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Int J Biol Macromol. 2015 Mar;74:530-40. doi: 10.1016/j.ijbiomac.2015.01.003. Epub 2015 Jan 10.

Anti-HSV1 activity of brown algal polysaccharides and possible relevance to the treatment of Alzheimer's disease.

Author information

1
Faculty of Life Sciences, The University of Manchester, 3.545 Stopford Building, Oxford Road, Manchester M13 9PT, UK. Electronic address: matthew.wozniak@tinyonline.co.uk.
2
The Ferrier Research Institute, Victoria University of Wellington, PO Box 31-310, Lower Hutt, New Zealand. Electronic address: Tracey.Bell@vuw.ac.nz.
3
Laboratory of Molecular Neuroendocrinology, Institute of Experimental Medicine, Hungarian Academy of Sciences, Szigony u 43, Budapest H 1083, Hungary. Electronic address: denes.adam@koki.mta.hu.
4
The Ferrier Research Institute, Victoria University of Wellington, PO Box 31-310, Lower Hutt, New Zealand. Electronic address: r.falshaw@xtra.co.nz.
5
Faculty of Life Sciences, The University of Manchester, 3.545 Stopford Building, Oxford Road, Manchester M13 9PT, UK. Electronic address: ruth.itzhaki@manchester.ac.uk.

Abstract

Herpes simplex virus type 1 (HSV1) induces the formation of the characteristic abnormal molecules of Alzheimer's disease (AD) brains, beta-amyloid, and abnormally phosphorylated, AD-like tau (P-tau). Formation of these molecules is inhibited by treatment with the antiviral agent acyclovir (ACV), which prevents viral DNA replication. A totally different mechanism of antiviral action against herpes simplex viruses is shown by sulfated fucans. The antiviral activity of sulfated fucans from five brown algae (Scytothamnus australis, Marginariella boryana, Papenfussiella lutea, Splachnidium rugosum and Undaria pinnatifida) was investigated in relation to the HSV1-induced formation of beta-amyloid, and AD-like tau. Antiviral activity was also related to specific structural features of these polysaccharides. Four sulfated fucan extracts each prevented the accumulation of HSV1-induced beta-amyloid and AD-like tau in HSV1-infected Vero cells. The structures of these extracts had some similarities but also key differences, indicating that a number of structural features can cause antiviral activity. The most active sulfated fucan combined with acyclovir was particularly effective, so may be particularly suitable for further experimental testing in order to develop treatment protocols for AD patients, with the aim of slowing or stopping disease progression.

KEYWORDS:

Alzheimer's disease; Antiviral; Fucan

PMID:
25583021
DOI:
10.1016/j.ijbiomac.2015.01.003
[Indexed for MEDLINE]

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