Abstract | BACKGROUND:
Amyloid fibrils such as Semen-Derived Enhancer of Viral Infection (SEVI) or amyloid-β- peptide (Aβ) enhance HIV-1 attachment and entry. Inhibitors destroying or converting those fibrils into non-amyloidogenic aggregates effectively reduce viral infectivity. Thus, they seem to be suitable as therapeutic drugs expanding the current HIV-intervening repertoire of antiretroviral compounds. FINDINGS: In this study, we demonstrate that the small D- amino acid peptide D3, which was investigated for therapeutic studies on Alzheimer's disease (AD), significantly reduces both SEVI and Aβ fibril boosted infectivity of HIV-1. CONCLUSIONS: Since amyloids could play an important role in the progression of AIDS dementia complex (ADC), the treatment of HIV-1 infected individuals with D3, that inhibits Aβ fibril formation and converts preformed Aβ fibrils into non-amyloidogenic and non-fibrillar aggregates, may reduce the vulnerability of the central nervous system of HIV patients for HIV associated neurological disorders.
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Authors | Marek Widera, Antonia Nicole Klein, Yeliz Cinar, Susanne Aileen Funke, Dieter Willbold, Heiner Schaal |
Journal | AIDS research and therapy
(AIDS Res Ther)
Vol. 11
Issue 1
Pg. 1
(Jan 14 2014)
ISSN: 1742-6405 [Print] England |
PMID | 24422713
(Publication Type: Journal Article)
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