Heptad repeat 1-derived N peptide inhibitors improve broad-spectrum anti-HIV-1 activity

七肽重复序列1衍生的N肽抑制剂可增强广谱抗HIV-1活性

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Abstract

BACKGROUND: HIV-1 N-peptide inhibitor (NPI) derived from N-terminal heptad-repeat region (HR1) of gp41 can target C-terminal heptad-repeat region (HR2) or the HR1 to interfere with the formation of endogenous six-helix bundle (6HB). However, the NPI is less active than the C-peptide inhibitor. In this study, we reported three HR1-derived NPIs designed by adding fusion peptide proximal region (FPPR) of gp41 or a trimeric motif MTQ into the N36 peptide and then evaluated their anti-HIV-1 activities. METHODS: Molecular modeling was performed using Swiss Model. The inhibitory activity of NPIs on HIV-1 was assessed by Env-pseudovirus infection assays and cell-cell fusion assays. Interaction between NPIs and HR2 peptides was evaluated by circular dichroism and Native PAGE. RESULTS: The three newly designed NPIs, FPPR-N36, MTQ-N36, and MTQ-FPPR-N36, exhibited higher anti-HIV-1 activity than N36. The stability of the coiled-coil core formed by three designed NPIs or the 6HB formed by C34 and these NPIs were significantly higher than those of corresponding monomer N36 or isoleucine zipper-engineered trimeric N36 (IZN36). The 50 % inhibitory concentrations (IC(50)) of MTQ-N36 against HIV-1 infection were at a nanomolar level, lower than those of other tested NPIs. The FPPR-N36 could also inhibit infection of HIV-1 strains that were resistant to N36 and IZN36. CONCLUSIONS: The three newly designed NPIs had inhibitory activity against HIV-1 infection. Among them, MTQ-N36 exhibited a higher potential to inhibit HIV-1 entry than other peptides, and FPPR-N36 might be a promising candidate NPI for suppressing HIV-1 strains that are resistant to conventional NPIs.

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