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

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

  • Double-stranded (ds) DNA virus.
  • Member of the herpesvirus (human α-herpesvirus family).
  • Single serotype (one attack of chickenpox gives lifelong immunity).
  • Humans are the only known reservoir hosts.
Different phases of varicella-zoster virus infection
Different phases of varicella-zoster virus infection (Image source: Ref-1)



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.


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 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.


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)
  • Chicken pox-like lesions occur in restricted areas (dermatome) that are innervated by a single ganglion;
  • The vesicles appear in a dermatomal distribution, almost always unilaterally
  • Skin lesions: Usually in the thorax.
  • Shingles of an intercostal nerve produces vesicular eruptions and burning pain in the affected dermatome
  • Chronic burning or itching pain called post-herpetic neuralgia
  • Maculopapular with an erythematous base, and usually heal in about two weeks.
  • Reactivation can affect the eye via the trigeminal nerve and the brain via the cranial nerve VII and VIII.
  • In immunocompromised life-threatening disseminated pneumonia may occur


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.


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

  • Gershon AA, Breuer J, Cohen JI, et al. Varicella zoster virus infection. Nat Rev Dis Primers. 2015;1:15016. Published 2015 Jul 2. doi:10.1038/nrdp.2015.16
  • Laing KJ, Ouwendijk WJD, Koelle DM, Verjans GMGM. Immunobiology of Varicella-Zoster Virus Infection [published correction appears in J Infect Dis. 2019 Apr 16;219(9):1514]. J Infect Dis. 2018;218(suppl_2):S68-S74. doi:10.1093/infdis/jiy403
  • De Paschale M, Clerici P. Microbiology laboratory and the management of mother-child varicella-zoster virus infection. World J Virol. 2016;5(3):97-124. doi:10.5501/wjv.v5.i3.97

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.

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.

Recent Posts