Varicella-zoster virus

Biological properties and classification

The causative agent of the infection, Varicella-zoster virus (VZV), was discovered in 1911 by H.E. Aragão. According to modern taxonomy, it belongs to the family Herpesviridae, genus Varicellovirus, and is classified as human herpesvirus type 3 (HHV-3).

Its structure is typical of its family, yet it has the smallest genome size among all herpesviruses. The virus is non-pathogenic to animals, meaning it is a strict anthroponosis. In laboratory conditions, it is cultured on human diploid fibroblasts. It multiplies more slowly than herpes simplex virus, affecting a narrower range of cells. Replication is accompanied by a characteristic cytopathic effect: the formation of intranuclear inclusions and multinucleated giant cells—symplasts—in culture.

Outside the human body, the pathogen is extremely unstable. It is easily destroyed by disinfectants and fat solvents. The virus is also thermolabile: heating to 60 °C destroys it in just 30 minutes.

Epidemiology and pathogenesis

The infection is characterized by high population susceptibility. The source of infection is an infected person or virus carrier. An important epidemiological feature is that an adult patient with shingles can be a source of the virus for susceptible individuals (e.g., children), causing typical chickenpox in them.

Main routes of transmission of VZV:

• Airborne (the leading mechanism).
• Contact (via direct contact with vesicular fluid).
• Vertical (transplacental).

The portal of entry for the infection is the mucous membranes of the upper respiratory tract. From there, the virus enters the bloodstream (viremia develops) and spreads to organs. The pathogen exhibits pronounced dermatotropic action: its main target is the epithelium of the skin and mucous membranes.

After the acute phase resolves, the virus does not disappear, but enters a stage of persistence. It persists for life in the dorsal root ganglia of the spinal cord or cranial nerve ganglia.

Two forms of infection: chickenpox and shingles

The virus is unique for its ability to cause two completely different diseases:

1. Chickenpox (varicella). This is a primary infection typically affecting children aged 2 months to 10 years. The patient is contagious from the end of the incubation period (which lasts 11–23 days) and for another 5 days after the rash appears. It manifests with fever, intoxication, and a generalized papulovesicular rash on the face, neck, trunk, extremities, and mucous membranes. Clear-fluid vesicles rupture and dry up within 1–3 days. Unlike smallpox, scars do not form after the crusts fall off. In infants under one year and adults, the disease can be severe, carrying a risk of pneumonia, encephalitis, and hepatitis (against the background of immunodeficiency).

1. Shingles (herpes zoster). This is an endogenous infection in adults, resulting from the reactivation of the dormant virus. Awakening of the virus is triggered by a decline in immunity (trauma, hypothermia, underlying pathologies). The pathogen migrates from the spinal ganglia to the skin. The leading clinical symptom is pronounced pain syndrome. The vesicular rash is distributed asymmetrically along nerve trunks (often intercostal, forming a "hoop" around the torso) or along the trigeminal nerve. In severe cases, a gangrenous (necrotic) form may develop.

Diagnostics, immunity, and treatment

After the infection, lifelong cell-mediated and humoral immunity is formed. However, it is non-sterile: the virus persists in the body, which creates the risk of developing shingles in the future.

For laboratory diagnostics, blood, nasopharyngeal discharge, and vesicular fluid are used. The following methods are applied:

• Microscopic: Romanowsky-Giemsa staining of smears reveals symplasts and intranuclear Lipschütz bodies.
• Virological: cultivation on fibroblasts followed by identification (ELISA, DFA, CF).
• Serological: detection of antibodies in blood serum (ELISA, CF).

Therapy includes etiotropic drugs (acyclovir, vidarabine) and immunomodulators (interferons). Rash elements are treated locally with potassium permanganate solutions (1–2%) or brilliant green. For specific prevention, a live attenuated vaccine is used, and immunoglobulins are administered to immunocompromised children for passive protection.

Briefly: answers to topical questions

Class and exam questions

What else to study on this topic

• Mechanisms of formation of non-sterile lifelong immunity in herpesvirus infections
• Differential diagnosis of rashes in chickenpox and smallpox
• Complications of chickenpox: pathogenesis of viral pneumonias and encephalitis
• Features of Varicella-zoster virus cultivation and types of cytopathic effect
• Pathogenesis of VZV persistence in spinal and cerebral ganglia

Other topics in the section "DNA viruses (parvoviruses, papillomaviruses, adenoviruses, hepatitis B, herpes viruses, poxviruses, anelloviruses)"

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