Interaction Mechanism Between the HSV-1 Glycoprotein B and the Antimicrobial Peptide Amyloid-β.

Autor:	Bourgade K; Research Center on Aging, Geriatric Division, Department of Medicine, Faculty of Medicine and Health Sciences, Université de Sherbrooke, Sherbrooke, QC, Canada., Frost EH; Department of Microbiology and Infectious diseases, Faculty of Medicine and Health Sciences, Université de Sherbrooke, Sherbrooke, QC, Canada., Dupuis G; Department of Biochemistry, Graduate Program in Immunology, Faculty of Medicine and Health Sciences, University of Sherbrooke, Sherbrooke, QC, Canada., Witkowski JM; Department of Pathophysiology, Medical University of Gdansk, Gdansk, Poland., Laurent B; Research Center on Aging, Department of Biochemistry and Functional Genomics, Faculty of Medicine and Health Sciences, Université de Sherbrooke, Sherbrooke, QC, Canada., Calmettes C; INRS-Centre Armand-Frappier Santé-biotechnologie, Laval, QC, Canada., Ramassamy C; INRS-Centre Armand-Frappier Santé-biotechnologie, Laval, QC, Canada., Desroches M; MathNeuro Team, Inria Sophia Antipolis Méditerranée, France.; Université Côte d'Azur, Nice, France., Rodrigues S; Ikerbasque, The Basque Foundation for Science, Bilbao, Spain.; BCAM - The Basque Center for Applied Mathematics, Bilbao, Spain., Fülöp T Jr; Research Center on Aging, Geriatric Division, Department of Medicine, Faculty of Medicine and Health Sciences, Université de Sherbrooke, Sherbrooke, QC, Canada.
Jazyk:	angličtina
Zdroj:	Journal of Alzheimer's disease reports [J Alzheimers Dis Rep] 2022 Sep 24; Vol. 6 (1), pp. 599-606. Date of Electronic Publication: 2022 Sep 24 (Print Publication: 2022).
DOI:	10.3233/ADR-220061
Abstrakt:	Background: Unravelling the mystery of Alzheimer's disease (AD) requires urgent resolution given the worldwide increase of the aging population. There is a growing concern that the current leading AD hypothesis, the amyloid cascade hypothesis, does not stand up to validation with respect to emerging new data. Indeed, several paradoxes are being discussed in the literature, for instance, both the deposition of the amyloid-β peptide (Aβ) and the intracellular neurofibrillary tangles could occur within the brain without any cognitive pathology. Thus, these paradoxes suggest that something more fundamental is at play in the onset of the disease and other key and related pathomechanisms must be investigated. Objective: The present study follows our previous investigations on the infectious hypothesis, which posits that some pathogens are linked to late onset AD. Our studies also build upon the finding that Aβ is a powerful antimicrobial agent, produced by neurons in response to viral infection, capable of inhibiting pathogens as observed in in vitro experiments. Herein, we ask what are the molecular mechanisms in play when Aβ neutralizes infectious pathogens? Methods: To answer this question, we probed at nanoscale lengths with FRET (Förster Resonance Energy Transfer), the interaction between Aβ peptides and glycoprotein B (responsible of virus-cell binding) within the HSV-1 virion. Results: The experiments show an energy transfer between Aβ peptides and glycoprotein B when membrane is intact. No energy transfer occurs after membrane disruption or treatment with blocking antibody. Conclusion: We concluded that Aβ insert into viral membrane, close to glycoprotein B, and participate in virus neutralization. Competing Interests: The authors declare no conflicts of interest. (© 2022 – The authors. Published by IOS Press.)
Databáze:	MEDLINE
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