This title appears in the Scientific Report :
2014
Please use the identifier:
http://dx.doi.org/10.1186/1742-6405-11-1 in citations.
Please use the identifier: http://hdl.handle.net/2128/5907 in citations.
The D-amino acid peptide D3 reduces amyloid fibril boosted HIV-1 infectivity
The D-amino acid peptide D3 reduces amyloid fibril boosted HIV-1 infectivity
BackgroundAmyloid 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...
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Personal Name(s): | Widera, Marek |
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Klein, Antonia Nicole / Cinar, Yeliz / Funke, Susanne (Corresponding author) / Willbold, Dieter / Schaal, Heiner (Corresponding Author) | |
Contributing Institute: |
Strukturbiochemie; ICS-6 |
Published in: | AIDS research and therapy, 11 (2014) 1, S. 1 - 7 |
Imprint: |
London
BioMed Central
2014
|
DOI: |
10.1186/1742-6405-11-1 |
PubMed ID: |
24422713 |
Document Type: |
Journal Article |
Research Program: |
Structural Biology |
Link: |
Get full text OpenAccess |
Publikationsportal JuSER |
Please use the identifier: http://hdl.handle.net/2128/5907 in citations.
BackgroundAmyloid 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.FindingsIn 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.ConclusionsSince 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 |