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Open Access Short report

The D-amino acid peptide D3 reduces amyloid fibril boosted HIV-1 infectivity

Marek Widera1, Antonia Nicole Klein2, Yeliz Cinar2, Susanne Aileen Funke24*, Dieter Willbold235* and Heiner Schaal15*

Author Affiliations

1 Institut für Virologie, Heinrich-Heine-Universität, D-40225 Düsseldorf, Germany

2 Forschungszentrum Jülich, ICS-6, Jülich, 52425, Germany

3 Institut für Physikalische Biologie, Heinrich-Heine-Universität, Düsseldorf, 40225, Germany

4 Bioanalytik, Fakultät für Angewandte Naturwissenschaften, Hochschule für Angewandte Wissenschaften Coburg, 96450 Coburg, Germany

5 Biologisch und Medizinisches Forschungszentrum (BMFZ), Heinrich-Heine-Universität Düsseldorf, Düsseldorf, Germany

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AIDS Research and Therapy 2014, 11:1  doi:10.1186/1742-6405-11-1

Published: 14 January 2014

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.

Keywords:
HIV-1 infection; SEVI; D3; Amyloid-beta; Alzheimer’s disease; D-enantiomeric peptide; Drugs; Monomers; Oligomers