Varicella-zoster virus

Etiology

Taxonomy

| Order = Herpesvirales | Family = Herpesviridae | Genus = Varicellovirus | Species = Human herpesvirus 3

Description

The earliest reports of the rashes caused by the varicella-zoster virus can be dated back to ancient civilizations. However, it was not until 1888 that a link between the varicella-zoster virus and chickenpox was suggested. Since there was no animal host, much of the evidence needed to be obtained through clinical and epidemiological observations. Developments in the understanding of the varicella-zoster virus were made throughout the second half of the twentieth century with the link being proven in the 1950s, the introduction of the live attenuated vaccine virus in 1974, and treatment with the drug aciclovir in the 1980s. In 1986, the complete DNA sequence of VZV was established. [1]

The varicella-zoster virus has the potential to cause two diseases: chickenpox (varicella) and shingles (herpes zoster). Before the development of a varicella vaccine in 1994, chickenpox was a common contagious childhood illness. It would produce itchy blisters throughout the body but rarely led to any serious problems. Once an individual has had chickenpox, the varicella-virus is able to lay dormant in the nerves and can reemerge as shingles. Although shingles is not life threatening, it is characterized by a painful rash of blisters. Some people that have acquired shingles can develop a condition called postherpetic neuralgia which results in pain in the skin even after the rash is gone. Shingles is most common in people over 60 and in those with a weakened immune system. A herpes zoster vaccine is available to reduce the risk of developing shingles.[2]

Genome

Varicella-zoster virus is an alphaherpesvirus that is in the same subfamily as herpes simplex virus 1 and 2. The varicella-zoster virus genome contains at least 70 genes, and all but 6 have homologs in the herpes simplex virus. The complete sequence of the varicella-zoster virus was determined in 1986, and the prototype strand, VZV Dumas is 124,884 base pairs in length. The genome consists of a unique long region which is bound by terminal long and internal long repeats and a unique short region which is bound by internal short and terminal short repeats. The unique short region is able to orientate in either of two directions, while the unique long region is rarely able to change its orientation. Therefore, there are usually two isomers of the genome in an infected cell. The genome is linear in virions, and there is an unpaired nucleotide at each end. In cells infected with the virus, the ends pair and the genome circularizes. There are five repeat regions in the genome. Repeat region 1 is located in open reading frame 11, R2 is in open reading frame 14 (glycoprotein C), R3 is in open reading frame 22, R4 is between open reading frame 62 and the origin of viral replication, and R5 is found between open reading frame 60 and 61. The length of the repeat regions vary among strains and can be used to distinguish different strains of the virus.

Prevention

The varicella vaccine is an active immunizing agent that is able to protect against the varicella-zoster virus. It causes the body to produce its own antibodies against the virus. Immunization is recommended for anyone 12 months of age or older who has not had chickenpox. In order to be considered immune to chickenpox without having the infection at some point, an individual must have received 1 dose of the vaccination if between 12 months and 12 years of age or 2 doses if 13 years of age or older. Zostavax® is used for protection against herpes zoster (commonly known as shingles) in people of age 50 and over [3].

References

1 Wood MJ. History of Varicella Zoster Virus. Oct. 2000
2 University of Maryland Medical Center. Varicella-zoster virus
3 Cohen, Jeffrey. The Varicella-Zoster Virus Genome. 7 Aug 2012
4 Mayo Clinic. Varicella Virus Vaccine (Subcutaneous Route)