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

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.

Result

SUBMITTER: Yuan C 

PROVIDER: S-EPMC11910682 | biostudies-literature | 2025

REPOSITORIES: biostudies-literature