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The varicella-zoster virus (VZV) causes two distinct infections: varicella and herpes zoster. Varicella, commonly known as chickenpox, manifests as the primary infection with VZV, which is a member of the family of herpesviruses. VZV then remains dormant within the sensory neurons, reactivating later in life to cause herpes zoster, commonly known as shingles.1

More than 99% of immunocompetent persons in the United States aged older than 40 years show serologic evidence of past primary VZV infection.2 Therefore, this population of older adults is susceptible to herpes zoster.

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Herpes zoster develops in approximately 1 of every 3 persons in the United States in their lifetime, with an estimated annual incidence of 1 million cases. The risk for herpes zoster increases with age; about half of all cases occur in adults aged 60 years and older.3-5

Risk factors, signs, and symptoms

The major risk factors for herpes zoster are immunosuppression, particularly a decline of cell-mediated immunity, and increasing age (Table 1).6 The condition commonly begins with prodromal symptoms of malaise, headache, mild fever, and abnormal skin sensations such as itching and burning.

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A rash begins as pink, maculopapular lesions in a unilateral dermatomal distribution along a sensory nerve tract. The rash is extremely sensitive to touch, and the pain is described as aching, shock-like, stabbing, or burning. The rash may cause intense pruritus. The lesions progress to clear vesicles, crust, and heal over the course of 2 to 4 weeks. More than one dermatomal region can be involved. The rash is often distributed over thoracic, cervical, or trigeminal dermatomes.7,8

Which of the following antiviral drugs do you most frequently prescribe for patients with shingles?

Pathophysiology of varicella and herpes zoster

Primary VZV infection typically occurs during childhood when wild-type VZV invades the respiratory tract and nasopharyngeal lymphoid tissue. The incubation period is 10 to 21 days, and children typically transmit the virus to one another via nasopharyngeal secretions.

During this period, the virus travels to the sensory nerves of the epidermis, causing the typical rash known as chickenpox. Pink, maculopapular lesions usually begin on the trunk and face and spread to the extremities. The lesions are pruritic and evolve from papular to vesicular, crust over, and heal. After the initial infection subsides, the virus lies dormant in the sensory dorsal root ganglia. Mainly cell-mediated immunity is involved in controlling the virus and keeping it dormant.9,10

Later in life, VZV reactivates to cause herpes zoster, in which intact virions in sensory neurons migrate through axons, spread from cell to cell, and penetrate the epidermis. A painful, vesicular rash develops along the dermatomal distribution of a sensory nerve. Affected ganglia show neuronal destruction and loss, which are usually accompanied by mononuclear inflammatory infiltrates, regional necrosis, and hemorrhage.11

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