Human Herpesvirus 3 (Varicella-Zoster Virus)

2016 ◽  
pp. 951-964
Keyword(s):  
Varicella Zoster Virus ◽  
Human Herpesvirus ◽  
Varicella Zoster

Herpesvirus Infections

2018 ◽  
Author(s):  
Martin S. Hirsch
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Varicella Zoster Virus ◽  
Ganglion Cells ◽  
Human Herpesvirus ◽  
Herpes Infection ◽  
Varicella Zoster ◽  
Clinical Syndromes ◽  
Simplex Virus ◽  
Human Herpesviruses

The herpes group of viruses is composed of at least eight human viruses and numerous animal viruses. The human herpesviruses include herpes simplex virus types 1 and 2 (HSV-1 and HSV-2), varicella-zoster virus (VZV), cytomegalovirus (CMV), Epstein-Barr virus (EBV), and human herpesvirus types 6 (HHV-6), 7 (HHV-7), and 8 (HHV-8, also known as Kaposi sarcoma–associated herpesvirus). Human herpesviruses share the properties of latency and reactivation. Members of the group can cause productive lytic infections, in which infectious virus is produced and cells are killed, or nonproductive lytic infections, in which viral DNA persists but complete replication does not occur and cells survive. After acute lytic infections, herpesviruses often persist in a latent form for years; periodic reactivations are followed by recurrent lytic infections. Sites of latency vary: HSV and VZV persist in neural ganglion cells, EBV persists in B cells, and CMV probably remains latent in many cell types. The sites of latency for HHV-6 and HHV-7 have not been identified, although both herpesviruses have been detected in salivary glands. All human herpesviruses have a worldwide distribution. Considerable efforts are being directed toward the development of vaccines and antiviral agents that will be active against herpesviruses. This chapter discusses the epidemiology, pathogenesis, diagnosis, prevention, and treatment of herpes simplex virus and varicella-zoster virus and their clinical syndromes. The descriptions of the clinical syndromes include complications and clinical features, as well as descriptions of symptoms. Tables provide information on chemotherapy for primary genital and mucocutaneous herpes infection, suppression of severe and recurring genital herpes infection, and varicella-zoster infection. Figures provide photographic illustrations of the various clinical syndromes. A sidebar about herpesvirus information on the Internet provides further detail. This review contains 123 references, 4 tables, and 6 highly rendered figures.

Herpesvirus Infections

2014 ◽  
Author(s):  
Martin S. Hirsch
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Varicella Zoster Virus ◽  
Ganglion Cells ◽  
Human Herpesvirus ◽  
Herpes Infection ◽  
Varicella Zoster ◽  
Clinical Syndromes ◽  
Simplex Virus ◽  
Human Herpesviruses

The herpes group of viruses is composed of at least eight human viruses and numerous animal viruses. The human herpesviruses include herpes simplex virus types 1 and 2 (HSV-1 and HSV-2), varicella-zoster virus (VZV), cytomegalovirus (CMV), Epstein-Barr virus (EBV), and human herpesvirus types 6 (HHV-6), 7 (HHV-7), and 8 (HHV-8, also known as Kaposi sarcoma–associated herpesvirus). Human herpesviruses share the properties of latency and reactivation. Members of the group can cause productive lytic infections, in which infectious virus is produced and cells are killed, or nonproductive lytic infections, in which viral DNA persists but complete replication does not occur and cells survive. After acute lytic infections, herpesviruses often persist in a latent form for years; periodic reactivations are followed by recurrent lytic infections. Sites of latency vary: HSV and VZV persist in neural ganglion cells, EBV persists in B cells, and CMV probably remains latent in many cell types. The sites of latency for HHV-6 and HHV-7 have not been identified, although both herpesviruses have been detected in salivary glands. All human herpesviruses have a worldwide distribution. Considerable efforts are being directed toward the development of vaccines and antiviral agents that will be active against herpesviruses. This chapter discusses the epidemiology, pathogenesis, diagnosis, prevention, and treatment of herpes simplex virus and varicella-zoster virus and their clinical syndromes. The descriptions of the clinical syndromes include complications and clinical features, as well as descriptions of symptoms. Tables provide information on chemotherapy for primary genital and mucocutaneous herpes infection, suppression of severe and recurring genital herpes infection, and varicella-zoster infection. Figures provide photographic illustrations of the various clinical syndromes. A sidebar about herpesvirus information on the Internet provides further detail. This review contains 123 references, 4 tables, and 6 highly rendered figures.

