Albano, C.

Bajetto, G.

Biolatti, M.

De Andrea, M.

Dell’Oste, Valentina

Griffante, G.

Gugliesi, F.

Landolfo, S.

Mina, E.

Pasquero, S.

Porporato, P.

Trifirò, L.

English

Institutional Research Information System University of Turin

© tomeyk/rh2010 - stock.adobe.com8th  EUROPEAN CONGRESS OFVIROLOGY 2023ABSTRACTSwww.eusv-congress.euISBN 978-3-948023-30-0Gdansk Poland4 –7 May 2023545  PP 337 Exploiting lipid metabolism by HSV-1 – a challenge to rethink new therapies for Alzheimer's disease L. Trifirò1, C. Albano1, S. Pasquero1, F. Gugliesi1, G. Griffante2, G. Bajetto3, W. Hewelt-Belka4, E. Mina5, P. Porporato5, D. Cairns6, D. Kaplan6, A. Mullis6, S. Landolfo1, M. De Andrea1,3, V. Dell’Oste1, M. Biolatti1 1University of Turin, Department of Public Health and Pediatric Sciences, Turin, Italy 2University of Piemonte Orientale, Department of Translational Medicine, Novara, Italy 3University of Piemonte Orientale, Center for Translational Research on Autoimmune and Allergic Disease - CAAD, Novara, Italy 4Gdańsk University of Technology, Department of Analytical Chemistry, Gdańsk, Poland 5University of Turin, Department of Molecular Biotechnology and Health Sciences, Turin, Italy 6Tufts University, Department of Biomedical Engineering, Medford, MA, United States Herpes simplex virus-1 (HSV-1) establishes a life-long latent infection and can enter the brain via retrograde axonal transport. Recurrent reactivation of HSV-1 may lead to neurodegenerative disorders, including Alzheimer"s disease (AD), although the underlying mechanisms have not been fully elucidated yet. Lipids constitute the bulk of the brain dry mass and alteration of lipid metabolism is a key component in AD. Considering that the mechanisms for remodeling of metabolism by HSV-1 are still poorly understood, we aim at dissecting the host metabolic pathways modulated by infection in a neuronal-like cell line to identify pathways that might be targeted to prevent AD. Specifically, we found an increase in both de novo synthesis and lipid storage following HSV-1 infection. In addition, anti-AD compounds targeting lipid metabolism (e.g. CMS121, C75) impaired HSV-1 infectivity. Overall, our data unveil new aspects of HSV-1-AD interplay and uncover new potential targets to rethink new possible therapies.   

Exploiting lipid metabolism by HSV-1 – a challenge to rethink new therapies for Alzheimer's disease

https://iris.unito.it/bitstream/2318/1910650/1/ECV_abstract_book_trifiro_.pdf

Exploiting lipid metabolism by HSV-1 – a challenge to rethink new therapies for Alzheimer's disease

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