Varicella zoster virus
Human alphaherpesvirus 3 | |
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Electron micrograph of a Human alphaherpesvirus 3 virion
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Virus classification | |
(unranked): | Virus |
Realm: | Duplodnaviria |
Kingdom: | Heunggongvirae
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Phylum: | Peploviricota |
Class: | Herviviricetes |
Order: | Herpesvirales |
Family: | Orthoherpesviridae
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Genus: | Varicellovirus |
Species: | Human alphaherpesvirus 3
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Synonyms | |
Varicella zoster virus (VZV), also known as human herpesvirus 3 (HHV-3, HHV3) or Human alphaherpesvirus 3 (taxonomically), is one of nine known herpes viruses that can infect humans. It causes chickenpox (varicella) commonly affecting children and young adults, and shingles (herpes zoster) in adults but rarely in children. VZV infections are species-specific to humans. The virus can survive in external environments for a few hours.[3]
VZV multiplies in the tonsils, and causes a wide variety of symptoms. Similar to the herpes simplex viruses, after primary infection with VZV (chickenpox), the virus lies dormant in neurons, including the cranial nerve ganglia, dorsal root ganglia, and autonomic ganglia. Many years after the person has recovered from initial chickenpox infection, VZV can reactivate to cause shingles.[4]
Epidemiology
Chickenpox
Primary varicella zoster virus infection results in
Shingles
In about a third of cases,[7] VZV reactivates in later life, producing a disease known as shingles or herpes zoster. The individual lifetime risk of developing herpes zoster is thought to be between 20% and 30%, or approximately 1 in 4 people. However, for people aged 85 and over, this risk increases to 1 in 2.[8] In a study in Sweden by Nilsson et al. (2015) the annual incidence of herpes zoster infection is estimated at a total of 315 cases per 100,000 inhabitants for all ages and 577 cases per 100,000 for people 50 years of age or older.[9]
VZV can also infect the central nervous system, with a 2013 article reporting an incidence rate of 1.02 cases per 100,000 inhabitants in Switzerland, and an annual incidence rate of 1.8 cases per 100,000 inhabitants in Sweden.[10]
Shingles lesions and the associated pain, often described as burning, tend to occur on the skin that is innervated by one or two adjacent sensory nerves, almost always on one side of the body only. The skin lesions usually subside over the course of several weeks, while the pain often persists longer. In 10–15% of cases the pain persists more than three months, a chronic and often disabling condition known as
Morphology
VZV is closely related to the
Genomes
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The
Evolution
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Commonality with HSV1 and HSV2 indicates a common ancestor; five genes (out of about 70) do not have corresponding HSV genes. Relation with other human herpes viruses is less strong, but many homologues and conserved gene blocks are still found.
There are at least five clades of this virus.[15] Clades 1 and 3 include European/North American strains; clade 2 are Asian strains, especially from Japan; and clade 5 appears to be based in India. Clade 4 includes some strains from Europe but its geographic origins need further clarification. There are also four genotypes that do not fit into these clades.[16] Allocation of VZV strains to clades required sequence of whole virus genome. Practically all molecular epidemiological data on global VZV strains distribution are obtained with targeted sequencing of selected regions.
