in the nucleus of host cells. Primary infection often occurs via mucocutaneous contact, producing painful vesicular lesions on an erythematous base that ulcerate. Classic presentations include herpetic gingivostomatitis (children), herpes labialis/cold sores (HSV-1 reactivation), genital herpes (HSV-2, though HSV-1 genital infections are increasing), herpetic whitlow (finger infection in healthcare workers/children), and herpes gladiatorum (wrestlers). HSV can cause keratoconjunctivitis (dendritic corneal ulcers, a leading cause of infectious blindness), and in neonates, disseminated HSV infection acquired during vaginal delivery can be life-threatening (hepatitis, encephalitis, skin/eye/mouth disease). HSV encephalitis, often HSV-1, classically affects the temporal lobes and presents with fever, altered mental status, and seizures; diagnosis is via CSF PCR, and it requires urgent IV acyclovir due to high mortality if untreated. Latency is established in sensory ganglia (trigeminal for HSV-1, sacral dorsal root ganglia for HSV-2) via episomal viral DNA that evades immune clearance; reactivation is triggered by stress, fever, UV exposure, menstruation, or immunosuppression (e.g., HIV). Diagnosis is primarily clinical but can be confirmed via Tzanck smear (showing multinucleated giant cells, though not specific for HSV vs VZV), viral culture, direct fluorescent antibody testing, or PCR (gold standard, especially for CNS disease). Histologically, HSV causes characteristic intranuclear Cowdry type A inclusion bodies. Treatment includes acyclovir, valacyclovir, or famciclovir, which are guanosine analogs requiring viral thymidine kinase for activation—a mechanism exploited for relative selectivity for infected cells. Resistance can occur via thymidine kinase mutations, particularly in immunocompromised patients, requiring foscarnet as an alternative (does not require viral TK). HSV is a major congenital infection (TORCH complex) and can cause erythema multiforme as a hypersensitivity reaction.
Sources
- First Aid for the USMLE Step 1
- Sherris Medical Microbiology
- UpToDate: Epidemiology, clinical manifestations, and diagnosis of herpes simplex virus infection
- Robbins and Cotran Pathologic Basis of Disease
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