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Chapter 21 : Varicella-Zoster Virus

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Varicella-Zoster Virus, Page 1 of 2

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Abstract:

Varicella-zoster virus (VZV) is the etiologic agent of two diseases, varicella (chickenpox) and zoster (shingles). Researchers performed the first successful in vitro studies and showed that viruses isolated from patients with varicella and zoster are immunologically similar. There are minor differences in DNA sequence among VZV isolates, and at least seven genotypes have now been identified, which on the basis of single nucleotide polymorphisms are classified as European, Japanese, or Mosaics. Cell-to-cell spread is thought to be the major means of spread of VZV in the body and would explain the importance of cellular immunity rather than antibodies in host defense against this virus. The other form of spread is by cell-free virus. There is little available information on the stability of VZV, but it is usually classified as a rather labile agent. Prevention of varicella may be accomplished with either active or passive immunization. In one study, about two-thirds of cases of breakthrough varicella were classified as mild. A recent study showed no difference in outcome in older patients with zoster whether they were treated with therapeutic oral acyclovir (ACV) for 7 or 21 days. In this study, recovery was no more rapid, nor was postherpetic neuralgia (PHN) less likely to occur, if a 3-week course of tapering prednisolone (beginning at 40 mg/day) was given along with ACV.

Citation: Gershon A, Silverstein S. 2009. Varicella-Zoster Virus, p 451-473. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch21

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Image of FIGURE 1
FIGURE 1

A suggested mechanism of VZV virion entry. ( ) The incoming virion initially attaches to cellular heparan sulfate proteoglycan (HSPG), facilitating specific interaction with cellular receptor, e.g., MPR ( ). This leads to receptor-mediated (clathrin-dependent) endocytosis ( ) and delivery to an endosomal compartment ( ). Within this structure, the virion is exposed to cofactors for membrane fusion, possibly including the insulin-degrading enzyme (IDE) and/or altered pH. ( ) Following triggered membrane fusion, the VZV nucleocapsid is delivered to the cytoplasm. Cholesterol may play a role at each stage. (Reprinted from reference with permission.)

Citation: Gershon A, Silverstein S. 2009. Varicella-Zoster Virus, p 451-473. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch21
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Image of FIGURE 2
FIGURE 2

Putative route of intracellular transport and maturation of VZV in human embryonic lung fibroblasts. Structures are not drawn to scale. (Top) Nucleocapsids assemble in the nuclei of infected cells and bud through the nuclear envelope to reach the perinuclear cisternarough endoplasmic reticulum (RER). A temporary, primary viral envelope is acquired from the inner nuclear membrane. This envelope fuses with the RER, delivering unenveloped nucleocapsids to the cytosol. The nucleocapsids move through the cytosol to reach the -Golgi network (TGN). (Bottom) The glycoproteins (gps) of the viral envelope are synthesized in the RER independently of the nucleocapsids and are integral membrane proteins. Tegument proteins are probably synthesized by free ribosomes and are transported to the Golgi stack, as are the gps. Virions receive their final envelope by wrapping the TGN-derived sac and are delivered to acidic structures, identified as prelysosomes. (Reprinted from reference with permission.)

Citation: Gershon A, Silverstein S. 2009. Varicella-Zoster Virus, p 451-473. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch21
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Image of FIGURE 3
FIGURE 3

VZV propagated in human embryonic lung fibroblasts after several days in culture. The specimen was stained with fluorescein-tagged monoclonal antibodies to gE of VZV. The arrow indicates gE in the -Golgi network, and the arrowheads indicate gE at the cell surface.

Citation: Gershon A, Silverstein S. 2009. Varicella-Zoster Virus, p 451-473. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch21
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Image of FIGURE 4
FIGURE 4

Diagram showing proposed pathogenesis of varicella regarding events during the incubation period. (Reprinted from reference with permission.)

Citation: Gershon A, Silverstein S. 2009. Varicella-Zoster Virus, p 451-473. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch21
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Image of FIGURE 5
FIGURE 5

Skin vesicle from a patient in the early stages of varicella. The vesicle has not been unroofed. (A) The specimen was stained with fluorescein-tagged monoclonal antibodies to gE of VZV. (B) Same specimen as in panel A, viewed by Nomarski interference contrast microscopy. V, vesicular space; S, outer surface of epidermis.

Citation: Gershon A, Silverstein S. 2009. Varicella-Zoster Virus, p 451-473. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch21
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Image of FIGURE 6
FIGURE 6

Proposed pathogenesis of zoster. (Reprinted from reference with permission.)

Citation: Gershon A, Silverstein S. 2009. Varicella-Zoster Virus, p 451-473. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch21
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Image of FIGURE 7
FIGURE 7

Varicella on day 5 in an otherwise healthy 2-year-old boy, showing the typical distribution of skin lesions.

Citation: Gershon A, Silverstein S. 2009. Varicella-Zoster Virus, p 451-473. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch21
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Image of FIGURE 8
FIGURE 8

Hemorrhagic fatal varicella in a child with underlying lymphoma.

Citation: Gershon A, Silverstein S. 2009. Varicella-Zoster Virus, p 451-473. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch21
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Image of FIGURE 9
FIGURE 9

Chronic VZV skin lesion in a child with underlying HIV infection.

Citation: Gershon A, Silverstein S. 2009. Varicella-Zoster Virus, p 451-473. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch21
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Image of FIGURE 10
FIGURE 10

Chest radiograph of a patient with primary varicella pneumonia. (Courtesy of Walter Berdon.)

Citation: Gershon A, Silverstein S. 2009. Varicella-Zoster Virus, p 451-473. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch21
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Image of FIGURE 11
FIGURE 11

Zoster in a 10-year-old boy with underlying leukemia, showing the unilateral lumbar distribution of the skin lesions.

Citation: Gershon A, Silverstein S. 2009. Varicella-Zoster Virus, p 451-473. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch21
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Image of FIGURE 12
FIGURE 12

Kaplan-Meier product limit analysis of the probability of remaining free of zoster in 96 children with leukemia who had naturally acquired varicella before or after the diagnosis of leukemia. (Reprinted from reference with permission of the Massachusetts Medical Society. All rights reserved.)

Citation: Gershon A, Silverstein S. 2009. Varicella-Zoster Virus, p 451-473. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch21
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Tables

Generic image for table
TABLE 1

Summary of genetic information on VZV

Citation: Gershon A, Silverstein S. 2009. Varicella-Zoster Virus, p 451-473. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch21
Generic image for table
TABLE 2

Reported approximate incidence of zoster in various populations per 1,000 person-years of observation

Citation: Gershon A, Silverstein S. 2009. Varicella-Zoster Virus, p 451-473. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch21
Generic image for table
TABLE 3

Clinical data on over 100 reported infants with developmental defects whose mothers had VZV infections (over 95% with varicella) during the first or second trimester of pregnancy between 1947 and 2002

Citation: Gershon A, Silverstein S. 2009. Varicella-Zoster Virus, p 451-473. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch21
Generic image for table
TABLE 4

Drugs for treatment of VZV infections

Citation: Gershon A, Silverstein S. 2009. Varicella-Zoster Virus, p 451-473. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch21

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