Herpes Simplex Virus Type 1 Enhances Expression of the Synaptic Protein Arc for Its Own Benefit

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dc.contributor.authorAcuna-Hinrichsen, Francisca
dc.contributor.authorMunoz, Mariela
dc.contributor.authorHott, Melissa
dc.contributor.authorMartin, Carolina
dc.contributor.authorMancilla, Evelyn
dc.contributor.authorSalazar, Paula
dc.contributor.authorLeyton, Luis
dc.contributor.authorZambrano, Angara
dc.contributor.authorConcha, Margarita, I
dc.contributor.authorBurgos, Patricia, V
dc.contributor.authorOtth, Carole
dc.date.accessioned2025-01-23T21:19:34Z
dc.date.available2025-01-23T21:19:34Z
dc.date.issued2019
dc.description.abstractHerpes simplex virus type 1 (HSV-1) is a neurotropic virus able to reach the central nervous system (CNS) after primary infection in oronasal mucosa. HSV-1 establishes latency inside neurons due the repression of its gene expression process, which is related to periodic reactivations in response to cellular stress conditions, constituting a risk factor for neurodegenerative diseases such as Alzheimer's disease (AD). The immediate-early gene Arc plays an essential role in neuronal morphology, synaptic plasticity and memory formation. Arc acts as a hub protein, interacting with components of the endocytic machinery required for AMPA receptor (AMPAR) recycling as well as with proteins of the post-synaptic density and actin cytoskeleton. However, to date, no studies have evaluated whether persistent neurotropic HSV-1 infection modulates the expression or function of Arc protein in brain tissue. Here, we report that neuronal in vivo and in vitro infection of HSV-1 significantly increases Arc protein levels, showing a robust perinuclear distribution in neuronal cell lines, a process that is dependent on an active HSV-1 replication cycle. Finally, we found that silencing Arc protein caused a decrease in HSV-1 proteins and viral progeny, suggesting that Arc is involved in the lifecycle of HSV-1. Our studies strongly suggest that pathogenicity of HSV-1 neuronal reactivations in humans could be mediated in part by Arc neuronal upregulation and its potential role in endocytic trafficking and AMPA-neuronal function impairment. Further studies are necessary to define whether this phenomenon could have repercussions in cognition and learning processes in infected individuals.
dc.fuente.origenWOS
dc.identifier.doi10.3389/fncel.2018.00505
dc.identifier.issn1662-5102
dc.identifier.urihttps://doi.org/10.3389/fncel.2018.00505
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/101185
dc.identifier.wosidWOS:000455157500001
dc.language.isoen
dc.revistaFrontiers in cellular neuroscience
dc.rightsacceso restringido
dc.subjectHSV-1
dc.subjectneuronal dysfunction
dc.subjectArc
dc.subjectneurodegeneration
dc.subjectneuronal infection
dc.subjectAlzheimer's disease
dc.subjectneurotropic virus
dc.subject.ods03 Good Health and Well-being
dc.subject.odspa03 Salud y bienestar
dc.titleHerpes Simplex Virus Type 1 Enhances Expression of the Synaptic Protein Arc for Its Own Benefit
dc.typeartículo
dc.volumen12
sipa.indexWOS
sipa.trazabilidadWOS;2025-01-12
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