Varicella-zoster virus–induced apoptosis in MeWo cells is accompanied by down-regulation of Bcl-2 expression

Brazeau, Elizabeth; Mahalingam, Ravi; Gilden, Don; Wellish, Mary; Kaufer, Benedikt B.; Osterrieder, Nikolaus; Pugazhenthi, Subbiah

doi:10.3109/13550281003682547

Cited by 25 publications

(28 citation statements)

References 18 publications

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“…Apoptosis was reported 24 to 48 h after VZV infection of fibroblasts (7), 48 h after infection of T cells (25), 64 to 72 h after infection in MeWo cells (1), and 72 to 96 h after infection of Vero cells (24). We found that ORF12 protein inhibited apoptosis of VZV-infected MeWo cells early (Յ30 h) after infection.…”

Section: Discussionmentioning

confidence: 59%

Varicella-Zoster Virus ORF12 Protein Triggers Phosphorylation of ERK1/2 and Inhibits Apoptosis

Liu

Dowdell

et al. 2012

J Virol

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Section: Discussionmentioning

confidence: 59%

Varicella-Zoster Virus ORF12 Protein Triggers Phosphorylation of ERK1/2 and Inhibits Apoptosis

Liu

Dowdell

et al. 2012

J Virol

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“…Equimolar concentrations of all four HSV-1 isomers are packaged into the virion (Roizman, 1979), whilst only two isomers (both U S inversions) predominate in packaged VZV (Kinchington et al, 1985). The drastic reduction of U L inversions in VZV DNA within infectious virus particles is attributed to a DNA sequence uniquely located at the extreme left-end of the virus U L DNA that is responsible for cleavage of genome-size DNA during packaging (Kaufer et al, 2010). As this sequence is not present at the extreme right-end of VZV U L DNA, the single cleavage site does not permit U L inversions to be packaged into infectious virus particles.…”

Section: Introductionmentioning

confidence: 99%

“…At the single-cell level, the VZV lytic replication cycle culminates in 9-12 h (Reichelt et al, 2009), but it can take 3-5 days for the entire culture to show extensive VZV-induced syncytia (Grose & Brunel, 1978) and cell death either by lysis or apoptosis (Brazeau et al, 2010;Pugazhenthi et al, 2011). Whilst cell-free VZV preparations have been reported, virus yield remains extremely low: 10 5 p.f.u.…”

Section: Introductionmentioning

confidence: 99%

A comparison of herpes simplex virus type 1 and varicella-zoster virus latency and reactivation

Kennedy

Rovnak

Badani

et al. 2015

Journal of General Virology

133

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Herpes simplex virus type 1 (HSV-1; human herpesvirus 1) and varicella-zoster virus (VZV; human herpesvirus 3) are human neurotropic alphaherpesviruses that cause lifelong infections in ganglia. Following primary infection and establishment of latency, HSV-1 reactivation typically results in herpes labialis (cold sores), but can occur frequently elsewhere on the body at the site of primary infection (e.g. whitlow), particularly at the genitals. Rarely, HSV-1 reactivation can cause encephalitis; however, a third of the cases of HSV-1 encephalitis are associated with HSV-1 primary infection. Primary VZV infection causes varicella (chickenpox) following which latent virus may reactivate decades later to produce herpes zoster (shingles), as well as an increasingly recognized number of subacute, acute and chronic neurological conditions. Following primary infection, both viruses establish a latent infection in neuronal cells in human peripheral ganglia. However, the detailed mechanisms of viral latency and reactivation have yet to be unravelled. In both cases latent viral DNA exists in an 'end-less' state where the ends of the virus genome are joined to form structures consistent with unit length episomes and concatemers, from which viral gene transcription is restricted. In latently infected ganglia, the most abundantly detected HSV-1 RNAs are the spliced products originating from the primary latency associated transcript (LAT). This primary LAT is an 8.3 kb unstable transcript from which two stable (1.5 and 2.0 kb) introns are spliced. Transcripts mapping to 12 VZV genes have been detected in human ganglia removed at autopsy; however, it is difficult to ascribe these as transcripts present during latent infection as early-stage virus reactivation may have transpired in the post-mortem time period in the ganglia. Nonetheless, low-level transcription of VZV ORF63 has been repeatedly detected in multiple ganglia removed as close to death as possible. There is increasing evidence that HSV-1 and VZV latency is epigenetically regulated. In vitro models that permit pathway analysis and identification of both epigenetic modulations and global transcriptional mechanisms of HSV-1 and VZV latency hold much promise for our future understanding in this complex area. This review summarizes the molecular biology of HSV-1 and VZV latency and reactivation, and also presents future directions for study. Received 5 January 2015Accepted 18 March 2015 IntroductionHerpes simplex virus type 1 (HSV-1; human herpesvirus 1) and varicella-zoster virus (VZV; human herpesvirus 3) are human neurotropic alphaherpesviruses usually acquired early in life. Primary HSV-1 infection is usually localized and may be asymptomatic, although it can produce a more widespread systemic infection in neonates and immunocompromised adults, whilst primary VZV infection is systemic and results in childhood varicella (chickenpox). During primary infection, both viruses gain access to neurons most likely through retrograde transport from the site of cutaneous lesion...

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“…3). All 68 VZV genes are transcribed during productive virus infection in tissue culture cells [32] where virus spreads from cell to cell, resulting in extensive cytopathologic effects and apoptotic cell death in 3–5 days [33]. However, during latency VZV transcription is limited, no cytopathologic effects are evident, and production of infectious virions is inhibited.…”

Section: Vzv Latencymentioning

confidence: 99%

The Variegate Neurological Manifestations of Varicella Zoster Virus Infection

Gilden

Nagel

Cohrs

et al. 2013

Curr Neurol Neurosci Rep

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Varicella zoster virus (VZV) is an exclusively human neurotropic alphaherpesvirus. Primary infection causes varicella (chickenpox), after which the virus becomes latent in ganglionic neurons along the entire neuraxis. With advancing age or immunosuppression, cell-mediated immunity to VZV declines, and the virus reactivates to cause zoster (shingles), dermatomal distribution, pain, and rash. Zoster is often followed by chronic pain (postherpetic neuralgia), cranial nerve palsies, zoster paresis, vasculopathy, meningoencephalitis, and multiple ocular disorders. This review covers clinical, laboratory, and pathological features of neurological complications of VZV reactivation, including diagnostic testing to verify active VZV infection in the nervous system. Additional perspectives are provided by discussions of VZV latency, animal models to study varicella pathogenesis and immunity, and of the value of vaccination of elderly individuals to boost cell-mediated immunity to VZV and prevent VZV reactivation.

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Varicella-zoster virus–induced apoptosis in MeWo cells is accompanied by down-regulation of Bcl-2 expression

Cited by 25 publications

References 18 publications

Varicella-Zoster Virus ORF12 Protein Triggers Phosphorylation of ERK1/2 and Inhibits Apoptosis

Varicella-Zoster Virus ORF12 Protein Triggers Phosphorylation of ERK1/2 and Inhibits Apoptosis

A comparison of herpes simplex virus type 1 and varicella-zoster virus latency and reactivation

The Variegate Neurological Manifestations of Varicella Zoster Virus Infection

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