Abstract
Varicella zoster virus (VZV) is an exclusively human neurotropic alphaherpesvirus. Primary infection causes varicella (chickenpox), after which virus becomes latent in cranial nerve ganglia, dorsal root ganglia, and autonomic ganglia along the entire neuraxis. Years later, in association with a decline in cell-mediated immunity in elderly and immunocompromised individuals, VZV reactivates and causes a wide range of neurologic disease. This article discusses the clinical manifestations, treatment, and prevention of VZV infection and reactivation; pathogenesis of VZV infection; and current research focusing on VZV latency, reactivation, and animal models.
MeSH terms
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Analgesics, Opioid / therapeutic use
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Antidepressive Agents / therapeutic use
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Antiviral Agents / therapeutic use
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Chickenpox / physiopathology
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Chickenpox / transmission
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Chickenpox / virology
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Ganglia / virology
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Herpes Zoster / physiopathology
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Herpes Zoster / transmission
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Herpes Zoster / virology
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Herpes Zoster Vaccine / administration & dosage
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Herpesvirus 3, Human / isolation & purification*
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Humans
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Neuralgia, Postherpetic / drug therapy
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Neuralgia, Postherpetic / virology
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Retinal Necrosis Syndrome, Acute / cerebrospinal fluid
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Retinal Necrosis Syndrome, Acute / prevention & control
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Retinal Necrosis Syndrome, Acute / virology
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Time Factors
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Virus Diseases / physiopathology*
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Virus Diseases / prevention & control
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Virus Diseases / virology*
Substances
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Analgesics, Opioid
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Antidepressive Agents
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Antiviral Agents
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Herpes Zoster Vaccine