Herpes zoster pathophysiology
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Herpes zoster Microchapters |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; L. Katie Morrison, MD; Associate Editor(s)-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]
Nomenclature
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.
Morphology
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 hexagonal form. 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.
Human disease
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. 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.