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Chapter 26 : Herpes Simplex Viruses and Varicella Zoster Virus

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Herpes Simplex Viruses and Varicella Zoster Virus, Page 1 of 2

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Abstract:

The herpesviruses are classified in the family based on the characteristic large linear double-stranded DNA genome packaged within an enveloped icosahedral capsid. Members of this family have been identified in almost all animal species, and the specific herpesviruses are usually restricted to a single species. Nine human herpesviruses have been described: HSV-1, HSV-2, varicella zoster virus (VZV), Epstein-Barr virus (EBV), human cytomegalovirus (CMV), human herpesvirus 6A (HHV-6A), human herpesvirus 6B (HHV-6B), human herpesvirus 7 (HHV-7), and human herpesvirus 8 (HHV-8). All these viruses are structurally similar and encode a large number of biosynthetic enzymes involved in the synthesis of viral DNA as well as structure proteins that compose the capsid and tegument, as well as envelope glycoproteins that are required for infection.

Citation: James S, Prichard M. 2016. Herpes Simplex Viruses and Varicella Zoster Virus, p 363-371. In Loeffelholz M, Hodinka R, Young S, Pinsky B (ed), Clinical Virology Manual, Fifth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819156.ch26
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Figures

Image of FIGURE 1
FIGURE 1

Antiviral therapies for HSV and VZV. (A) Therapies for the treatment of HSV and VZV are shown with prodrugs shown in parentheses. The pyrophosphate analog foscarnet is approved for resistant therapies. Cidofovir is also active against resistant isolates, but it has not been approved for that indication. (B) Acyclovir, the therapy of choice, is initially phosphorylated exclusively by the TK enzymes encoded by HSV-1, HSV-2, and VZV to the level of the monophosphate (ACV-MP). Cellular kinases further phosphorylate the drug to the active triphosphate metabolite (ACV-TP) that inhibits the viral DNA polymerase. Most drug-resistant viruses contain mutations in the TK that impair its ability to phosphorylate the drug and limits the concentration of the active metabolite. Neither foscarnet nor cidofovir require the TK such that both drugs are active against drug-resistant isolates of the virus.

Citation: James S, Prichard M. 2016. Herpes Simplex Viruses and Varicella Zoster Virus, p 363-371. In Loeffelholz M, Hodinka R, Young S, Pinsky B (ed), Clinical Virology Manual, Fifth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819156.ch26
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Image of FIGURE 2
FIGURE 2

Algorithm for the diagnosis of HSV and VZV infections. If no lesions are present and time is not a critical factor, serological testing can identify patients infected with HSV or VZV. Further testing for HSV shown in the box can type the infection as being HSV-1 or HSV-2. If lesions are present, swab specimens can be cultured, and infected cultures can be further tested by fluorescent antibody to identify the infection as being HSV or VZV. For high-risk or time-critical specimens (or as an alternative to viral culture), PCR of specimens can be used to identify DNA from HSV or VZV. Many standard assays also distinguish between HSV-1 and HSV-2 at this stage.

Citation: James S, Prichard M. 2016. Herpes Simplex Viruses and Varicella Zoster Virus, p 363-371. In Loeffelholz M, Hodinka R, Young S, Pinsky B (ed), Clinical Virology Manual, Fifth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819156.ch26
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