Compounds that Target Host Cell Enzymes Prevent Varicella-zoster Virus Replication In Vitro, Ex Vivo, and in SCID-hu Mice

2009 ◽  
Vol 82 (2) ◽  
pp. A52 ◽  
Author(s):  
J. Rowe ◽  
R. Greenblatt ◽  
D. Liu ◽  
J. Moffat
Keyword(s):  
Varicella Zoster Virus ◽  
Host Cell ◽  
Virus Replication ◽  
Ex Vivo ◽  
Varicella Zoster

Resveratrol inhibition of varicella-zoster virus replication in vitro

2006 ◽  
Vol 72 (3) ◽  
pp. 171-177 ◽  
Author(s):  
John J. Docherty ◽  
Thomas J. Sweet ◽  
Erin Bailey ◽  
Seth A. Faith ◽  
Tristan Booth
Keyword(s):  
Varicella Zoster Virus ◽  
Virus Replication ◽  
Varicella Zoster

Inhibitory activity of oxyresveratrol on wild-type and drug-resistant varicella-zoster virus replication in vitro

2009 ◽  
Vol 84 (1) ◽  
pp. 95-97 ◽  
Author(s):  
Pattaraporn Sasivimolphan ◽  
Vimolmas Lipipun ◽  
Kittisak Likhitwitayawuid ◽  
Masaya Takemoto ◽  
Pornpen Pramyothin ◽  
...  
Keyword(s):  
Varicella Zoster Virus ◽  
Virus Replication ◽  
Inhibitory Activity ◽  
Drug Resistant ◽  
Wild Type ◽  
Varicella Zoster

scholarly journals Role of the protein kinase PKR in the inhibition of varicella-zoster virus replication by beta interferon and gamma interferon

2005 ◽  
Vol 86 (1) ◽  
pp. 1-6 ◽  
Author(s):  
Nathalie Desloges ◽  
Markus Rahaus ◽  
Manfred H. Wolff
Keyword(s):  
Protein Kinase ◽  
Varicella Zoster Virus ◽  
Virus Replication ◽  
Type I ◽  
Double Stranded Rna ◽  
Varicella Zoster ◽  
Antiviral Effects ◽  
Simplex Virus

Varicella-zoster virus (VZV) is sensitive to type I and type II interferons (IFNs), which mediate antiviral effects. In this study, it was demonstrated that IFN-β and IFN-γ inhibited the replication of VZV in vitro. Although IFN-β was more effective than IFN-γ, the level of inhibition of VZV replication achieved by the combination of both IFNs was more than additive and it was concluded that these two cytokines acted synergistically. Expression of the IFN-induced, double-stranded RNA-activated protein kinase PKR and its phosphorylation level were not modulated strongly during ongoing replication of VZV. However, in the presence of IFN-β, but not IFN-γ, PKR expression and its phosphorylation were increased, explaining in part the inhibition of virus replication by IFNs. The expression of herpes simplex virus Us11, a viral protein with several functions, including prevention of PKR activation, strongly increased the level of VZV replication.

scholarly journals Downregulation of Varicella-Zoster Virus (VZV) Immediate-Early ORF62 Transcription by VZV ORF63 Correlates with Virus Replication In Vitro and with Latency

2006 ◽  
Vol 80 (7) ◽  
pp. 3459-3468 ◽  
Author(s):  
Susan E. Hoover ◽  
Randall J. Cohrs ◽  
Zoila G. Rangel ◽  
Donald H. Gilden ◽  
Peter Munson ◽  
...  
Keyword(s):  
Varicella Zoster Virus ◽  
Virus Replication ◽  
Deletion Mutant ◽  
Recombinant Adenovirus ◽  
Parental Virus ◽  
Reading Frame ◽  
Fourfold Increase ◽  
Varicella Zoster ◽  
In Cells

ABSTRACT Varicella-zoster virus (VZV) open reading frame 63 (ORF63) protein is expressed during latency in human sensory ganglia. Deletion of ORF63 impairs virus replication in cell culture and establishment of latency in cotton rats. We found that cells infected with a VZV ORF63 deletion mutant yielded low titers of cell-free virus and produced very few enveloped virions detectable by electron microscopy compared with those infected with parental virus. Microarray analysis of cells infected with a recombinant adenovirus expressing ORF63 showed that transcription of few human genes was affected by ORF63; a heat shock 70-kDa protein gene was downregulated, and several histone genes were upregulated. In experiments using VZV transcription arrays, deletion of ORF63 from VZV resulted in a fourfold increase in expression of ORF62, the major viral transcriptional activator. A threefold increase in ORF62 protein was observed in cells infected with the ORF63 deletion mutant compared with those infected with parental virus. Cells infected with ORF63 mutants impaired for replication and latency (J. I. Cohen, T. Krogmann, S. Bontems, C. Sadzot-Delvaux, and L. Pesnicak, J. Virol. 79:5069-5077, 2005) showed an increase in ORF62 transcription compared with those infected with parental virus. In contrast, cells infected with an ORF63 mutant that is not impaired for replication or latency showed ORF62 RNA levels equivalent to those in cells infected with parental virus. The ability of ORF63 to downregulate ORF62 transcription may play an important role in virus replication and latency.

scholarly journals Molecular Aspects of Varicella-Zoster Virus Latency

2018 ◽  
Author(s):  
Daniel P. Depledge ◽  
Tomohiko Sadaoka ◽  
Werner J. D. Ouwendijk
Keyword(s):  
Varicella Zoster Virus ◽  
Molecular Mechanisms ◽  
Neurological Complications ◽  
In Vitro Models ◽  
New Era ◽  
Varicella Zoster ◽  
Virus Latency ◽  
Technological Advances ◽  
Molecular Aspects

Primary varicella-zoster virus (VZV) infection causes varicella (chickenpox) and the establishment of a lifelong latent infection in ganglionic neurons. VZV reactivates in about one-third of infected individuals to cause herpes zoster, often accompanied by neurological complications. The restricted host range of VZV and, until recently, the lack of suitable in vitro models to study VZV latency have seriously hampered molecular studies of viral latency. Nevertheless, recent technological advances facilitated a series of exciting studies that resulted in the discovery of a VZV latency-associated transcript (VLT) and have redefined our understanding of VZV latency and factors that initiate reactivation. Together, these findings pave the way for a new era of research that may finally unravel the precise molecular mechanisms that govern latency. In this review, we will summarize the implications of recent discoveries in the VZV latency field from both a virus and host perspective and provide a roadmap for future studies.

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