Latency of varicella zoster virus a persistently perplexing state

Kinchington, Paul R.

doi:10.2741/a422

Cited by 6 publications

(4 citation statements)

References 76 publications

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“…VZV gene expression in latently infected human ganglia is restricted to transcription of a limited number of viral genes (Cohrs et al ., 1996 ; Kinchington, 1999 ). SVV gene expression in ganglia of latently infected monkeys has not yet been defined.…”

Section: Full Textmentioning

confidence: 99%

Viral gene expression during acute simian varicella virus infection

Gray

Mullis

Soike

2002

Journal of General Virology

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Simian varicella virus (SVV) causes a natural varicella-like disease in nonhuman primates. Outbreaks of simian varicella occur sporadically in primate facilities. Simian varicella is used as a model for investigation of varicella-zoster virus (VZV) pathogenesis and latency. In this study, SVV gene expression and histopathology were analysed in tissues of acutely infected vervet monkeys. RT-PCR analysis demonstrated expression of specific SVV immediate early, early and late genes in the skin, lung, liver and ganglia tissues of acutely infected monkeys. Viral antigen expression and histopathology, including necrosis and inflammation, were detected in the skin, lungs, liver and spleen of infected monkeys by immunohistochemical analysis. Viral antigen expression, but little or no histopathology, was evident in the neural ganglia, the eventual site of viral latency. The study provides a foundation for further investigation on the role of viral genes in varicella pathogenesis and latency.

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Section: Full Textmentioning

confidence: 99%

Viral gene expression during acute simian varicella virus infection

Gray

Mullis

Soike

2002

Journal of General Virology

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“…Varicella results from primary infection and is a common highly contagious childhood illness, associated with fever and generalized vesicular rashes [18] . Following the resolution of primary infection by the host immune system, VZV migrates along neuronal cell axon to reach dorsal root ganglia where it establishes a lifelong latent infection [19] . Reactivation from latency, due to a weakness of the immune system, leads to herpes zoster.…”

Section: Introductionmentioning

confidence: 99%

The Varicella-Zoster Virus ORF47 Kinase Interferes with Host Innate Immune Response by Inhibiting the Activation of IRF3

et al. 2011

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The innate immune response constitutes the first line of host defence that limits viral spread and plays an important role in the activation of adaptive immune response. Viral components are recognized by specific host pathogen recognition receptors triggering the activation of IRF3. IRF3, along with NF-κB, is a key regulator of IFN-β expression. Until now, the role of IRF3 in the activation of the innate immune response during Varicella-Zoster Virus (VZV) infection has been poorly studied. In this work, we demonstrated for the first time that VZV rapidly induces an atypical phosphorylation of IRF3 that is inhibitory since it prevents subsequent IRF3 homodimerization and induction of target genes. Using a mutant virus unable to express the viral kinase ORF47p, we demonstrated that (i) IRF3 slower-migrating form disappears; (ii) IRF3 is phosphorylated on serine 396 again and recovers the ability to form homodimers; (iii) amounts of IRF3 target genes such as IFN-β and ISG15 mRNA are greater than in cells infected with the wild-type virus; and (iv) IRF3 physically interacts with ORF47p. These data led us to hypothesize that the viral kinase ORF47p is involved in the atypical phosphorylation of IRF3 during VZV infection, which prevents its homodimerization and subsequent induction of target genes such as IFN-β and ISG15.

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“…Cytoplasmic retention of IE63 could interfere with efficient transcription of VZV glycoprotein genes in neural cells (3,4,40). A single copy of ORF63 was sufficient to support VZV infection of neural cells in vivo.…”

Section: Figmentioning

confidence: 99%

“…V aricella-zoster virus (VZV) is a human alphaherpesvirus that causes varicella and herpes zoster (1)(2)(3)(4). VZV has a linear, double-stranded DNA genome encoding at least 70 proteins, including immediate early (IE) regulatory proteins that control viral gene transcription, early genes, such as viral kinases, and late genes, which are predominantly viral glycoproteins that comprise the virion envelope.…”

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confidence: 99%

Varicella-zoster virus infection of human neural cells in vivo

Baiker

Fabel

Cozzio

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

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Varicella-zoster virus (VZV) establishes latency in sensory ganglia and causes herpes zoster upon reactivation. These investigations in a nonobese diabetic severe combined immunodeficient mousehuman neural cell model showed that VZV infected both neurons and glial cells and spread efficiently from cell to cell in vivo. Neural cell morphology and protein synthesis were preserved, in contrast to destruction of epithelial cells by VZV. Expression of VZV genes in neural cells was characterized by nuclear retention of the major viral transactivating protein and a block in synthesis of the predominant envelope glycoprotein. The attenuated VZV vaccine strain retained infectivity for neurons and glial cells in vivo. VZV gene expression in differentiated human neural cells in vivo differs from neural infection by herpes simplex virus, which is characterized by latency-associated transcripts, and from lytic VZV replication in skin. The chimeric nonobese diabetic severe combined immunodeficient mouse model may be useful for investigating other neurotropic human viruses.

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Latency of varicella zoster virus a persistently perplexing state

Cited by 6 publications

References 76 publications

Viral gene expression during acute simian varicella virus infection

Viral gene expression during acute simian varicella virus infection

The Varicella-Zoster Virus ORF47 Kinase Interferes with Host Innate Immune Response by Inhibiting the Activation of IRF3

Varicella-zoster virus infection of human neural cells in vivo

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