Zoster, a recrudescence of VZ virus infection.

Pathogenesis Varicella and zoster are different clinical manifestations caused by the same (VZ) virus. Infection of a previously uninfected person produces varicella or in some cases an inapparent infection. Zoster is believed to result from the activation of VZ virus which has been present, but inactive, in the patient's dorsal root ganglion cells and/or his skin cells. Most are 'immune' to a second exogenous VZ virus infection but during recovery from varicella the VZ virus presumably assumes a latent state within the patient's cells. Opinion varies on the route by which the infectious virus reaches the ganglion cells. Zoster tends to involve skin served by one or two adjacent ganglia, suggesting that the virus does not reach the ganglion via the blood stream for if it did it would be expected to infect all ganglia. Nonetheless haematogenous spread has not been ruled out. Evidence of cerebrospinal fluid passage along spinal nerves in pigs and sheep has provided support for the theory that VZ virus could reach the ganglion cells by centripetal passage along a nerve from a skin lesion of varicella (Steer & Horne, 1968). Virus has not been isolated during the hypothesized latent state assumed by the VZ virus in the ganglion cells of man. However, the prophage state of lambda bacteriophage in Escherichia coli offers biologic precedent for the latency concept (Lwoff, 1961). Lambda can enter a latent or prophage state in the bacteria during which the bacteriophage genetic material associates and multiplies in synchrony with the bacterial nucleoprotein. Certain stimuli will cause rapid multiplication of the phage and consequent destruction of the host cell. In the human, herpes simplex is also considered an example of viral latency but like zoster has not been proved. Varicella-zoster virus The association between varicella and zoster was first noted by von Bokay in 1909 (Blank & Rake, 1955). By 1925, Kundratiz (quoted by Blank & Rake, 1955) had demonstrated that children inoculated with zoster vesicle fluid would develop and transmit varicella; children with a history of varicella did not develop disease. Electron microscopic and immunologic investigations have confirmed the impression that varicella and zoster are caused by the same virus and have substantially increased our knowledge of the VZ virus. The zoster virus was first seen with the electron microscope in 1948 by Rake and his collaborators. It was found to be morphologically indistinguishable from the varicella virus. More sophisticated electron micrographs of negatively stained specimens have shown the VZ virus to consist of a central capsid covered by hollow identically sized capsomeres (Almeida, Howatson & Williams, 1962) (Fig. 1).