In this paper, iVibrio cholerae/i, the causative agent of cholera, is examined with focus on its genetic evolution, phage interactions, and modern gene-editing strategies for control. Cholera remains a pressing global health issue, especially in regions with inadequate sanitation. The bacterium’s virulence depends on acquiring the CTXφ bacteriophage, which integrates cholera toxin genes into its chromosome. Advances in CRISPR-Cas and recombineering now enable precise genetic manipulation to block CTXφ infection by targeting phage receptors like the toxin-coregulated pilus (TCP) or essential phage genes. The emergence of the O139 “Bengal” strain in the 1990s marked a major epidemiological event, illustrating how horizontal gene transfer and microevolution fuel epidemic potential. Genome plasticity, facilitated by SXT elements and chromosomal fusion, drives antimicrobial resistance and adaptability. Between 2015 and 2018, chromosome-fused V. cholerae strains in Dhaka highlighted ongoing recombination as an evolutionary force. Environmental isolates also serve as reservoirs for virulence genes such as ctxAB, tcpA, toxR, and toxT, showing that aquatic habitats sustain genetic exchange and the emergence of new variants. The stringent-response gene relA further links nutritional stress to virulence regulation and phage immunity. Horizontal gene transfer through the conjugative SXT element enables dissemination of resistance and virulence determinants across bacterial species. Emerging CRISPR-Cas and BREX/DISARM systems enhance phage resistance and genome stability. Together, these insights underscore how gene editing, synthetic biology, and genomic surveillance could revolutionize cholera prevention by designing phage-resistant, low-virulence, and ecologically stable V. cholerae strains for sustainable disease control.
Elihaika Lyimo (Fri,) studied this question.