Research Article
A Review on Engineering Phage Resistance in Vibrio cholerae: A Gene Editing Perspective
Elihaika Charles Lyimo*
Issue:
Volume 12, Issue 1, March 2026
Pages:
1-9
Received:
17 December 2025
Accepted:
29 December 2025
Published:
23 January 2026
Abstract: In this paper, Vibrio cholerae, 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.
Abstract: In this paper, Vibrio cholerae, 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, ...
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Research Article
Opioid-Induced Dysregulation of BDNF Signalling: A Study of Acute, Sub-Chronic, and Chronic Exposure in a Rodent Model
Issue:
Volume 12, Issue 1, March 2026
Pages:
10-16
Received:
18 January 2026
Accepted:
2 February 2026
Published:
21 February 2026
DOI:
10.11648/j.bs.20261201.12
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Abstract: Brain-derived neurotrophic factor (BDNF) is a critical regulator of neuronal survival, synaptic plasticity, and cognitive function, making it a key biomarker in understanding the neurobiological impact of opioid exposure. This study investigated the effects of opioids (codeine and tramadol) on brain-derived neurotrophic factor (BDNF) levels in male Wistar rats. A total of 75 male Wistar rats (120-140g) were used for the study in acute, sub-chronic and chronic phases, using 25 rats for each phase. In each phase, 25 male Wistar rats were divided into 5 groups of 5 animals each. Group 1 served as the control and received distilled water, groups 2 and 3 were treated with tramadol at 20 and 60 mg/kg, respectively, while groups 4 and 5 were supplemented with codeine at 10 and 30 mg/kg, respectively. Treatment by oral gavage lasted for 14, 28 and 56 days for the acute, sub-chronic and chronic studies, respectively. Serum and hippocampal BDNF assays were analysed following standard laboratory protocols. Results showed dose and time-dependent significant reductions (p < 0.05) in BDNF levels across all treatment groups compared to controls, with the most pronounced decreases observed in codeine 30mg/kg and tramadol 60mg/kg groups. These findings suggest that prolonged opioid exposure disrupts neurotrophic signalling, potentially contributing to neurodegenerative conditions.
Abstract: Brain-derived neurotrophic factor (BDNF) is a critical regulator of neuronal survival, synaptic plasticity, and cognitive function, making it a key biomarker in understanding the neurobiological impact of opioid exposure. This study investigated the effects of opioids (codeine and tramadol) on brain-derived neurotrophic factor (BDNF) levels in male...
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