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

AIDS Research and Therapy

Marek Widera⁴  Antonia Nicole Klein³  Yeliz Cinar³  Susanne Aileen Funke²  Dieter Willbold¹  Heiner Schaal¹ 

[1] Biologisch und Medizinisches Forschungszentrum (BMFZ), Heinrich-Heine-Universität Düsseldorf, Düsseldorf, Germany

[2] Bioanalytik, Fakultät für Angewandte Naturwissenschaften, Hochschule für Angewandte Wissenschaften Coburg, 96450 Coburg, Germany

[3] Forschungszentrum Jülich, ICS-6, Jülich, 52425, Germany

[4] Institut für Virologie, Heinrich-Heine-Universität, D-40225 Düsseldorf, Germany

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

Others  :  789552
DOI  :  10.1186/1742-6405-11-1

 received in 2013-07-24, accepted in 2014-01-09,  发布年份 2014

【 摘 要 】

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.

【 授权许可】

   
2014 Widera et al.; licensee BioMed Central Ltd.

【 图 表 】

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