9 Varicella-Zoster Virus: The Paradox of Immune Mediation and Immunocompromise

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Varicella-zoster virus (VZV) causes both chicken pox and zoster (shingles). It is a double-stranded DNA virus with a lipid coat belonging to the herpesvirus family. Chicken pox is usually considered a benign febrile disease. However, several studies have documented serious complications in previously well children, with an increased frequency of serious complications of chicken pox in adults. Damage to the peripheral nervous system gives rise to denervation, limb hypoplasia, and scarring. Virus may be isolated from fresh vesicle fluid and from cells at the base of the vesicle. Humoral antibody rises quickly after appearance of the rash in an amnestic fashion. Emergence from latency is associated with diverse pathogenic mechanisms in the central nervous system (CNS) and peripheral nervous system. While infrequent, there is evidence for VZV replication as the basis for certain syndromes, particularly in the immunocompromised patient. Immune-mediated mechanisms have long been thought to be involved in light of the "parainfectious" timing of many of the syndromes in relation to the cutaneous manifestations of VZV. VZV is one of the causes of viral retinitis in which the diagnosis can be made by PCR on vitreous specimens. There have been few pathological studies of cases clinically diagnosed as disseminated VZV encephalitis. Myelitis can occur in the immunocompetent or immunosuppressed as part of a complex of signs and symptoms of brain, meninges, spinal roots, and/or cranial nerves, or on its own, with or without cutaneous vesicles.

Citation: Booss J, Esiri M. 2003. 9 Varicella-Zoster Virus: The Paradox of Immune Mediation and Immunocompromise, p 127-139. In Viral Encephalitis in Humans. ASM Press, Washington, DC. doi: 10.1128/9781555817831.ch9
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Image of FIGURE 9.1

Granulomatous arteritis associated with trigeminal zoster, (a) Low-power view of perivascular inflammation, (b) Low-power view of small microinfarct in basal ganglia associated with small vessel angiitis at periphery, (c) Higher-power view of inflammation, including a multinucleate giant cell.

Citation: Booss J, Esiri M. 2003. 9 Varicella-Zoster Virus: The Paradox of Immune Mediation and Immunocompromise, p 127-139. In Viral Encephalitis in Humans. ASM Press, Washington, DC. doi: 10.1128/9781555817831.ch9
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Image of FIGURE 9.2

Brain stem encephalitis associated with geniculate herpes zoster. Perivascular lymphocytic cuffing of the ipsilateral medulla. Hematoxylin and eosin stain. × 350.

Citation: Booss J, Esiri M. 2003. 9 Varicella-Zoster Virus: The Paradox of Immune Mediation and Immunocompromise, p 127-139. In Viral Encephalitis in Humans. ASM Press, Washington, DC. doi: 10.1128/9781555817831.ch9
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Image of FIGURE 9.3

Multifocal VZV leukoencephalitis, (a) Whole mount stained for myelin demonstrating multiple separate and confluent areas of demyelination. The patient was a woman with underlying Hodgkin's disease. (Courtesy of Marc K. Rosenblum, Memorial Sloan-Kettering Cancer Center, New York, N.Y.). (b) Enhanced Tl-weighted MRI image demonstrating multiple foci of demyelination in frontal and parietal lobes, right side (left side of figure) greater than left. Minimal mass effect is seen. The patient was a man with HIV. (Courtesy of Lisa M. DeAngelis, Memorial Sloan-Kettering Cancer Center.)

Citation: Booss J, Esiri M. 2003. 9 Varicella-Zoster Virus: The Paradox of Immune Mediation and Immunocompromise, p 127-139. In Viral Encephalitis in Humans. ASM Press, Washington, DC. doi: 10.1128/9781555817831.ch9
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Neurological complications of zoster: syndromes and circumstances

Citation: Booss J, Esiri M. 2003. 9 Varicella-Zoster Virus: The Paradox of Immune Mediation and Immunocompromise, p 127-139. In Viral Encephalitis in Humans. ASM Press, Washington, DC. doi: 10.1128/9781555817831.ch9

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