Journal
SCIENCE TRANSLATIONAL MEDICINE
Volume 2, Issue 63, Pages -Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/scitranslmed.3001697
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Funding
- Ministry of Science and Innovation [CONSOLIDER CSD2009-00088]
- State of Lower Saxony
- Deutsche Forschungsgemeinschaft
- Bundesministerium fur Bildung und Forschung
- European Aids Treatment Network (NEAT)
- Innovationsfond des Landes Niedersachsen
- Helmholtz-Zentrum fur Infektionsforschung [IG-SCID-TwinPro02]
- Boehringer-Ingelheim
- GlaxoSmithKline
- Roche
- Tibotec
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To infect host cells, most enveloped viruses must insert a hydrophobic fusion peptide into the host cell membrane. Thus, fusion peptides may be valuable targets for developing drugs that block virus entry. We have shown previously that a natural 20-residue fragment of alpha(1)-antitrypsin, designated VIRus-Inhibitory Peptide (VIRIP), that binds to the gp41 fusion peptide of HIV-1 prevents the virus from entering target cells in vitro. Here, we examine the efficacy of 10-day monotherapy with the optimized VIR-576 derivative of VIRIP in treatment-naive, HIV-1-infected individuals with viral RNA loads of >= 10,000 copies per ml. We report that at the highest dose (5.0 grams per day), intravenous infusion of VIR-576 reduced the mean plasma viral load by 1.23 log(10) copies per ml without causing severe adverse effects. Our results are proof of concept that fusion peptide inhibitors suppress viral replication in human patients, and offer prospects for the development of a new class of drugs that prevent virus particles from anchoring to and infecting host cells.
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