Journal Article

FZJ-2014-01123

http://join2-wiki.gsi.de/foswiki/pub/Main/Artwork/join2_logo100x88.png The D-amino acid peptide D3 reduces amyloid fibril boosted HIV-1 infectivity

Widera, M. ; Klein, A. N.FZJ* ; Cinar, Y. ; Funke, S. (Corresponding author) ; Willbold, D.FZJ* ; Schaal, H. (Corresponding Author)

2014
BioMed Central London

This record in other databases:      

Please use a persistent id in citations: http://hdl.handle.net/2128/5907  doi:10.1186/1742-6405-11-1

Abstract: 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

---

Contributing Institute(s):

1. Strukturbiochemie (ICS-6)

Research Program(s):

1. 452 - Structural Biology (POF2-452) (POF2-452)

Appears in the scientific report 2014

---

Database coverage:
; ; ; ; NCBI Molecular Biology Database ; SCOPUS

---