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Herpes Simplex Virus (HSV) Ocular Manifestations
Cornea
1. Virology & Pathobiology
Clinical Analogy
- Think of HSV as a sleeping wolf in the trigeminal ganglion. It enters through the cornea or oral mucosa in
childhood, travels up sensory axons to its den (ganglion), and sleeps for years. The wolf awakens - selectively, unpredictably - whenever the host's immune vigilance drops: UV light, fever, stress, immunosuppression. Each awakening causes fresh corneal damage through two entirely different mechanisms: direct viral cytopathology (epithelial disease) and immune-mediated collateral damage (stromal/endothelial disease). Distinguishing these two mechanisms governs every management decision.
2. Taxonomy and Structure
- Herpes simplex virus (HSV) belongs to the Alphaherpesvirinae subfamily within Orthoherpesviridae.
- The virion is 150–200 nm and has four structural components: core (double-stranded DNA, ~152 kb), icosahedral capsid (162 capsomers), structurally complex and poorly defined tegument containing many viral and possibly some host proteins, and a lipid envelope that is a bilayer containing multiple integral viral glycoproteins, including gB, gC, gD, and gH/gL. Envelope glycoproteins have roles in host-cell adsorption and penetration.
| Feature | Herpes simplex virus type 1 (HSV-1) | Herpes simplex virus type 2 (HSV-2) |
|---|---|---|
| Primary site | • Orofacial (trigeminal) | • Genital (sacral spinal segments 2–4) |
| Ocular tropism | • Dominant cause of ocular herpes simplex virus (HSV) (~95%) | • Rare; neonatal ocular herpes simplex virus (HSV) • Acute retinal necrosis (ARN) in adults |
| Latency site | • Trigeminal ganglion; the specific V1-to-V2 predominance is not established here. | • Sacral dorsal root ganglia |
| Reactivation rate | • 20–40% of the population experience recurrent orolabial herpes simplex virus infection at some stage. | • Lower recurrence rate oculofacially |
| Seroprevalence (global) | • 64% of the global population under age 50 (2020 estimate) | • 13% of people aged 15–49 years worldwide (2020 estimate) |
| Relation to acute retinal necrosis (ARN) | • Acute retinal necrosis (ARN) in older/immunocompetent patients. | • Acute retinal necrosis (ARN) in younger patients • Comparative aggressiveness is not established here. |
| Neonatal disease | • Intrapartum exposure to herpes simplex virus type 1 (HSV-1) is possible. | • Herpes simplex virus type 2 (HSV-2) causes many cases of neonatal herpes simplex virus (HSV), but herpes simplex virus type 1 (HSV-1) causes approximately one-third to one-half. • Ocular involvement is part of localized skin, eye, and/or mouth disease and may be severe. |
| Feature | Herpes simplex virus type 1 (HSV-1) | Herpes simplex virus type 2 (HSV-2) |
|---|---|---|
| Primary site | • Orofacial (trigeminal) | • Genital (sacral spinal segments 2–4) |
| Ocular tropism | • Dominant cause of ocular herpes simplex virus (HSV) (~95%) | • Rare; neonatal ocular herpes simplex virus (HSV) • Acute retinal necrosis (ARN) in adults |
| Latency site | • Trigeminal ganglion; the specific V1-to-V2 predominance is not established here. | • Sacral dorsal root ganglia |
| Reactivation rate | • 20–40% of the population experience recurrent orolabial herpes simplex virus infection at some stage. | • Lower recurrence rate oculofacially |
| Seroprevalence (global) | • 64% of the global population under age 50 (2020 estimate) | • 13% of people aged 15–49 years worldwide (2020 estimate) |
| Relation to acute retinal necrosis (ARN) | • Acute retinal necrosis (ARN) in older/immunocompetent patients. | • Acute retinal necrosis (ARN) in younger patients • Comparative aggressiveness is not established here. |
| Neonatal disease | • Intrapartum exposure to herpes simplex virus type 1 (HSV-1) is possible. | • Herpes simplex virus type 2 (HSV-2) causes many cases of neonatal herpes simplex virus (HSV), but herpes simplex virus type 1 (HSV-1) causes approximately one-third to one-half. • Ocular involvement is part of localized skin, eye, and/or mouth disease and may be severe. |
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Keep reading Herpes Simplex Virus (HSV) Ocular Manifestations
31 more sections are included with the Clinical plan.
- Latency and Reactivation Biology
- Primary vs Recurrent Infection
- Mechanisms of Corneal Damage
- HSV Blepharitis / Vesicular Eruption
- Neonatal Ocular Herpes
- Conjunctival Disease