Background: Amyloid fibrils such as Semen-Derived Enhancer of Viral Infection (SEVI) or amyloid-beta-peptide (Abeta) 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 Abeta 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 Abeta fibril formation and converts preformed Abeta 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. © 2014 Widera et al.; licensee BioMed Central Ltd.
CITATION STYLE
M., W., A.N., K., Y., C., S.A., F., D., W., & H., S. (2014). The D-amino acid peptide D3 reduces amyloid fibril boosted HIV-1 infectivity. AIDS Research and Therapy. S.A. Funke, Forschungszentrum Julich, ICS-6, Julich, 52425, Germany. E-mail: aileen.funke@hs-coburg.de: BioMed Central Ltd. (Floor 6, 236 Gray’s Inn Road, London WC1X 8HB, United Kingdom). Retrieved from http://www.aidsrestherapy.com/content/11/1/1
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