Varicella-zoster virus ORF 58 gene is dispensable for viral replication in cell culture

Yoshii, Hironori; Sadaoka, Kay; Matsuura, M.; Nagaike, Kazuhiro; Takahashi, Michiaki; Yamanishi, Koichi; Mori, Yasuko

doi:10.1186/1743-422x-5-54

Cited by 8 publications

(3 citation statements)

References 19 publications

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“…Varicella zoster virus (VZV) is the causative agent of chickenpox and shingles. Several studies have utilized VZV BACs to study the role of specific VZV genes [ 21 – 23 , 59 , 118 ], and there has also been a recent global mutagenesis study to determine which VZV genes are essential for viral replication [ 53 ]. (For more information about global analysis of gene function in VZV, see the next section.)…”

Section: Studies Of Specific Herpesvirus Bacsmentioning

confidence: 99%

Herpesvirus BACs: Past, Present, and Future

Warden

Tang

Zhu

2010

BioMed Research International

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The herpesviridae are a large family of DNA viruses with large and complicated genomes. Genetic manipulation and the generation of recombinant viruses have been extremely difficult. However, herpesvirus bacterial artificial chromosomes (BACs) that were developed approximately 10 years ago have become useful and powerful genetic tools for generating recombinant viruses to study the biology and pathogenesis of herpesviruses. For example, BAC-directed deletion mutants are commonly used to determine the function and essentiality of viral genes. In this paper, we discuss the creation of herpesvirus BACs, functional analyses of herpesvirus mutants, and future applications for studies of herpesviruses. We describe commonly used methods to create and mutate herpesvirus BACs (such as site-directed mutagenesis and transposon mutagenesis). We also evaluate the potential future uses of viral BACs, including vaccine development and gene therapy.

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Section: Studies Of Specific Herpesvirus Bacsmentioning

confidence: 99%

Herpesvirus BACs: Past, Present, and Future

Warden

Tang

Zhu

2010

BioMed Research International

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“…ORFs 37 and 60 are late genes encoding Glycoproteins H and L, respectively [12], while ORF 42 may be involved in the encapsidation process [13]. The candidacy of the other two transcripts is less of an issue in this regard, as ORF 32 encodes a small polypeptide with unknown function [14], and ORF 58 encodes a nuclear phosphoprotein [15]. At this juncture, it is uncertain whether these ORFs remain "latency candidates" that justify further experimentation or if they can only be classified as transcripts detected in latent tissue and are more likely to be representative of low-level VZV reactivation.…”

Section: Discussionmentioning

confidence: 99%

Variable Gene Expression in Human Ganglia Latently Infected with Varicella-Zoster Virus

Kennedy

Montague

2022

Viruses

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Varicella-Zoster virus (VZV) is a pathogenic human herpes virus that causes varicella (“chicken pox”) as a primary infection, following which it becomes latent in neuronal cells in human peripheral ganglia. It may then reactivate to cause herpes zoster (“shingles”). Defining the pattern of VZV gene expression during latency is an important issue, and four highly expressed VZV genes were first identified by Randall Cohrs in 1996 using cDNA libraries. Further studies from both his and other laboratories, including our own, have suggested that viral gene expression may be more widespread than previously thought, but a confounding factor has always been the possibility of viral reactivation after death in tissues obtained even at 24 h post-mortem. Recent important studies, which Randall Cohrs contributed to, have clarified this issue by studying human trigeminal ganglia at 6 h after death using RNA-Seq methodology when a novel spliced latency-associated VZV transcript (VLT) was found to be mapped antisense to the viral transactivator gene 61. Viral gene expression could be induced by a VLT-ORF 63 fusion transcript when VZV reactivated from latency. Prior detection by several groups of ORF63 in post-mortem-acquired TG is very likely to reflect detection of the VLT-ORF63 fusion and not canonical ORF63. The contributions to the VZV latency field by Randall Cohrs have been numerous and highly significant.

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“…The introduction of GFP also deleted the stop codon of ORF58. Both ORF57 and ORF58 are not essential for VZV growth in vitro [37][38][39] . After two days of infection with pOka-Δ57-GFP, we stimulated the cells with IFN-γ for another day and then quantified ICAM1 protein levels by flow cytometry (Supplementary Fig.…”

Section: Ifn-γ-mediated Icam1 Expression Increases In Epithelial Cell...mentioning

confidence: 99%

Viral modulation of type II interferon increases T cell adhesion and virus spread

Jacobsen,

Plückebaum,

Ssebyatika

et al. 2024

Nat Commun

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During primary varicella zoster virus (VZV) infection, infected lymphocytes drive primary viremia, causing systemic dissemination throughout the host, including the skin. This results in cytokine expression, including interferons (IFNs), which partly limit infection. VZV also spreads from skin keratinocytes to lymphocytes prior to secondary viremia. It is not clear how VZV achieves this while evading the cytokine response. Here, we show that VZV glycoprotein C (gC) binds IFN-γ and modifies its activity, increasing the expression of a subset of IFN-stimulated genes (ISGs), including intercellular adhesion molecule 1 (ICAM1), chemokines and immunomodulatory genes. The higher ICAM1 protein level at the plasma membrane of keratinocytes facilitates lymphocyte function-associated antigen 1-dependent T cell adhesion and expression of gC during infection increases VZV spread to peripheral blood mononuclear cells. This constitutes the discovery of a strategy to modulate IFN-γ activity, upregulating a subset of ISGs, promoting enhanced lymphocyte adhesion and virus spread.

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Varicella-zoster virus ORF 58 gene is dispensable for viral replication in cell culture

Cited by 8 publications

References 19 publications

Herpesvirus BACs: Past, Present, and Future

Herpesvirus BACs: Past, Present, and Future

Variable Gene Expression in Human Ganglia Latently Infected with Varicella-Zoster Virus

Viral modulation of type II interferon increases T cell adhesion and virus spread

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