Etiology: properties of the VZV virus
The causative agent of chickenpox and shingles is varicella-zoster virus (VZV), a DNA-containing virus of the Alphaherpesvirinae subfamily. It is characterized by epitheliotropism: active replication occurs in the cells of the stratum spinosum of the epidermis.
The virion reaches 120–200 nm in diameter and has a complex structure:
- Genome: double-stranded DNA capable of fragment repositioning (isometry), leading to mutations.
- Capsid: icosahedral (162 capsomeres).
- Tegument: a layer containing viral proteins to initiate replication.
- Supercapsid (envelope): formed from the host cell nuclear membrane with the addition of viral glycoproteins.
Upon entering the cell, the virus uses its own enzymes (DNA polymerase, thymidine kinase) for synthesis, making it a convenient target for antiviral therapy. By multiplying, VZV causes neighboring infected cells to fuse, forming giant multinucleated symplasts. Billions of virus copies accumulate inside them, inaccessible to antibodies. Meanwhile, the virus is extremely unstable in the external environment (killed by ultraviolet light and disinfectants), but withstands freezing exceptionally well.
Epidemiology
Chickenpox is a typical anthroponosis. The source is a person sick with chickenpox or (more rarely) shingles. Human susceptibility is colossal (90–95%), the only exception being infants in their first months of life who are protected by maternal antibodies.
The primary transmission route is airborne. VZV possesses incredible volatility and can spread with air currents over distances exceeding 20 meters. Extremely rarely, the infection is transmitted by contact (via vesicle fluid). There is also a vertical route: if a pregnant woman falls ill in the late stages, there is a high risk of severe infection in the newborn.
The disease most frequently affects children aged 5–9 years and exhibits autumn-winter seasonality. Recovery confers lifelong immunity; reinfection is possible only in the setting of severe immunodeficiency.
Pathogenesis of chickenpox
The development of the disease goes through several stages:
- Incubation period (10–23 days). The virus invades the mucous membranes of the respiratory tract, multiplies, is engulfed by macrophages, and disseminates via lymph and blood.
- Prodromal period. Almost imperceptible in children, in adults it manifests as intoxication due to viremia and interferon production.
- Eruptive period (2–10 days). The virus settles in the skin and mucous membranes. Cells fuse into symplasts. The immune system attacks them (cytolysis), which clinically manifests as a vesicular rash.
- Convalescence. Antibody production, disappearance of viremia, healing of the rash.
A crucial feature of pathogenesis is "immune evasion". Evading the immune system, some viruses travel along nerve fibers to sensory ganglia (spinal or cranial). There VZV enters a dormant state (episome in the neuronal nucleus) for the rest of the host's life. Its reactivation in the future will lead to shingles.
Tissue changes (pathomorphology)
The primary target of the virus is the stratum spinosum of the epidermis. Here, cell vacuolization and symplast formation occur, leading to the appearance of unilocular vesicles with serous exudate. Then the fluid is reabsorbed, and a crust forms. Since the germinative (basal) layer of the skin is not damaged, chickenpox heals without scarring. Scarring is possible only upon scratching or bacterial superinfection.
On mucous membranes, vesicles rapidly turn into erosions. In severe visceral forms, foci of necrosis and specific intranuclear inclusions can be found in internal organs and nervous tissue.
Briefly: answers to topical questions
What specific symptoms manifest intoxication during the prodromal period of chickenpox in adults?
During the prodromal period of chickenpox in adults, intoxication manifests as low-grade fever, weakness, and dyspeptic disorders. This period in adults lasts 1–3 days, whereas in children it is most often absent or mildly expressed. Also during this period, some patients may experience a brief appearance of an early nonspecific micropapular or macular rash.
What specific nervous system complications can chickenpox cause?
Specific central nervous system complications of chickenpox include encephalitis and meningoencephalitis.
- Encephalitis is listed among the complications of chickenpox; sources also note that encephalitis accounts for 90% of neurological complications.
- Meningoencephalitis is listed among specific CNS complications.
These neurological complications occur during the crusting period, and their development is not related to the severity of the disease course.
What antiviral drugs are used for etiotropic therapy of chickenpox?
For etiotropic antiviral therapy of chickenpox, the drug acyclovir is used. It is indicated for severe forms of the disease, as well as in patients with immunodeficiency.
- Tablet form is prescribed orally at 800 mg 5 times daily for 5–7 days.
- Parenteral form is used for central nervous system involvement; the drug is administered intravenously at a dose of 10–15 mg/kg every 8 hours for a prolonged course of 2 to 3 weeks.
Remembering the causative agent is easy: Chickenpox (Vetryanaya Ospas) = Airborne-Awesome (highly volatile) and Unilocular (rash).
Class and exam questions
Why do people get chickenpox once, but shingles at an older age?
Chickenpox leaves lasting immunity against reinfection from the outside. But the virus itself hides in nerve ganglia and, when immunity decreases (with age or due to stress), wakes up, causing local inflammation of the nerve and skin — shingles.
Are crusts contagious in chickenpox?
No. The virus is present in the air from the patient's breathing and in the vesicle fluid. When the rash dries and crusts over, the virus is no longer present in them.
Do scars remain after chickenpox?
Normally no, because the inflammation does not affect the deep germinative layer of the epidermis. Scars form only if the vesicle is scratched off or a bacterial infection is introduced.
What else to study on this topic
- Features of viral protein translation (early alpha, beta, and late gamma proteins)
- Mechanism of symplast formation at the cellular level
- Effect of VZV on the fetus depending on the trimester of pregnancy
- Pathomorphology of the visceral form of chickenpox and CNS lesions
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