Mycobacterium Survival Strategy Translated to Develop a Lipo-Peptide Based Fusion Inhibitor

07 May 2020, Version 1
This content is a preprint and has not undergone peer review at the time of posting.

Abstract

The entry of enveloped viruses requires fusion of viral and host cell membranes. An effective fusion inhibitor aiming at impeding such virus-host cell membrane fusion may emerge as a broad-spectrum antiviral agent to neutralize the infection from an increasing diversity of harmful new viruses. Mycobacterium survives inside the phagosome of the host cells by inhibiting phagosome-lysosome fusion with the help of a coat protein coronin 1. Structural analysis of coronin 1 and other WD40-repeat containing protein suggest that the tryptophan-aspartic acid (WD) sequence is placed at distorted β-meander motif (more exposed) whereas the WD resides in regular β-meander motif in other WD40 proteins. The unique structural feature of coronin 1 was explored to identify a simple lipo-peptide sequence (lipid-WD), which effectively inhibit the membrane fusion by increasing interfacial order and decreasing water penetration, surface potential. The effective fusion inhibitory role of mycobacterium inspired lipo-dipeptide was applied to combat type 1 influenza virus (H1N1) infection as a ‘broad spectrum’ antiviral agent.

Keywords

Membrane fusion
Enveloped Virus
lipo-peptide inhibitor
Water Penetration
broad-spectrum antivirals

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