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Chapter 26 : Herpes Simplex Viruses

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Herpes Simplex Viruses, Page 1 of 2

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Abstract:

Herpes simplex virus (HSV) types 1 (HSV-1) and 2 (HSV-2) are members of the family Herpesviridae. They belong to the subfamily Alphaherpesvirinae and the genus Simplexvirus. The majority of the replicative intermediates are long concatemers apparently generated through sequence replacement or insertion. The rate of neonatal herpes projected by this study was 33 of 100,000 live births, and it was highest in the seronegative women. Using this process, trigeminal and sacral dorsal root ganglia were respectively identified as the most common sites for latent HSV-1 and HSV-2 infections, but latency can also be established in the central nervous system (CNS), primarily in the brain stem. The current routine procedure increases the sensitivity and specificity of the antigen detection assays by amplification through short-term (16 to 24 h) growth in tissue culture. The original goals of vaccination were to induce mucosal and systemic immunity to prevent HSV-2 infection and transmission. Oncolytic viruses are promising tools for cancer gene therapy. Cancer gene therapy approach (known as suicide) is based on the ability of HSV thymidine kinase (TK) to preferentially activate ganciclovir, thereby killing tumor cells that contain the TK gene as well as surrounding tumor cells.

Citation: Aurelian L. 2009. Herpes Simplex Viruses, p 424-453. In Specter S, Hodinka R, Young S, Wiedbrauk D (ed), Clinical Virology Manual, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815974.ch26
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Figures

Image of FIGURE 1
FIGURE 1

Structure. (A) Negatively stained virus particles. Capsid consists of 162 capsomers that are 9.5 by 12.5 nm (longitudinal section) and have a 4-nm-diameter channel that runs from the surface along the long axis. The capsid is surrounded by an asymmetrical fibrous-like tegument. The envelope is decorated with spikes projecting from its surface that consist of glycoproteins. Magnification, ×250,000. (B) The HSV genome has two covalently linked components consisting of unique sequences (UL and US) bracketed by inverted repeats (IRL/TRL and IRS/TRS) and contains 3 origins of replication (1 oriL and 2 oriS).

Citation: Aurelian L. 2009. Herpes Simplex Viruses, p 424-453. In Specter S, Hodinka R, Young S, Wiedbrauk D (ed), Clinical Virology Manual, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815974.ch26
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Image of FIGURE 2
FIGURE 2

Replicative cycle. Schematic representation includes temporally regulated transcription of IE (α), E (β), and L (γ) genes and viral DNA replication.

Citation: Aurelian L. 2009. Herpes Simplex Viruses, p 424-453. In Specter S, Hodinka R, Young S, Wiedbrauk D (ed), Clinical Virology Manual, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815974.ch26
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Image of FIGURE 3
FIGURE 3

Virus replication. Thin sections of HSV-2-infected cell (12 h after infection) stained with uranyl acetate and lead citrate show nuclear (N) and cytoplasmic (C) compartments. (A) Intranuclear capsids are in different stages of assembly, and the nucleus shows chromatin margination. (B) Virion assembly documents budding through the inner nuclear membrane, de-envelopment at the outer nuclear membrane, and reenvelopment in the trans-Golgi network. Magnification, ×55,700.

Citation: Aurelian L. 2009. Herpes Simplex Viruses, p 424-453. In Specter S, Hodinka R, Young S, Wiedbrauk D (ed), Clinical Virology Manual, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815974.ch26
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Image of FIGURE 4
FIGURE 4

Clinical manifestations. HSV-2-induced lesions of the penis (A), vulva (B and D), and cervix (E). Clinical HSV-1 manifestation is gingivostomatitis (C).

Citation: Aurelian L. 2009. Herpes Simplex Viruses, p 424-453. In Specter S, Hodinka R, Young S, Wiedbrauk D (ed), Clinical Virology Manual, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815974.ch26
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Image of FIGURE 5
FIGURE 5

Schematic representation of latency establishment and reactivation. Following replication in the skin, capsids are axonally transported to nerve cell bodies where viral DNA is maintained as a circularized episome. Reactivating stimuli cause reverse axonal transport of virus progeny.

Citation: Aurelian L. 2009. Herpes Simplex Viruses, p 424-453. In Specter S, Hodinka R, Young S, Wiedbrauk D (ed), Clinical Virology Manual, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815974.ch26
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Image of FIGURE 6
FIGURE 6

Proposed mechanism of HSV-2 latency reactivation. Reactivating stimuli upregulate AP-1 factors, thereby causing ICP10 overload. ICP10 supplies the PK activity, which is required for IE gene transcription and a feedback amplification loop through activation of the Ras survival pathway. It also supplies the ribonucleotide reductase (RR) activity that is required for DNA synthesis. The outcome is initiation of the lytic cascade.

Citation: Aurelian L. 2009. Herpes Simplex Viruses, p 424-453. In Specter S, Hodinka R, Young S, Wiedbrauk D (ed), Clinical Virology Manual, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815974.ch26
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Image of FIGURE 7
FIGURE 7

HSV-1 and HSV-2 activate distinct signaling pathways related to pathogenicity. Schematic representation of signaling pathways activated by neuronal cell infection with HSV-1 or HSV-2. HSV-1 activates the proapoptotic JNK/c-Jun pathway and triggers apoptosis, likely mediated by the ICP0 protein. HSV-2 activates the MEK/ERK, phosphatidylinositol 3-kinase (PI3K)/Akt, and adenylate cyclase (AC)/PKA survival pathways and blocks apoptosis, mediated by the PK function of the R1 protein (also known as ICP10). PARP, poly(ADP-ribose) polymerase.

Citation: Aurelian L. 2009. Herpes Simplex Viruses, p 424-453. In Specter S, Hodinka R, Young S, Wiedbrauk D (ed), Clinical Virology Manual, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815974.ch26
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Tables

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TABLE 1

Properties of HSV serotypes

Citation: Aurelian L. 2009. Herpes Simplex Viruses, p 424-453. In Specter S, Hodinka R, Young S, Wiedbrauk D (ed), Clinical Virology Manual, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815974.ch26
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TABLE 2

Spectrum of diseases associated with or caused by HSV

Citation: Aurelian L. 2009. Herpes Simplex Viruses, p 424-453. In Specter S, Hodinka R, Young S, Wiedbrauk D (ed), Clinical Virology Manual, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815974.ch26
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TABLE 3

Methods for the diagnosis of HSV infections

Citation: Aurelian L. 2009. Herpes Simplex Viruses, p 424-453. In Specter S, Hodinka R, Young S, Wiedbrauk D (ed), Clinical Virology Manual, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815974.ch26
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TABLE 4

ICP10ΔPK has therapeutic HSV-2 vaccine activity in guinea pigs a

Citation: Aurelian L. 2009. Herpes Simplex Viruses, p 424-453. In Specter S, Hodinka R, Young S, Wiedbrauk D (ed), Clinical Virology Manual, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815974.ch26
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TABLE 5

ICP10ΔPK has therapeutic activity in phase II trials a

Citation: Aurelian L. 2009. Herpes Simplex Viruses, p 424-453. In Specter S, Hodinka R, Young S, Wiedbrauk D (ed), Clinical Virology Manual, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815974.ch26
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TABLE 6

CDC treatment recommendations for genital HSV

Citation: Aurelian L. 2009. Herpes Simplex Viruses, p 424-453. In Specter S, Hodinka R, Young S, Wiedbrauk D (ed), Clinical Virology Manual, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815974.ch26

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