Related Experiment Video
Updated: May 27, 2025
09:40
Phage Phenomics: Physiological Approaches to Characterize Novel Viral Proteins
Published on: June 11, 2015
12.1K
Capturing dynamic phage-pathogen coevolution by clinical surveillance
Yamini Mathur1, Caroline M Boyd1, Jeannette E Farnham1
1Department of Plant and Microbial Biology, University of California, Berkeley, Berkeley, CA 94720, USA.
Biorxiv : the Preprint Server for Biology
|February 20, 2025
Summary
Bacteria and viruses engage in a constant evolutionary battle. A mobile genetic element (MGE) called PLE11 emerged, protecting *Vibrio cholerae* from phage predation and driving pathogen evolution during a major cholera outbreak.
Area of Science:
- Microbiology
- Evolutionary Biology
- Genetics
Background:
- Bacteria possess defense systems against phage predation, often encoded on mobile genetic elements (MGEs).
- Phages and bacteria engage in a dynamic evolutionary arms race, particularly relevant in human disease contexts.
- A higher burden of the lytic phage ICP1 in *Vibrio cholerae* correlates with reduced diarrheal disease severity, but direct evidence of phage-driven selection is lacking.
Purpose of the Study:
- To investigate the molecular basis of phage-driven selection in *Vibrio cholerae* during a cholera outbreak.
- To identify the anti-phage mechanisms and evolutionary dynamics between *V. cholerae* and its phage ICP1.
Main Methods:
- Clinical surveillance in cholera-endemic Bangladesh to track MGE acquisition.
- Experimental evolution to study phage counteradaptations.
- Molecular characterization of phage-defense interactions and MGE-mediated manipulation of phage components.
Main Results:
- The acquisition of a parasitic anti-phage MGE, PLE11, was observed, coinciding with a major cholera outbreak and a selective sweep in *V. cholerae*.
- PLE11 provided potent anti-phage activity against ICP1 via the Rta protein, which restricts phage tail assembly.
- Experimental evolution revealed phage counteradaptations and the emergence of ICP1 variants capable of overcoming PLE11 defenses, including the formation of chimeric phage-MGE tails.
Conclusions:
- PLE11-mediated phage resistance drove the natural selection of *Vibrio cholerae* during a significant cholera epidemic.
- PLEs can hijack phage structural proteins for horizontal transmission and manipulate phage tail assembly, revealing a novel mechanism of co-evolution.
- This study elucidates the molecular underpinnings of pathogen-virus co-evolution in a clinically relevant setting.
Related Concept Videos
01:30Lytic Cycle of Bacteriophages
70.1K
Bacteriophages, also known as phages, are specialized viruses that infect bacteria. A key characteristic of phages is their distinctive “head-tail” morphology. A phage begins the infection process (i.e., lytic cycle) by attaching to the outside of a bacterial cell. Attachment is accomplished via proteins in the phage tail that bind to specific receptor proteins on the outer surface of the bacterium. The tail injects the phage’s DNA genome into the bacterial cytoplasm. In the...
70.1K
00:43Lysogenic Cycle of Bacteriophages
61.7K
In contrast to the lytic cycle, phages infecting bacteria via the lysogenic cycle do not immediately kill their host cell. Instead, they combine their genome with the host genome, allowing the bacteria to replicate the phage DNA along with the bacterial genome. The incorporated copy of the phage genome is called the prophage. Some prophages can re-activate and enter the lytic cycle. This often occurs in response to a perturbation, such as DNA damage, but can also transpire in the absence of...
61.7K
00:36Viral Mutations
32.1K
A mutation is a change in the sequence of bases of DNA or RNA in a genome. Some mutations occur during replication of the genome due to errors made by the polymerase enzymes that replicate DNA or RNA. Unlike DNA polymerase, RNA polymerase is prone to errors because it is not capable of “proofreading” its work. Viruses with RNA-based genomes, like HIV, therefore accrue mutations faster than viruses with DNA-based genomes. Because mutation and recombination provide the raw material...
32.1K
00:57Viral Recombination
23.2K
Cells are sometimes infected by more than one virus at once. When two viruses disassemble to expose their genomes for replication in the same cell, similar regions of their genomes can pair together and exchange sequences in a process called recombination. Alternatively, viruses with segmented genomes can swap segments in a process called reassortment.
23.2K
01:10Retrovirus Life Cycles
45.6K
Retroviruses have a single-stranded RNA genome that undergoes a special form of replication. Once the retrovirus has entered the host cell, an enzyme called reverse transcriptase synthesizes double-stranded DNA from the retroviral RNA genome. This DNA copy of the genome is then integrated into the host’s genome inside the nucleus via an enzyme called integrase. Consequently, the retroviral genome is transcribed into RNA whenever the host’s genome is transcribed, allowing the...
45.6K
01:20Infection
7.0K
When a pathogen enters the body and reproduces, it can cause an infection, damage body cells, and cause illness symptoms that eventually lead to disease. Therefore, its prevention requires breaking the chain of infection.
The chain begins with pathogens: bacteria, viruses, fungi, prions, or parasites such as protozoa helminths. These can be present on the skin as transient or resident flora, or they can be acquired from the environment. Identifying and treating the type of infection and...
The chain begins with pathogens: bacteria, viruses, fungi, prions, or parasites such as protozoa helminths. These can be present on the skin as transient or resident flora, or they can be acquired from the environment. Identifying and treating the type of infection and...
7.0K