Chickenpox (varicella) was rarely recognized until the sixteenth century. The name is thought to be derived from the Old English gican, meaning "itch". While shingles (herpes zoster) has been recognized as a unique clinical entity, varicella was differentiated from smallpox by the English physician Heberden in 1767. The relationship between chickenpox and shingles was first noted in 1898 by the Hungarian pediatrician Bokay. In 1952, the American virologists Weller and Stoddard first isolated the etiologic agent of varicella and zoster, the varicella-zoster virus (VZV), in cell cultures from varicella vesicle fluid. Weller had been able to establish in 1958 that there were no biologic and immunologic differences between the viruses isolated from patients with varicella and subsequent zoster. In 1974, a live-attenuated varicella vaccine was established by a Japanese group under Takahashi after isolating and attenuating the virus from a child with chickenpox named Oka. Straus proved in 1984 the identity of viral DNA by using the restriction endonuclease analysis.
The VZV is a member of the Alphaherpesvirinae subfamily within the family Herpesviridae. The spherical, 120-300 nm large particle of virus consists of a linear double-stranded DNA genome with about 125,000 base pairs and an icosahedric capsid composed of 162 capsomers. This nucleocapsid is surrounded by the tegument made up of glycoproteins as well as a trilaminar glycoprotein- and lipid-containing envelope. VZV cannot be distinguished from other herpesviruses electron microscopically. Some VZV genes have homologues in the genome of herpes simplex virus (HSV). Anti-VZV drugs such as aciclovir act on the virus-encoded thymidine kinase and DNA polymerase. There is only one serotype of VZV, and little antigenic variations have been noted between different isolates. VZV particles are exceedingly labile. Growth is highly cell-associated and almost exclusively restricted to cells of human and simian origin.
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