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Varicella zoster virus
From Wikipedia, the free encyclopedia
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 Micrograph of VZV.
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The Varicella zoster virus (VZV) is one of the eight herpes viruses known to affect humans (and other vertebrates).
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Multiple names are used to refer to same virus, creating some confusion. Varicella virus, zoster virus, human herpes 3 (HHV-3), and Varicella Zoster Virus (VZV) all refer to the same viral pathogen. The disease caused by this pathogen is called chickenpox or Varicella disease during the initial infection. A reactivation of the infection is commonly called shingles, herpes zoster or simply zoster.
Primary VZV infection results in chickenpox (varicella), which may rarely result in complications including VZV encephalitis or pneumonia. Even when clinical symptoms of varicella have resolved, VZV remains dormant in the nervous system of the host in the trigeminal and dorsal root ganglia.[1] In about 10-20% of cases, VZV reactivates later in life producing a disease known as herpes zoster or shingles. Serious complications of shingles include post-herpetic neuralgia, zoster multiplex, myelitis, herpes ophthalmicus, or zoster sine herpete.
VZV is closely related to the herpes simplex viruses (HSV), sharing much genome homology. The known envelope glycoproteins (gB, gC, gE, gH, gI, gK, gL) correspond with those in HSV, however there is no equivalent of HSV gD. VZV virons are spherical and 150-200 nm in diameter. Their lipid envelope encloses the nucleocapsid of 162 capsomeres arranged in a icosahedral form.[2] Its DNA is a single, linear, double-stranded molecule, 125,000 nt long.
The virus is very susceptible to disinfectants, notably sodium hypochlorite. Within the body it can be treated by a number of drugs and therapeutic agents including aciclovir, zoster-immune globulin (ZIG), and vidarabine.
A live attenuated VZV Oka/Merck strain vaccine is available and is marketed under the trade name Varivax. It was developed by Merck, Sharp & Dohme in the 1980s from the Oka strain virus isolated and attenuated by Michiaki Takahashi and colleagues in the 1970s. It was submitted to the U.S. Food and Drug Administration for approval in 1990 and was approved in 1995. Since then, it has been added to the recommended vaccination schedules for children in Australia, the United States, and many other countries, causing controversy because it is only expected to be effective for about twenty years, leaving adults vulnerable to the most dangerous forms of infection by this virus. The use of varicella virus vaccine live (Varivax) has been limited by practitioner concerns that adults vaccinated as children could develop severe varicella infection complications if immunity provided by the vaccine does not last for a lifetime. So far, clinical data has proved that the vaccine is effective for over 10 years in preventing varicella infection in healthy individuals and when breakthrough infections do occur, illness is typically mild.[3]
In 2006, the FDA approved Zostavax for the prevention of shingles. Zostavax is a more concentrated formulation of the Varivax vaccine, designed to elicit an immune response in the eldery whose immunity to VZV wanes with advancing age. [4]
- ^ Steiner I, Kennedy PG, Pachner AR (2007). "The neurotropic herpes viruses: herpes simplex and varicella-zoster". Lancet Neurol 6 (11): 1015–28. doi:10.1016/S1474-4422(07)70267-3. PMID 17945155.
- ^ Herpes Simplex Virus and Varicella Zoster Virus Anatomy, Microbiology, Epidemiology, and Diagnosis & Management of Ocular Disease William James Reinhart MD February, 2005 Ohio Ophthalmologic Society Quote: "Characteristics of HSV 1 & 2...Icosahedral protein shell (capsid), 162 capsomeres"
- ^ Centers for Disease Control and Prevention (CDC). Prevention of varicella: recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR 1996;45(No.RR-11)
- ^ Poland, Gregory. "The Growing Paradigm of Preventing Disease." Annals of Internal Medicine. 2005;143539-541.