Detection of Human Herpesvirus 6 and Varicella-Zoster Virus in Tear Fluid of Patients with Bell's Palsy by PCR

2000 ◽  
Vol 38 (7) ◽  
pp. 2753-2755 ◽  
Author(s):  
A. Pitkäranta ◽  
H. Piiparinen ◽  
L. Mannonen ◽  
M. Vesaluoma ◽  
A. Vaheri
Keyword(s):  
Varicella Zoster Virus ◽  
Human Herpesvirus ◽  
Bell’S Palsy ◽  
Tear Fluid ◽  
Healthy Controls ◽  
Human Herpesvirus 6 ◽  
Bell's Palsy ◽  
Varicella Zoster ◽  
Herpesvirus 6 ◽  
Human Herpesviruses

Human herpesvirus 6 DNA was detected by PCR in the tear fluid of 7 (35%) of 20 patients with Bell's palsy and of 1 (5%) of 20 healthy controls. Varicella-zoster virus was detected by PCR in the tear fluid of 2 of 20 Bell's palsy patients but in none of the tear fluids from 20 healthy controls. These findings suggest an association between human herpesviruses and Bell's palsy.

scholarly journals Varicella-Zoster Virus (VZV) Small Noncoding RNAs Antisense to the VZV Latency-Encoded Transcript VLT Enhance Viral Replication

2020 ◽  
Vol 94 (13) ◽  
Author(s):  
Punam Bisht ◽  
Biswajit Das ◽  
Paul R. Kinchington ◽  
Ronald S. Goldstein
Keyword(s):  
Gene Expression ◽  
Herpes Zoster ◽  
Varicella Zoster Virus ◽  
Noncoding Rnas ◽  
Human Herpesvirus ◽  
Varicella Zoster ◽  
Small Noncoding Rnas ◽  
Viral Spread ◽  
Additional Layer ◽  
Virally Encoded

ABSTRACT Small noncoding RNAs (sncRNA), including microRNA (miR), are expressed by many viruses to provide an additional layer of gene expression regulation. Our work has shown that varicella-zoster virus (VZV; also called human herpesvirus 3 [HHV3]), the human alphaherpesvirus causing varicella and herpes zoster, expresses 24 virally encoded sncRNA (VZVsncRNA) in infected cells. Here, we demonstrate that several VZVsncRNA can modulate VZV growth, including four VZVsncRNA (VZVsncRNA10, -11, -12, and -13) that are antisense to VLT, a transcript made in lytic infections and associated with VZV latency. The influence on productive VZV growth and spread was assessed in epithelial cells transfected with locked nucleotide analog antagonists (LNAA). LNAA to the four VZVsncRNA antisense to VLT significantly reduced viral spread and progeny titers of infectious virus, suggesting that these sncRNA promoted lytic infection. The LNAA to VZVsncRNA12, encoded in the leader to ORF61, also significantly increased the levels of VLT transcripts. Conversely, overexpression of VZVsncRNA13 using adeno-associated virus consistently increased VZV spread and progeny titers. These results suggest that sncRNA antisense to VZV may regulate VZV growth, possibly by affecting VLT expression. Transfection of LNAA to VZVsncRNA14 and VZVsncRNA9 decreased and increased VZV growth, respectively, while LNAA to three other VZVsncRNA had no significant effects on replication. These data strongly support the conclusion that VZV replication is modulated by multiple virally encoded sncRNA, revealing an additional layer of complexity of VZV regulation of lytic infections. This may inform the development of novel anti-sncRNA-based therapies for treatment of VZV diseases. IMPORTANCE Varicella-zoster virus (VZV) causes herpes zoster, a major health issue in the aging and immunocompromised populations. Small noncoding RNAs (sncRNA) are recognized as important actors in modulating gene expression. This study extends our previous work and shows that four VZVsncRNA clustering in and near ORF61 and antisense to the latency-associated transcript of VZV can positively influence productive VZV infection. The ability of multiple exogenous small oligonucleotides targeting VZVsncRNA to inhibit VZV replication strengthens the possibility that they may inform development of novel treatments for painful herpes zoster.

scholarly journals Recombination of Globally Circulating Varicella-Zoster Virus

2015 ◽  
Vol 89 (14) ◽  
pp. 7133-7146 ◽  
Author(s):  
Peter Norberg ◽  
Daniel P. Depledge ◽  
Samit Kundu ◽  
Claire Atkinson ◽  
Julianne Brown ◽  
...  
Keyword(s):  
Varicella Zoster Virus ◽  
Genetic Recombination ◽  
Human Herpesvirus ◽  
Infectious Laryngotracheitis Virus ◽  
Live Attenuated Vaccine ◽  
Herpes Simplex Viruses ◽  
Varicella Zoster ◽  
Laryngotracheitis Virus

