Varicella zoster virus

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A Microbial Biorealm page on the genus Varicella zoster virus

Classification

Order: Herpesvirales; Family: Herpesviridae; Subfamily: Alphaherpesvirinae; Genus: Varicellovirus; Species: Human herpesvirus 3; Commonly known as Varicella Zoster Virus (VZV)

Description and significance

The isolation of Varicella Zoster Virus was first published in 1958. This virus is the causative agent of chicken pox, a disease characterized by a blister-like rash on the skin and often accompanied by fever. This disease is highly contagious, transmitted by sneezing or coughing, direct contact, or aerosol transmission of virus from skin lesions. This is known as varicella.

After recovering from the varicella disease, a person may develop shingles, also known as zoster or herpes zoster, due to the virus remaining in the dorsal root ganglia. Shingles is characterized by a painful rash on one side of the body, typically preceeded by pain, itching, or tingling in that area. It may also be accompanied by fever, headache, chills, or upset stomach. The risk of developing shingles increases with age, especially after 50 years of age. Almost 1 out of every 3 Americans will develop shingles, and 1 million cases are estimated to occur in this country each year.

Disease caused by the Varicella Zoster Virus can be prevented by the varicella vaccine; two doses of the vaccine are recommended. People who have been vaccinated may still get the disease, but if they do it will be milder, and there is a much lower chance of such infection. Before the vaccine became widely available (1995), an estimated 4 million cases of varicella occured each year in the U.S.; rates have decreased by 53-88% as of 2004.

Genome structure

Varicella zoster virus has a variable genome size (from just above 124,000 bp to more than 126,000 bp), but the obtained sequence published consisted of 124,884 base pairs containing 70 genes distributed roughly equally over the two DNA strands. G + C content is 46.02%.

The genome is a linear double-stranded DNA molecule made up of two segments (L and S) joined covalently. Each segment comprises a unique sequence (100,000 bp in L, 5,232 bp in S) flanked by a large (7319.5 bp, in S) or small (88.5 bp, in L) inverted repeat. These terminal repeat components have higer G + C content, which is common in herpesvirus genomes. A small proportion of virions have been reported to contain superhelical circular DNA molecules.

80 potentially protein-encoding open reading frames (more than 150 amino acid residues) were identified, though 14 were designated unlikely to encode proteins. 5 more open reading frames could potentially encode proteins of less than 150 amino acid residue, for a total of 71 predicted protein-encoding open reading frames.

In analysis of the genome, splicing was predicted to be rare in the VZV genome due to imprecise consensus splice acceptor and donor sites and analogy with another herpesvirus, HSV-1, which has only 4 spliced genes confirmed. However, the possibility could not be reasonably dismissed.

Of the 71 protein-encoding open reading frames predicted, ORFs 42 and 45 are represented as a spliced transcript, resulting in 70 genes, three of which are duplicated in the S-segment inverted repeats, so only 67 identified genes are unique.

The VZV genome is very economical, consisting almost solely of code for viral protein, with control regions likely in coding regions of adjacent genes.

The gene layout of VSV is similar to that of HSV-1, but 6 HSV-1 genes have no counterpart in VZV, and many local differences exist.

Cell structure, metabolism & life cycle

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Ecology (including pathogenesis)

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Interesting feature

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References

Arvin, A.M. "Varicella-Zoster Virus". Clinical Microbiology Reviews. 1996. p. 361-381

Davison, A.J., and J.E. Scott. "The Complete DNA Sequence of Varicella-Zoster Virus". Journal of General Virology. 1986. Volume 67. p. 1759-1816.

International Committee on Taxonomy of Viruses. Accessed October 31, 2011.

"Varicella-Zoster Virus Infection" National Center for Infectious Diseases. Page last reviewed July 14, 2011. Accessed October 31, 2011.

Weller, T.H., H.M. Whitton, and E.J. Bell. "The etiologic agents of varicella and herpes zoster". Journal of Experimental Medicine. 1958. Volume 108. p.843-868