Phylogenetic analysis of VZV genomic sequences resolves wild-type strains into nine genotypes (E1, E2, J, M1, M2, M3, M4, VIII and IX).[17][18] Complete sequences for M3 and M4 strains are unavailable, but targeted analyses of representative strains suggest they are stable, circulating VZV genotypes. Sequence analysis of VZV isolates identified both shared and specific markers for every genotype and validated a unified VZV genotyping strategy. Despite high genotype diversity no evidence for intra-genotypic recombination was observed. Five of seven VZV genotypes were reliably discriminated using only four single nucleotide polymorphisms (SNP) present in ORF22, and the E1 and E2 genotypes were resolved using SNP located in ORF21, ORF22 or ORF50. Sequence analysis of 342 clinical varicella and zoster specimens from 18 European countries identified the following distribution of VZV genotypes: E1, 221 (65%); E2, 87 (25%); M1, 20 (6%); M2, 3 (1%); M4, 11 (3%). No M3 or J strains were observed.[17] Of 165 clinical varicella and zoster isolates from Australia and New Zealand typed using this approach, 67 of 127 eastern Australian isolates were E1, 30 were E2, 16 were J, 10 were M1, and 4 were M2; 25 of 38 New Zealand isolates were E1, 8 were E2, and 5 were M1.[19]
The mutation rate for synonymous and nonsynonymous mutation rates among the herpesviruses have been estimated at 1 × 10−7 and 2.7 × 10−8 mutations/site/year, respectively, based on the highly conserved gB gene.[20]
Treatment
Within the human body it can be treated by a number of drugs and therapeutic agents including
Vaccination
A live attenuated VZV Oka/Merck strain
In 2006, the FDA approved
History
Chickenpox-like rashes were recognized and described by ancient civilizations; the relationship between zoster and chickenpox was not realized until 1888.[29] In 1943, the similarity between virus particles isolated from the lesions of zoster and those from chickenpox was noted.[30] In 1974 the first chickenpox vaccine was introduced.[31]
The varicella zoster virus was first isolated by Evelyn Nicol while she was working at Cleveland City Hospital.[32] Thomas Huckle Weller also isolated the virus and found evidence that the same virus was responsible for both chickenpox and herpes zoster.[33]
The etymology of the name of the virus comes from the two diseases it causes, varicella and herpes zoster. The word varicella is possibly derived from variola, a term for smallpox coined by Rudolph Augustin Vogel in 1764.[34]
See also
- Herpes simplex virus
- Progressive outer retinal necrosis
- Simian varicella virus
References
- ^ "ICTV 9th Report (2011) Herpesviridae". International Committee on Taxonomy of Viruses (ICTV). Archived from the original on December 22, 2018. Retrieved 9 January 2019.
Human herpesvirus 3 Human herpesvirus 3 [X04370=NC_001348] (HHV-3) (Varicella-zoster virus)
- ^ "ICTV Taxonomy history: Human alphaherpesvirus 3". International Committee on Taxonomy of Viruses (ICTV). Retrieved 9 January 2019.
- ^ "Pathogen Safety Data Sheets: Infectious Substances – Varicella-zoster virus". canada.ca. Pathogen Regulation Directorate, Public Health Agency of Canada. 2012-04-30. Retrieved 2017-10-10.
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- ^ a b Tortora G. Microbiology: An Introduction. Pearson. pp. 601–602.
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- ^ Han DH (25 October 2017). "General Characteristics and Epidemiology of varicella-zoster virus (VZV)". The Lecturio Medical Concept Library. Medical Professionals Reference (MPR). Retrieved 2021-06-14.
- PMID 3018124.
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- ^ PMID 19019403.
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- ^ Cornelissen CN (2013). Lippincott's illustrated reviews: Microbiology (3rd ed.). Philadelphia: Lippincott Williams & Wilkins Health. pp. 255–272.
- PMID 8668119.
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- ^ Gruber MF (20 October 2017). "Biologics License Application (BLA) for Zoster Vaccine Recombinant, Adjuvant" (PDF). Office of Vaccines Research and Review, Center for Biologics Evaluation and Research, US Food and Drug Administration. Retrieved 16 November 2018.
- ^ Han HD (25 October 2017). "ACIP: New Vaccine Recommendations for Shingles Prevention". Medical Professionals Reference (MPR). Retrieved October 30, 2017.
- PMID 25371534.
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- S2CID 11118674.
- PMID 4139526.
- ^ Frellick M (July 1, 2020). "Pioneering Molecular Biologist Dies of COVID-19 at 89". Medscape. Retrieved Sep 19, 2022.
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External links
- "Varicella (Chickenpox) Vaccination". Centers for Disease Control and Prevention (CDC). 2017-07-07.