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Updated: Jul 10, 2026

Laboratory Techniques Used to Maintain and Differentiate Biotypes of Vibrio cholerae Clinical and Environmental Isolates
Published on: May 30, 2017
A bacteriophage encoding a pathogenicity island, a type-IV pilus and a phage receptor in cholera bacteria
D K Karaolis1, S Somara, D R Maneval
1Center for Vaccine Development, Division of Hospital Epidemiology, University of Maryland School of Medicine, Baltimore 21201, USA. karaolis@umaryland.edu
Abstract:
The virulence properties of many pathogenic bacteria are due to proteins encoded by large gene clusters called pathogenicity islands, which are found in a variety of human pathogens including Escherichia coli, Salmonella, Shigella, Yersinia, Helicobacter pylori, Vibrio cholerae, and animal and plant pathogens such as Dichelobacter nodosus and Pseudomonas syringae. Although the presence of pathogenicity islands is a prerequisite for many bacterial diseases, little is known about their origins or mechanism of transfer into the bacterium. The bacterial agent of epidemic cholera, Vibrio cholerae, contains a bacteriophage known as cholera-toxin phage (CTXphi), which encodes the cholera toxin, and a large pathogenicity island called the VPI (for V. cholerae pathogenicity island) which itself encodes a toxin-coregulated pilus that functions as a colonization factor and as a CTXphi receptor. We have now identified the VPI pathogenicity island as the genome of another filamentous bacteriophage, VPIphi. We show that VPIphi is transferred between V. cholerae strains and provide evidence that the TcpA subunit of the toxin-coregulated type IV pilus is in fact a coat protein of VPIphi. Our results are the first description of a phage that encodes a receptor for another phage and of a virus-virus interaction that is necessary for bacterial pathogenicity.
Insights
Pathogenicity islands, crucial for bacterial virulence, were previously poorly understood. This study reveals the V. cholerae pathogenicity island (VPI) is a bacteriophage (VPIphi), detailing its transfer and role in disease.
Area of Science:
- Microbiology
- Virology
- Genetics
Background:
- Pathogenicity islands (PAIs) are large gene clusters encoding virulence factors in many bacterial pathogens.
- The origins and transfer mechanisms of PAIs remain largely unknown.
- Vibrio cholerae utilizes a PAI (VPI) encoding a colonization factor and CTXphi receptor.
Purpose of the Study:
- To elucidate the origin and transfer mechanism of the V. cholerae pathogenicity island (VPI).
- To investigate the nature of the VPI and its relationship with other mobile genetic elements.
- To understand the virus-virus interaction in bacterial pathogenicity.
Main Methods:
- Genomic analysis to identify the VPI as a bacteriophage genome.
- Bacterial conjugation experiments to demonstrate VPI transfer between V. cholerae strains.
- Protein analysis to identify VPI components.
Main Results:
- The VPI pathogenicity island was identified as the genome of a filamentous bacteriophage, VPIphi.
- VPIphi is transferable between V. cholerae strains.
- The TcpA subunit of the toxin-coregulated pilus is a VPIphi coat protein.
- This represents the first description of a phage encoding a receptor for another phage.
Conclusions:
- The VPI pathogenicity island is a bacteriophage (VPIphi) capable of horizontal gene transfer.
- VPIphi plays a critical role in Vibrio cholerae pathogenicity by mediating colonization and phage receptor functions.
- This study reveals a novel virus-virus interaction essential for bacterial virulence.
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