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. © 2014 Widera et al.; licensee BioMed Central Ltd.
Widera, M., Klein, A. N., Cinar, Y., Funke, S. A., Willbold, D., & Schaal, H. (2014). The D-amino acid peptide D3 reduces amyloid fibril boosted HIV-1 infectivity. AIDS Research and Therapy, 11(1). https://doi.org/10.1186/1742-6405-11-1