Varicella‑zoster virus (VZV), also known as human herpesvirus 3, is a double‑stranded DNA virus with an icosahedral capsid, tegument and lipid envelope. It belongs to the alpha herpesvirus subfamily and is the causative agent of varicella (chickenpox) and herpes zoster (shingles).
Biology and Pathogenesis
VZV is highly contagious and spreads through respiratory droplets or direct contact with lesion fluid. During primary infection, the virus replicates in the nasopharynx and regional lymph nodes, leading to viremia that disseminates the virus to the skin and mucous membranes. This results in varicella, characterized by a diffuse vesicular rash that progresses from macules to papules to vesicles and crusts. After resolution of the rash, VZV migrates along sensory neurons and establishes latency in the dorsal root ganglia. Reactivation of latent VZV occurs years later, especially in older adults or immunocompromised individuals, producing herpes zoster. In shingles, viral replication and spread occur along a single sensory nerve, resulting in a unilateral vesicular eruption confined to a dermatome. VZV infection is almost universal; serologic evidence of past infection is present in about 95 percent of adults. Host immunity, mediated by interferons and cellular and humoral responses, limits the severity of primary infection and helps prevent reactivation, but immunity wanes with age or immunosuppression. Complications of primary infection include bacterial superinfection of lesions, varicella pneumonia, encephalitis and cerebellar ataxia, while herpes zoster can lead to postherpetic neuralgia. Vaccines based on attenuated VZV effectively prevent primary infection and reduce the risk of shingles.
Distinctive Manifestations
In varicella, rash typically starts on the face and trunk and spreads centripetally, with lesions at various stages present simultaneously. The vesicles are pruritic and fever is usually mild. In immunocompetent children the illness is self‑limited, but adults are at higher risk of severe disease such as pneumonia. Herpes zoster presents with prodromal pain followed by clusters of vesicles along a single dermatome, most commonly the thoracic or trigeminal dermatomes. Pain may precede the rash by days and can persist for months as postherpetic neuralgia. Disseminated shingles occurs when VZV reactivates and spreads beyond the initial dermatome, usually in immunocompromised patients. Vaccination and early antiviral therapy can reduce the severity and complications of both varicella and shingles. Varicella‑zoster virus is a ubiquitous DNA virus that causes chickenpox during primary infection and shingles upon reactivation. After initial replication in the respiratory tract and dissemination to the skin, it establishes lifelong latency in sensory ganglia. Reactivation results in dermatomal vesicular eruptions, and vaccines are key for prevention. Related Terms: Herpes Simplex Virus 2, Herpes Simplex Virus 1, Epstein–Barr Virus, Cytomegalovirus, Human Herpesvirus 6