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Roles of variable linker length in dual acting virucidal entry inhibitors on HIV-1 potency via on-the-fly free energy molecular simulations
Journal article   Open access   Peer reviewed

Roles of variable linker length in dual acting virucidal entry inhibitors on HIV-1 potency via on-the-fly free energy molecular simulations

Steven T Gossert, Bibek Parajuli, Irwin Chaiken and Cameron F Abrams
Protein science, v 29(11), pp 2304-2310
Nov 2020
PMID: 32926485
url
https://doi.org/10.1002/pro.3949View
Published, Version of Record (VoR)Maybe Open Access (Publisher Bronze) Open

Abstract

HIV Envelope Protein gp41 - genetics HIV-1 - chemistry Recombinant Fusion Proteins - genetics Lectins - genetics Structure-Activity Relationship Lectins - chemistry Recombinant Fusion Proteins - chemistry HIV Envelope Protein gp41 - chemistry HIV-1 - genetics Molecular Dynamics Simulation
The Dual-Acting Virolytic Entry Inhibitors, or DAVEI's, are a class of recombinant chimera fusion proteins consisting of a lectin, a flexible polypeptide linker, and a fragment of the membrane-proximal external region (MPER) of HIV-1 gp41. DAVEIs trigger virolysis of HIV-1 virions through interactions with the trimeric envelope glycoprotein complex (Env), though the details of these interactions are not fully determined as yet. The purpose of this work was to use structural modeling to rationalize a dependence of DAVEI potency on the molecular length of the linker connecting the two components. We used temperature accelerated molecular dynamics and on-the-fly parameterization to compute free energy versus end-to-end distance for two different linker lengths, DAVEI L0 (His ) and DAVEI L2 ([Gly Ser] His ). Additionally, an envelope model was created based on a cryo-electron microscopy-derived structure of a cleaved, soluble Env construct, with high-mannose glycans added which served as putative docking locations for the lectin, along with MPER added that served as a putative docking location for the MPER region of DAVEI (MPER ). Using MD simulation, distances between the lectin C-terminus and Env gp41 MPER were measured. We determined that none of the glycans were close enough to gp41 MPER to allow DAVEI L0 to function, while one, N448, will allow DAVEI L2 to function. These findings are consistent with the previously determined dependence of lytic function on DAVEI linker lengths. This supports the hypothesis that DAVEI's engage Env at both glycans and the Env MPER in causing membrane poration and lysis.

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Web of Science research areas
Biochemistry & Molecular Biology
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