A Cell Culture Model of Latent and Lytic Herpes Simplex Virus Type 1 Infection in Spiral Ganglion

Liu, Yuehong; Li, Shufeng

doi:10.1159/000381679

Cited by 6 publications

(3 citation statements)

References 31 publications

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“…For this purpose, we infected primary murine neurons with neuropathogenic and non-neuropathogenic EHV-1 strains in the presence or absence of the antiviral drug ACV suppressing productive infection. Trichostatin A (TSA) was used to stimulate productive infection after ACV removal, as it is a known chemical reactivator of HSV-1 (14). No significant differences in replication kinetics were shown between Jan-E and 26 strains, which was also demonstrated previously (7).…”

Section: Resultsmentioning

confidence: 91%

Acyclovir and trichostatin A modulate EHV-1 replication in murine neurons in vitro

Golke¹,

Cymerys²,

Tucholska³

et al. 2017

Medycyna Weterynaryjna

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SummaryEquine herpesvirus type 1 (EHV-1) is a major viral pathogen of horses, causing respiratory disease, abortions, and equine herpes myeloencephalopathy (EHM). Like other alphaherpesviruses, EHV-1 establishes latency in neurons, but mechanisms involved in this process are still elusive. In the present study, we used antiviral drug acyclovir (ACV) to completely suppress EHV-1 replication in primary murine neuron culture. Trichostatin A (TSA), a known chemical reactivator of other herpesviruses, was used to stimulate productive EHV-1 infection. Moreover, gene expression of some cytokines was simultaneously evaluated, in order to check, whether the maintenance conditions of such a model may influence host cell response. Changes observed in IFN-α, IFN-β, and IL-10 mRNA gene expression depended on the EHV-1 strain. Although infection with either of the two EHV-1 strains investigated led to in an increase in type I IFNs gene expression, only the neuropathogenic strain caused a decrease in anti-inflammatory IL-10 gene expression. Unlike EHV-1 infection, the addition of neither ACV nor TSA caused significant changes in the expression of the above genes. We may therefore conclude that the in vitro model presented in the study is suitable for detailed investigation of the host cell-virus relationship on the molecular level.

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Section: Resultsmentioning

confidence: 91%

Acyclovir and trichostatin A modulate EHV-1 replication in murine neurons in vitro

Golke¹,

Cymerys²,

Tucholska³

et al. 2017

Medycyna Weterynaryjna

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“…The ACV concentration that effectively inhibits EHV-1 replication was established previously (Golke et al, 2017). Trichostatin A was used to stimulate productive EHV-1 infection, after ACV removal, as it is a known chemical reactivator of HHV-1 (Liu and Li, 2015). The replication kinetics of both EHV-1 strains in primary murine neurons and influence of ACV and TSA was determined previously (Golke et al, 2017).…”

Section: Methodsmentioning

confidence: 99%

Neuropathogenic and non-neuropathogenic EHV-1 strains induce the accumulation of hyperphosphorylated Tau in primary murine neurons

Cymerys¹,

Słońska²,

Chodkowski³

et al. 2020

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Equid herpesvirus 1 (EHV-1) causes respiratory disease, abortion and neurological disorders in horses. Similarly, to other alphaherpesviruses, EHV-1 is neurotropic and establishes latency in the neurons of its natural host. Despite the fact that many studies have been devoted to the pathogenesis of various clinical forms of EHV-1 infection, mechanisms of the neuronal damage are still not fully understood. The aim of this study was to define the phosphorylation status of tau protein in neuronal cell culture infected with EHV-1. Phosphorylation of tau was tested at tau-ser199/ser202, tau-ser404, tau-ser262, tau-thr181, tau-thr217 and tau-thr205 sites. we described, for the first time, that EHV-1 infection leads to the accumulation of hyperphosphorylated tau in primary murine neurons. we showed that non-neuropathogenic and neuropathogenic EHV-1 strains specifically induce hyperphosphorylation of tau-ser199/ser202, tau-ser404 and tau-thr205 during long-term infection and after a controlled activation of productive infection.

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“…Computed tomography (CT) and MRI scans of their brains showed common bilateral lesions in the auditory cortex [ 52 ]. The reactivation of latent HSV-1 infection after infancy can also cause hearing loss [ 53 ]. Rabinstein et al described a 61-year-old woman with severe bilateral hearing loss who experienced serological reactivation of a previously latent HSV-1 virus.…”

Section: Herpesvirusesmentioning

confidence: 99%

The Pathogenesis of Cytomegalovirus and Other Viruses Associated with Hearing Loss: Recent Updates

Shi

Liu

Sun

2023

Viruses

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Virus infection is one of the most common etiologies of hearing loss. Hearing loss associated with viral infection can be unilateral or bilateral, mild or severe, sudden or progressive, and permanent or recoverable. Many viruses cause hearing loss in adults and children; however, the pathogenesis of hearing loss caused by viral infection is not fully understood. This review describes cytomegalovirus, the most common virus causing hearing loss, and other reported hearing loss-related viruses. We hope to provide a detailed description of pathogenic characteristics and research progress on pathology, hearing phenotypes, possible associated mechanisms, treatment, and prevention measures. This review aims to provide diagnostic and treatment assistance to clinical workers.

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A Cell Culture Model of Latent and Lytic Herpes Simplex Virus Type 1 Infection in Spiral Ganglion

Cited by 6 publications

References 31 publications

Acyclovir and trichostatin A modulate EHV-1 replication in murine neurons in vitro

Acyclovir and trichostatin A modulate EHV-1 replication in murine neurons in vitro

Neuropathogenic and non-neuropathogenic EHV-1 strains induce the accumulation of hyperphosphorylated Tau in primary murine neurons

The Pathogenesis of Cytomegalovirus and Other Viruses Associated with Hearing Loss: Recent Updates

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