期刊
AIDS RESEARCH AND THERAPY
卷 11, 期 -, 页码 -出版社
BMC
DOI: 10.1186/1742-6405-11-1
关键词
HIV-1 infection; SEVI; D3; Amyloid-beta; Alzheimer's disease; D-enantiomeric peptide; Drugs; Monomers; Oligomers
资金
- DFG [SCHA 909/3 1]
- Stiftung fur AIDS-Forschung, Dusseldorf
- BMBF-Kompetenznetz Degenerative Demenzen [KNDD FKZ 01GI1010A]
- DFG Graduate School [1033]
- Jurgen Manchot Stiftung
Background: Amyloid fibrils such as Semen-Derived Enhancer of Viral Infection (SEVI) or amyloid-beta-peptide (A beta) 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 A beta 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 A beta fibril formation and converts preformed A beta 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.
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