Abstract

Morganella morganii is one of the main etiological agents of hospital-acquired infections and no licensed vaccine is available against the pathogen. Herein, we designed a multi-epitope-based vaccine against M. morganii. Predicted proteins from fully sequenced genomes of the pathogen were subjected to a core sequences analysis, followed by the prioritization of non-redundant, host non-homologous and extracellular, outer membrane and periplasmic membrane virulent proteins as vaccine targets. Five proteins (TonB-dependent siderophore receptor, serralysin family metalloprotease, type 1 fimbrial protein, flagellar hook protein (FlgE), and pilus periplasmic chaperone) were shortlisted for the epitope prediction. The predicted epitopes were checked for antigenicity, toxicity, solubility, and binding affinity with the DRB*0101 allele. The selected epitopes were linked with each other through GPGPG linkers and were joined with the cholera toxin B subunit (CTBS) to boost immune responses. The tertiary structure of the vaccine was modeled and blindly docked with MHC-I, MHC-II, and Toll-like receptors 4 (TLR4). Molecular dynamic simulations of 250 nanoseconds affirmed that the designed vaccine showed stable conformation with the receptors. Further, intermolecular binding free energies demonstrated the domination of both the van der Waals and electrostatic energies. Overall, the results of the current study might help experimentalists to develop a novel vaccine against M. morganii.

Highlights

  • IntroductionAntibiotic resistance (AR) is a global health crisis

  • Antibiotic resistance (AR) is a subset of antimicrobial resistance (AMR) and happens when bacteria evolve mechanisms to withstand attacks by antibiotics

  • AR can evolve by natural courses forced by the continued misuse of antibiotics [1]

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Summary

Introduction

Antibiotic resistance (AR) is a global health crisis. AR is a subset of antimicrobial resistance (AMR) and happens when bacteria evolve mechanisms to withstand attacks by antibiotics. AR can evolve by natural courses forced by the continued misuse of antibiotics [1]. The resistance is mounting to seriously high levels across all countries of the world. Novel resistance mechanisms are evolving and spreading worldwide, making our efforts to treat common infectious diseases less effective [2]. Infections caused by bacterial pathogens are becoming tough to treat, even sometimes impossible to

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