Herpes Simplex Virus Type 1 Neuronal Infection Elicits Cellular and Molecular Mechanisms of Neuroinflammation and Neurodegeneration in in vitro and in vivo Mice Models

Otth, Carola; Leyton, Luis; Salamin, Marukel; Acuña‐Hinrichsen, Francisca; Martin, Carolina; Concha, Miguel

doi:10.3233/jad-160508

Cited by 2 publications

(1 citation statement)

References 93 publications

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“…Otth et al . (106) proposed that HSV1 could activate the AMPK/Sirt1 axis as a strategy for establishing latency through inhibition of apoptosis and restoration of energy status. They demonstrated that HSV1 modulated the AMPK/Sirt1 axis differentially during infection, interfering with proapoptotic signaling and regulating mitochondrial biogenesis, both of which are essential processes in the lifetime of CNS neurons.…”

Section: Dna Damage and Repair In Ad And Hsv1mentioning

confidence: 99%

Herpes simplex virus type 1 and Alzheimer's disease: possible mechanisms and signposts

Itzhaki

2017

FASEB j.

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Support for the concept that herpes simplex virus type 1 (HSV1), when present in the brains of apolipoprotein E-ε4 carriers, is a major risk for Alzheimer's disease (AD) is increasing steadily, with over 120 publications providing direct or indirect evidence relevant to the hypothesis. No articles have contested the concept, apart from 3 published 13-18 yr ago. This review describes very recent studies on the role of HSV1 but refers also to older studies that provide background for some lesser-known related topics not covered in other recent reviews; these include the relevance of herpes simplex encephalitis and of epilepsy to AD, the action of IFN, and the possible relevance of the different types of DNA damage to AD-in particular, those caused by HSV1-and mechanisms of repair of damage. New epidemiologic data supporting previous studies on mild cognitive impairment and progression to AD are reviewed, as are those examining the relationship between total infectious burden (additive seropositivity to various microbes) and cognition/AD. The latter indicates the involvement of HSV1 and cytomegalovirus (and the necessity of taking into account any marked differences in sensitivity of antibody detection). Recent studies that provide further support for the occurrence of repeated reactivation of latent HSV1 in the brain in AD pathogenesis are also discussed.-Itzhaki, R. F. Herpes simplex virus type 1 and Alzheimer's disease: possible mechanisms and signposts.

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Section: Dna Damage and Repair In Ad And Hsv1mentioning

confidence: 99%

Herpes simplex virus type 1 and Alzheimer's disease: possible mechanisms and signposts

Itzhaki

2017

FASEB j.

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Herpes Simplex Virus type 1 neuronal infection triggers disassembly of key structural components of dendritic spines

Acuña‐Hinrichsen

Covarrubias‐Pinto

Ishizuka

et al. 2020

Preprint

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Herpes simplex virus type 1 (HSV-1) is a widespread neurotropic virus. The primary infection in facial epithelium leads to retrograde axonal transport to the central nervous system (CNS) where it establishes latency. Under stressful conditions, the virus reactivates, and new progeny is transported anterogradely to the primary site of infection. In late stages of neuronal infection, axonal damage is known to occur. However, the impact of HSV-1 infection on morphology and functional integrity at earlier stages of infection in neuronal dendrites is unknown. Previously, we demonstrated that acute HSV-1 infection in neuronal cell lines selectively enhances the expression of Arc protein -a major regulator of long-term synaptic plasticity and memory consolidation, known for being a protein-interaction hub in the postsynaptic dendritic compartment. Thus, HSV-1 induced Arc may alter the functionality of the infected neurons having an impact on dendritic spine dynamics. In this study we demonstrated that HSV-1 infection causes structural disassembly and functional deregulation in cultured cortical neurons, through protein homeostasis alteration with intracellular accumulation of Arc, and decreased expression of spine scaffolding-like proteins such as PSD-95, Drebrin and CaMKIIβ. Our findings reveal progressive deleterious effects of HSV-1 infection on excitatory neuronal synapse function and dendritic morphology, supporting the thesis of the infectious origin of neurodegenerative processes.

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Herpes Simplex Virus Type 1 Neuronal Infection Elicits Cellular and Molecular Mechanisms of Neuroinflammation and Neurodegeneration in in vitro and in vivo Mice Models

Cited by 2 publications

References 93 publications

Herpes simplex virus type 1 and Alzheimer's disease: possible mechanisms and signposts

Herpes simplex virus type 1 and Alzheimer's disease: possible mechanisms and signposts

Herpes Simplex Virus type 1 neuronal infection triggers disassembly of key structural components of dendritic spines

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