Herpes simplex virus type 1 in brain and risk of Alzheimer's disease

Itzhaki, Ruth F.; Lin, Woan-Ru; Shang, Dazhuang; Wilcock, Gordon; Faragher, Brian; Jamieson, Gordon A.

doi:10.1016/s0140-6736(96)10149-5

Cited by 553 publications

(495 citation statements)

References 24 publications

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“…Infection has been implicated as a potential trigger in the initiation of sporadic AD as infectious agents such as Chlamydophila (Chlamydia) pneumoniae, herpes simplex virus-1 (HSV-1), and spirochetes have been associated with AD [3,18,29]. In the initial report linking C. pneumoniae infection with AD, 90% of AD brains were PCR positive for C. pneumoniae, and the organism was detected in regions of the brain that exhibited AD pathology [3].…”

Section: Introductionmentioning

confidence: 99%

Chlamydia pneumoniae induces Alzheimer-like amyloid plaques in brains of BALB/c mice

Little

Hammond

MacIntyre

et al. 2004

Neurobiology of Aging

198

197

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Amyloid deposits resembling plaques found in Alzheimer's disease (AD) brains were formed in the brains of non-transgenic BALB/c mice following intranasal infection with Chlamydia pneumoniae. The mice were infected at 3 months of age with C. pneumoniae isolated from an AD brain. Infection was confirmed by light and electron microscopy in olfactory tissues of the mice. C. pneumoniae was still evident in these tissues 3 months after the initial infection indicating that a persistent infection had been established. Amyloid beta (A␤) 1-42 immunoreactive deposits were identified in the brains of infected BALB/c mice up to 3 months post-infection with the density, size, and number of deposits increasing as the infection progressed. A subset of deposits exhibited thioflavin-s labeling. Intracellular A␤1-42 labeling was observed in neuronal cells. Experimental induction of amyloid deposition in brains of non-transgenic BALB/c mice following infection with C. pneumoniae may be a useful model for furthering our understanding of mechanisms, linked to infection, involved in the initiation of the pathogenesis of sporadic AD.

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Section: Introductionmentioning

confidence: 99%

Chlamydia pneumoniae induces Alzheimer-like amyloid plaques in brains of BALB/c mice

Little

Hammond

MacIntyre

et al. 2004

Neurobiology of Aging

198

197

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“…7 Furthermore, animal models and acute HSV-1 encephaltitis patients show that the virus targets brain regions overlapping with AD: frontal and temporal cortices and the hippocampus. [99][100][101][102] Although HSV-1 preferentially lies dormant in neurons, the detection of HSV-1 DNA in the cerebrospinal fluid suggests that asymptomatic replication of HSV-1 may occur in the CNS under certain cirucumstances. 103,104 Given the intense interplay between HSV-1 and host cells, it is likely that recurrent HSV-1 reactivation may cumulatively arouse neuronal dysfunction, as demonstrated recently by Martin et al, 105 which shows that HSV-1 reactivation from latency induces neuroinflammation and the appearance of early neurodegenerative markers including MAPT/Tau phosphorylation.…”

Section: Hsv-1-associated Autophagy Dysfunction: a Risk Factor For Nementioning

confidence: 99%

Autophagy interaction with herpes simplex virus type-1 infection

O’Connell

Liang

2016

Autophagy

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More than 50% of the U.S. population is infected with herpes simplex virus type-I (HSV-1) and global infectious estimates are nearly 90%. HSV-1 is normally seen as a harmless virus but debilitating diseases can arise, including encephalitis and ocular diseases. HSV-1 is unique in that it can undermine host defenses and establish lifelong infection in neurons. Viral reactivation from latency may allow HSV-1 to lay siege to the brain (Herpes encephalitis). Recent advances maintain that HSV-1 proteins act to suppress and/or control the lysosome-dependent degradation pathway of macroautophagy (hereafter autophagy) and consequently, in neurons, may be coupled with the advancement of HSV-1-associated pathogenesis. Furthermore, increasing evidence suggests that HSV-1 infection may constitute a gradual risk factor for neurodegenerative disorders. The relationship between HSV-1 infection and autophagy manipulation combined with neuropathogenesis may be intimately intertwined demanding further investigation.

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“…La hipótesis que relaciona a HSV-1 con la patogénesis de la EA ha adquirido relevancia debido a que se han detectado secuencias de ADN viral 34,35,36 o antígenos virales y cuerpos de inclusión intranucleares en astrocitos 37 obtenidos de cerebros de personas que padecieron EA. Adicionalmente, se ha demostrado que la presencia de HSV-1 en el cerebro de portadores del alelo 4 de la apoliproteína E (apoE) constituye un fuerte factor de riesgo para desarrollar la EA [38][39][40] .…”

Section: Hsv-1 Como Factor De Riesgo Asociado Con La Enfermedad De Alunclassified

“…Además, el alelo 4 (a diferencia de los otros alelos) se asocia con una disminuida reparación del SNC después de lesiones 41,42 y además se ha demostrado que apoE 4 favorece la invasión del herpesvirus desde la sangre al cerebro 43 . Asimismo, se ha encontrado que la frecuencia de reactivación viral es mayor en personas homocigotas para el alelo 4 del gen de la apoE 34,36 , sugiriendo que factores virales y genéticos pueden estar involucrados en EA. En investigaciones recientes, se ha encontrado la presencia de anticuerpos anti-HSV en líquido cefalorraquídeo de personas con EA y en personas mayores sin antecedentes de EA, no así en líquido cefalorraquídeo en niños menores de 7 años 20 .…”

Section: Hsv-1 Como Factor De Riesgo Asociado Con La Enfermedad De Alunclassified

Herpes simplex virus tipo 1 como factor de riesgo asociado con la enfermedad de Alzheimer

et al. 2011

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Herpes simplex virus tipo 1 L a familia Herpesviridae, se encuentra ampliamente diseminada en la naturaleza. Existen más de 100 tipos diferentes de herpesvirus, los que presentan la misma estructura, ADN lineal de doble hebra dentro de una cápside icosaédrica, rodeada por un tegumento proteico y cubierto por una envoltura lipídica (Figura 1) 1,2 . Una característica que distingue a los herpesvirus, es su capacidad para establecer infecciones persistentes latentes en el hospedero infectado, estado en el cual el genoma viral se encuentra en forma episomal en el núcleo de la célula infectada, con una expresión limitada de genes específi cos para el mantenimiento del estado de latencia (transcritos LAT) y sin producir partículas virales infectivas 3,4 . Este tipo de infección se piensa que constituye una estrategia viral para evadir su detección por parte del sistema inmune. Bajo ciertas condiciones -incluyendo la exposición a radiación UV, estrés emocional, alteración del balance hormonal, depresión del sistema inmunológico, entre otros-se puede interrumpir el estado de latencia, induciendo una reactivación del genoma viral, con la consecuente producción de nuevas partículas virales infectivas que inician la recurrencia del cuadro clínico 1,4 . Sin embargo, los mecanismos celulares y moleculares de este proceso, aún se desconocen en detalle.En base al tipo de célula en que establecen latencia y otras características, los herpesvirus humanos han sido clasificados en distintas

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Herpes simplex virus type 1 in brain and risk of Alzheimer's disease

Cited by 553 publications

References 24 publications

Chlamydia pneumoniae induces Alzheimer-like amyloid plaques in brains of BALB/c mice

Chlamydia pneumoniae induces Alzheimer-like amyloid plaques in brains of BALB/c mice

Autophagy interaction with herpes simplex virus type-1 infection

Herpes simplex virus tipo 1 como factor de riesgo asociado con la enfermedad de Alzheimer

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