Biological Properties and Classification
The causative agent, Varicella-zoster virus (VZV), was discovered in 1911 by B.E. Aragão. According to current taxonomy, it belongs to the family Herpesviridae, genus Varicellovirus, and is classified as human herpesvirus 3 (HHV-3).
Its structure is typical of the herpesvirus family, though it possesses the smallest genome among all human herpesviruses. The virus is non-pathogenic to animals, making it a strict human pathogen. In laboratory settings, it is cultivated on human diploid fibroblasts. It replicates more slowly than herpes simplex virus and infects a narrower range of cell types. Replication is accompanied by a characteristic cytopathic effect: the formation of intranuclear inclusion bodies and multinucleated giant cells (syncytia) in cell culture.
Outside the human body, the pathogen is extremely unstable. It is readily inactivated by disinfectants and lipid 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 individual or virus carrier. An important epidemiological feature is that an adult patient with herpes zoster can transmit the virus to susceptible individuals (e.g., children), causing typical chickenpox in them.
Main routes of VZV transmission:
- Airborne droplets (the primary mechanism).
- Direct contact (via direct touch of vesicular fluid).
- Vertical transmission (transplacental).
Portal of entry includes the mucous membranes of the upper respiratory tract. From there, the virus enters the bloodstream (viremia) and disseminates to organs. The pathogen exhibits marked dermatotropism, targeting primarily the epithelium of the skin and mucous membranes.
Following the resolution of the acute phase, the virus does not clear but enters a phase of latency. It persists for life in the dorsal root ganglia of the spinal cord or cranial nerve ganglia.
Two Forms of Infection: Varicella and Herpes Zoster
The virus is unique in its ability to cause two entirely different clinical syndromes:
- Varicella (Chickenpox) (varicella). This is the primary infection, typically affecting children aged 2 months to 10 years. Patients are contagious from the end of the incubation period (which lasts 11–23 days) and for 5 days after the appearance of the rash. It presents with fever, malaise, and a generalized papulovesicular rash on the face, neck, trunk, limbs, and mucous membranes. Clear-fluid vesicles rupture and crust over within 1–3 days. Unlike smallpox, uncomplicated chickenpox heals without scarring. In infants under one year of age and immunocompromised adults, the disease can be severe, carrying risks of pneumonia, encephalitis, and hepatitis.
- Herpes Zoster (Shingles) (herpes zoster). This is an endogenous infection in adults resulting from the reactivation of dormant virus. Reactivation is triggered by declining cell-mediated immunity (e.g., trauma, hypothermia, concurrent illnesses). The pathogen migrates from the sensory ganglia to the skin. The hallmark clinical symptom is severe pain. The vesicular rash is distributed unilaterally along dermatomes (frequently intercostal, forming a band around the trunk, or along branches of the trigeminal nerve). Severe cases may present with gangrenous (necrotic) forms.
Diagnostics, Immunity, and Treatment
Primary infection confers lifelong cell-mediated and humoral immunity. However, this immunity is non-sterile: the virus persists in the body in a latent state, posing a lifelong risk of herpes zoster reactivation.
Laboratory diagnostics utilize blood samples, nasopharyngeal secretions, and vesicular fluid. Methods include:
- Microscopy: Romanowsky-Giemsa stained smears reveal multinucleated syncytia and intranuclear Cowdry bodies (Lipschütz bodies).
- Virological: Culture on fibroblasts followed by identification (ELISA, DFA, complement fixation).
- Serology: Detection of specific antibodies in serum (ELISA, complement fixation).
Therapy includes antiviral agents (acyclovir, vidarabine) and immunomodulators (interferons). Skin lesions may be treated topically with antiseptic solutions (e.g., potassium permanganate 1–2% or brilliant green). Specific prophylaxis involves a live-attenuated vaccine, while exposed immunocompromised children receive passive immunization with varicella-zoster immunoglobulin (VZIG).