English   español  
Please use this identifier to cite or link to this item: http://hdl.handle.net/10261/113226
logo share SHARE logo core CORE   Add this article to your Mendeley library MendeleyBASE

Visualizar otros formatos: MARC | Dublin Core | RDF | ORE | MODS | METS | DIDL
Exportar a otros formatos:


Herpes simplex virus type 1 induces nuclear accumulation of hyperphosphorylated tau in neuronal cells

AuthorsÁlvarez, Gema; Aldudo Jesús; Alonso, María ; Santana, Soraya; Valdivieso Amate, Fernando
Issue Date2012
PublisherJohn Wiley & Sons
CitationJournal of Neuroscience Research 90: 1020- 1029 (2012)
AbstractHerpes simplex virus type 1 (HSV-1) is a neurotropic virus that remains latent in host neurons. Viral DNA replication is a highly structured process in which the redistribution of nuclear proteins plays an important role. Although tau is most widely known as a microtubule-associated protein found in a hyperphosphorylated state in the brains of patients with Alzheimer's disease (AD), this protein has also been detected at other sites such as the nucleolus. Here, we establish that HSV-1 infection gives rise to an increase in tau phosphorylation and that hyperphosphorylated tau accumulates in the nucleus, forming defined structures in HSV-1-infected neuronal cells reminiscent of the common sites of viral DNA replication. When tau expression in human neuroblastoma cells was specifically inhibited using an adenoviral vector expressing a short hairpin RNA to tau, viral DNA replication was not affected, indicating that tau is not required for HSV-1 growth in neuronal cells. Given that HSV-1 is considered a risk factor for AD, our results suggest a new way in which to understand the relationships between HSV-1 infection and the pathogenic mechanisms leading to AD. © 2012 Wiley Periodicals, Inc.
Identifiersdoi: 10.1002/jnr.23003
issn: 0360-4012
Appears in Collections:(CBM) Artículos
Files in This Item:
File Description SizeFormat 
accesoRestringido.pdf15,38 kBAdobe PDFThumbnail
Show full item record
Review this work

Related articles:

WARNING: Items in Digital.CSIC are protected by copyright, with all rights reserved, unless otherwise indicated.