ABSTRACTVaricella-zoster virus (VZV) is a human herpesvirus, which during primary infection typically causes varicella (chicken pox) and establishes lifelong latency in sensory and autonomic ganglia. Later in life, the virus may reactivate to cause herpes zoster (HZ; also known as shingles). To prevent these diseases, a live-attenuated heterogeneous vaccine preparation, vOka, is used routinely in many countries worldwide. Recent studies of another alphaherpesvirus, infectious laryngotracheitis virus, demonstrate that live-attenuated vaccine strains can recombinein vivo, creating virulent progeny. These findings raised concerns about using attenuated herpesvirus vaccines under conditions that favor recombination. To investigate whether VZV may undergo recombination, which is a prerequisite for VZV vaccination to create such conditions, we here analyzed 115 complete VZV genomes. Our results demonstrate that recombination occurs frequently for VZV. It thus seems that VZV is fully capable of recombination if given the opportunity, which may have important implications for continued VZV vaccination. Although no interclade vaccine-wild-type recombinant strains were found, intraclade recombinants were frequently detected in clade 2, which harbors the vaccine strains, suggesting that the vaccine strains have already been involved in recombination events, eitherin vivoorin vitroduring passages in cell culture. Finally, previous partial and complete genomic studies have described strains that do not cluster phylogenetically to any of the five established clades. The additional VZV strains sequenced here, in combination with those previously published, have enabled us to formally define a novel sixth VZV clade.IMPORTANCEAlthough genetic recombination has been demonstrated to frequently occur for other human alphaherpesviruses, herpes simplex viruses 1 and 2, only a few ancient and isolated recent recombination events have hitherto been demonstrated for VZV. In the present study, we demonstrate that VZV also frequently undergoes genetic recombination, including strains belonging to the clade containing the vOKA strain.

scholarly journals Lineages of varicella-zoster virus

2009 ◽  
Vol 90 (4) ◽  
pp. 963-969 ◽  
Author(s):  
Duncan J. McGeoch
Keyword(s):  
Phylogenetic Tree ◽  
Varicella Zoster Virus ◽  
Human Herpesvirus ◽  
Nucleotide Polymorphisms ◽  
Single Group ◽  
Genome Sequences ◽  
Single Nucleotide ◽  
Unique Region ◽  
Varicella Zoster ◽  
Single Sequence

Relationships among varicella-zoster virus (VZV; Human herpesvirus 3) genome sequences were examined to evaluate descent of strains, structures of lineages and incidence of recombination events. Eighteen complete, published genome sequences were aligned and 494 single nucleotide polymorphisms (SNPs) extracted, each as two alleles. At 281 SNPs, a single sequence differed from all the others. Distributions of the remaining 213 SNPs indicated that the sequences fell into five groups, which coincided with previously recognized phylogenetic groupings, termed E1, E2, J, M1 and M2. The 213-SNP set was divisible into 104 SNPs that were specific to a single group, and 109 cross-group SNPs that defined relationships among groups. This last set was evaluated by criteria of continuities in relationships between groups and breaks in such patterns, to identify crossover points and ascribe them to lineages. For the 99 cross-group SNPs in the genome's long unique region, it was seen that the E2 and M2 groups were almost completely distinct in their SNP alleles, and the E1 group was derived from a recombinant of E2 and M2. A valid phylogenetic tree could thus be constructed for the four E2 and two M2 strains. There was no substantive evidence for recombination within the E2 group or the E1 group (ten strains). The J and M1 groups each contained only one strain, and both were interpreted as having substantial distinct histories plus possible recombinant elements from the E2 and M2 lineages. The view of VZV recombination and phylogeny reached represents a major clarification of deep relationships among VZV lineages.

Antiviral Activity of 2-Hydroxy Fatty Acids

1996 ◽  
Vol 7 (3) ◽  
pp. 138-141 ◽  
Author(s):  
D.R. Harper ◽  
R.L. Gilbert ◽  
T.J. O'Connor ◽  
D. Kinchington ◽  
N. Mahmood ◽  
...  
Keyword(s):  
Varicella Zoster Virus ◽  
Human Herpesvirus ◽  
Antiviral Effect ◽  
Adherent Cell ◽  
Cellular Functions ◽  
Varicella Zoster ◽  
Immunodeficiency Virus ◽  
Compound Screening ◽  
Uptake Assay ◽  
High Concentrations

Following an earlier demonstration of an antiviral effect against varicella-zoster virus (VZV, human herpesvirus 3) using 2-hydroxymyristic acid (2-hydroxytetradecanoic acid; 2-HM), an inhibitor of protein myristoylation, both 2-HM and 2-hydroxypalmitic acid (2-hydroxyhexadecanoic acid; 2-HP) have been tested against a range of viruses. Although both compounds inhibit the replication of varicella-zoster virus (VZV; human herpesvirus 3) they do not inhibit the replication of closely related herpesviruses. They do, however, inhibit the replication of both poliovirus (a member of the Picornaviridae) and the human immunodeficiency virus type 1 (HIV-1; a member of the Retroviridae). Neither compound is toxic to adherent cells by dye uptake assay, although limited toxicity is apparent to non-adherent cell lines at high concentrations. The mechanisms underlying these effects are discussed. A diminished effect of 2-hydroxymyristic acid when the compound is dissolved in dimethyl sulphoxide (DMSO) rather than ethanol is reported, and the implications for the use of DMSO as a ‘universal solvent’ for compound screening noted. Finally, it is suggested that targeting of ‘virus-essential’ cellular functions may provide an alternative route for inhibiting viral replication.

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