Varicella-Zoster Virus (VZV): Chicken Pox and Shingles

By Acharya Tankeshwar •  Created: 05/13/22 •  5 min read

Varicella-Zoster virus (VZV) is a DNA virus that belongs to the α-herpesvirus family. It causes chickenpox as a primary infection and herpes zoster (shingles) if reactivation occurs later in life.

  1. Varicella or chickenpox: It is a highly contagious viral skin infection characterized by generalized diffuse bilateral vesicular rashes.  Chickenpox occurs following primary infection and mostly affects children.
  2. Zoster or shingles: It occurs mostly in adult life, following reactivation of latent varicella-zoster virus present in the trigeminal or dorsal root ganglia. Vesicular rashes are unilateral and segmental (confined to the skin innervated by a single sensory ganglion).
Varicella-Zoster Virus (VZV)

Varicella is less contagious than measles, but more contagious than mumps and rubella.

Characteristics Feature of Virus

Different phases of varicella-zoster virus infection
Different phases of varicella-zoster virus infection (Image source: Ref-1)

Chickenpox

Transmission

Mode of transmission of chickenpox is direct contact with skin lesions, inhalation of aerosols from vesicular fluid of skin lesions of acute varicella or zoster, or aerosols of infected respiratory secretions. Person is contagious 1-2 days before the appearance of the rash until all blisters are crusted.

Pathogenesis

Varicella-zoster virus enters through the upper respiratory mucosa or the conjunctiva. VZV infects macrophages and pneumocytes in the respiratory mucosa. Virus spreads to the reticuloendothelial system, replicates in the regional lymph nodes, and enters the bloodstream (primary viremia). From the hematogenous route, it reaches the liver, and spleen and multiplies there. Secondary viremia occurs, and the VZV present in the infected mononuclear cells are transported to skin, respiratory tract, and neurons.

  1. Skin: Virus replication in the epithelial cells leads to the development of typical rashes. Swelling of epithelial cells, ballooning degeneration, and accumulation of tissue fluids result in the formation of vesicles.
  2. Respiratory tract: VZV is shed in the respiratory secretions of the infected individuals leading to the transmission of infection to other individuals.
  3. Neurons: VZV gains access to neurons and undergoes latency in dorsal root ganglia.
Vesicular rashes in chickenpox (Image source: CDC/PHIL)
Three types of lesions are most often seen in varicella-zoster infections;
maculopapular lesions (lesions with a raised red bump), vesicular lesions (blister-like or fluid-filled lesions), and scabbed or crusted lesions.

Clinical Manifestations

The incubation period of varicella is 10-21 days.

  1. Characteristics vesicular rash (chickenpox vesicle surrounded by an erythematous halo is described as a dewdrop on a rose petal) appears in about 10-23 days of VZV infections.
  2. Rashes are centripetal in distribution; the greatest concentration of lesions are seen on the trunk and the fewest lesions on distal extremities.
  3. Bilateral and diffuse in distribution.
  4. Rashes appear in multiple crops; lesions in various stages of evolution, such as maculopapular, vesicles, and scabs can be found in one area at the same time.
  5. Fever appears with each crop of rashes.
Distribution of chickenpox rashes

Chickenpox is a disease of childhood. If occurs in adults, it is more severe with bullous and hemorrhagic rashes. If a pregnant mother got a primary infection of VZV, she may develop congenital varicella syndrome.

Complications

Complications are more common in adults and in immunocompromised individuals. Secondary bacterial infection of the skin is the most common complication. Other complications are pneumonia, CNS involvement (cerebellar ataxia, encephalitis, and aseptic meningitis), Reye’s syndrome, myocarditis, nephritis, corneal lesion, and arthritis.

Shingles

Zoster or shingles is the recurrent form of varicella-zoster virus infection, which usually occurs later in life when the virus gets reactivated under stress or with immune suppression.

Shingles rash
Shingles rash (Image source: CDC/PHIL)

Diagnosis

The characteristic appearance of lesions both in primary varicella and zoster allows for a presumptive clinical diagnosis. Definitive diagnosis in the laboratory can be achieved by using samples from lesions or blood and testing by the following methods;

Virus culture: Virus can be isolated from the lesions using cell lines. VZV produces HSV-like cytopathic effects such as diffuse rounding and ballooning of infected cells. Virus-specific antigens can be detected in the culture fluids.

Tzanck cells (multinucleated giant cells in VZV lesions)
Tzanck test: Note the presence of a multinucleated giant cell (Tzanck cell) in the center. (Image source: CDC PHIL)

Cytopathology: Giemsa staining of scrapings from the ulcer base (Tzanck smear) reveals cytopathological changes similar to HSV infections, such as the formation of multinucleated giant cells.

Antigen detection

Specific viral antigens can be detected using direct immunofluorescence staining.

Serology

Primary VZV infection elicits immunoglobulin G (IgG), IgM, and IgA antibodies. Raise antibody titer can be detected using various serological methods. It is useful to diagnose varicella but less useful in the case of zoster.

Molecular Methods

Polymerase chain reactions (PCR) can be used to detect VZV-specific genes. The presence of the virus DNA can be demonstrated in tissues, vesicular fluid, maculopapular lesions, or crusts from lesions.

References and further readings

Acharya Tankeshwar

Hello, thank you for visiting my blog. I am Tankeshwar Acharya. Blogging is my passion. As an asst. professor, I am teaching microbiology and immunology to medical and nursing students at PAHS, Nepal. I have been working as a microbiologist at Patan hospital for more than 10 years.

Keep Reading

4 responses to “Measles virus: Structure, Pathogenesis, Lab Diagnosis”

  1. vijayalakshmi says:

    Sir ,thank u for info

  2. John Froude says:

    This is beautifully written. What is the structural difference between Measles virus and Rinderpest Virus? They are indistinguishable under EM.

  3. michael says:

    what where yoour souces for your data or bio

  4. muluye shemeles says:

    i want to know if there is vaccine escape measles mutation.which gene of measles should i study?

We love to get your feedback. Share your queries or comments

This site uses Akismet to reduce spam. Learn how your comment data is processed.

%d bloggers like this: