Time-course microscopy snapshots comparing cell morphology and cellular DNA content, as monitored using HU–mNeonGreen fusion (mNG), in WT and ΔWASA-1 backgrounds, following infection with ICP1-2006 at MOI 5.
A striking example of such an evolutionary arms race has just been uncovered by a team from École polytechnique fédérale de Lausanne (EPFL), who found that a notorious strain of cholera possesses a suite of sophisticated immune systems to fend off viral attack. According to ID proponents like William A. Dembski, both this cholera strain and the viruses that infect it should qualify as products of ‘complex, specified information’. Likewise, under Michael J. Behe’s definition, both would be considered ‘irreducibly complex’. By their logic, this makes them the result of intelligent design by a supernatural creator.
In other words, creationism’s designer god has supposedly created viruses that infect the cholera bacterium—then equipped the bacterium with complex machinery to defend itself.
To make matters worse for creationists, this virus-resistant cholera strain was behind a devastating epidemic across Latin America. That is, the designer god not only enabled the bacterium to resist viruses, but in doing so gave it a better chance of surviving to infect and harm humans—using its ‘intelligently designed’, ‘irreducibly complex’ viral defences.
The research is published open access in Nature Microbiology.
What information do you have on Cholera, particularly the West African–South American lineage? The West African–South American (WASA) lineage of Vibrio cholerae is a significant branch of the seventh cholera pandemic (7PET) lineage, notably responsible for the extensive cholera epidemic in Latin America from 1991 to 2001. This lineage is distinguished by unique genetic features that enhance its survival and virulence, particularly through sophisticated anti-phage defense mechanisms.[1.1, 2.1]
Key Genetic Features and Phage Defense Mechanisms
Recent research has identified two distinctive genetic signatures in the WASA lineage that contribute to its resilience against bacteriophage predation:[3.1]
- WASA-1 Prophage Encoding WonAB System: This system provides resistance to the lytic vibriophage ICP1, which is known to limit cholera outbreaks by infecting V. cholerae populations.[1.1]
- Unique Genes on Vibrio Seventh Pandemic Island II (VSP-II): These genes encode:
These defense systems likely contributed to the WASA lineage's epidemic success by enabling it to withstand phage attacks that typically curb cholera outbreaks. [2.1]
Epidemiological Impact
The WASA lineage was central to the cholera epidemic that began in Peru in 1991, rapidly spreading across Latin America and resulting in over a million infections and approximately 10,000 deaths. Genomic analyses suggest that this lineage may have originated from West Africa, highlighting the interconnectedness of cholera transmission between continents. [4.1]
Implications for Public Health and Research
Understanding the genetic adaptations of the WASA lineage underscores the importance of genomic surveillance in tracking cholera's evolution and spread. The presence of advanced phage defense systems in epidemic strains like WASA emphasizes the need for comprehensive strategies that consider bacterial resistance mechanisms when developing interventions and treatments.[5.1]
For a detailed exploration of the WASA lineage's genetic characteristics and its role in cholera pandemics, refer to the open-access study published in Nature Microbiology (the subject of this blog post).[1.1]
How cholera bacteria outsmart viruses
Author: Nik Papageorgiou
EPFL researchers uncover a notorious cholera strain that contains sophisticated immune systems to fend off viruses, which potentially helped it fuel a devastating epidemic across Latin America.
When we think of cholera, most of us picture contaminated water and tragic outbreaks in vulnerable regions. But behind the scenes, cholera bacteria are locked in a fierce, microscopic war—one that could shape the course of pandemics.
Cholera bacteria aren’t just battling antibiotics and public health measures—they are also constantly under attack from bacteriophages (phages), viruses that infect and kill bacteria. These viruses don’t just influence individual infections; they can make or break entire epidemics. In fact, certain bacteriophages are thought to limit the size and duration of cholera outbreaks by killing off Vibrio cholerae, the bacterium behind the disease.
Since the 1960s, the ongoing 7th cholera pandemic has been driven by what are known as “seventh pandemic El Tor” (7PET) strains of V. cholerae, which have spread globally in successive waves. In this evolutionary arms race, bacteria have adapted to fight back, developing defense mechanisms against these phages. For example, many bacterial strains carry mobile genetic elements that arm them with anti-viral tools. So why are certain cholera strains so successful at evading phage attacks? Could this either enable or enhance the pathogen’s devastating effect on human populations?
A secret revealed
One event stands out. In the early 1990s, a cholera epidemic swept through Peru and much of Latin America, infecting over 1 million people and causing thousands of deaths. The strains responsible belonged to the West African South American (WASA) lineage of V.cholerae. Why these WASA strains caused such a large outbreak in Latin America is still not fully understood.
New research by the group of Melanie Blokesch at EPFL’s Global Health Institute has now uncovered one secret behind these strains. The study, published in Nature Microbiology, shows that the WASA lineage acquired multiple distinct bacterial immune systems that have protected it from diverse types of phages. And this defense may have contributed to the massive scale of the Latin American epidemic.
The researchers looked at Peruvian cholera strains from the 1990s, testing their resistance against key phages, especially ICP1—a dominant virus that has been extensively studied in the cholera endemic area of Bangladesh where it is thought to contribute to restricting cholera outbreaks. Surprisingly, the Peruvian strains were immune to ICP1, while other strains representative of the 7th pandemic weren’t.
An expanded arsenal of defense systems
By deleting specific sections of the cholera strain’s DNA and inserting these genes into other bacterial strains to test their function, the team identified two major defense regions on the WASA strain’s genome, namely within the so-called WASA-1 prophage and the genomic island known as Vibrio seventh pandemic island II (VSP-II). These genomic regions encode specialized anti-phage systems that work together to create a bacterial immune system capable of defending against phage infections.
One such system, WonAB, triggers an “abortive infection” response that kills infected cells before phages can reproduce, sacrificing a few bacteria to save the larger population. This strategy is different to classical bacterial immune systems such as restriction-modification systems that degrade the phage DNA as it enters the cells.
Instead, it stops the phage from replicating but only after it has already hijacked the cholera bacterium's cellular machinery, effectively locking the infected bacteria in a standoff—but at least the phage doesn’t spread.
David Adams, co-lead author.
Laboratory of Molecular Microbiology
Global Health Institute
School of Life Sciences
Ecole Polytecnique Fédérale de Lausanne (EPFL), Lausanne, Switzerland.
Two further systems, GrwAB and VcSduA, contribute distinct protective functions: GrwAB targets phages with chemically modified DNA—a strategy employed by phages to camouflage their genomes and evade other bacterial immune systems. VcSduA on the other hand acts against different families of viruses including another common “vibriophage”, offering layered protection that broadens the bacterial population’s resistance spectrum.
Essentially, the WASA lineage of cholera bacteria harbors an expanded arsenal of anti-phage defense systems, which allows it to counteract a broad range of bacteriophages in addition to protection from its major predatory phage ICP1.
An alternative to antibiotic treatment
Understanding how epidemic bacteria resist phage predation is crucial, especially as interest in phage therapy—the use of viruses to treat bacterial infections— has re-emerged as an alternative to antibiotic treatment. If bacteria like V. cholerae can acquire increased transmission potential by obtaining viral defenses, this can reshape how we approach cholera control, monitoring, and treatment. It also underscores the importance of considering phage-bacteria dynamics when studying and managing infectious disease outbreaks.
Publication:
AbstractThis discovery presents a clear challenge to Intelligent Design (ID) creationism. At its core, ID asserts that complex biological systems are best explained by the action of an intelligent designer, rather than unguided natural processes. Yet, the arms race between cholera bacteria and bacteriophages reveals a dynamic of constant evolutionary pressure and counter-adaptation that is far better explained by natural selection than by design. The cholera strain has evolved complex molecular systems—such as restriction enzymes and novel Shedu-family proteins—not as parts of a grand design, but as responses to specific selective pressures from viral attack.
Our understanding of the factors underlying the evolutionary success of different lineages of pandemic Vibrio cholerae remains incomplete. The West African–South American (WASA) lineage of V. cholerae, responsible for the 1991–2001 Latin American cholera epidemic, is defined by two unique genetic signatures. Here we show that these signatures encode multiple distinct anti-phage defence systems. Firstly, the WASA-1 prophage encodes an abortive-infection system, WonAB, that renders the lineage resistant to the major predatory vibriophage ICP1, which, alongside other phages, is thought to restrict cholera epidemics. Secondly, a unique set of genes on the Vibrio seventh pandemic island II encodes an unusual modification-dependent restriction system targeting phages with modified genomes, and a previously undescribed member of the Shedu defence family that defends against vibriophage X29. We propose that these anti-phage defence systems likely contributed to the success of a major epidemic lineage of the ongoing seventh cholera pandemic.
Main
The ability of lytic bacteriophages to rapidly devastate bacterial populations has driven the evolution of multiple layers of defence, including a diverse array of specialized anti-phage defence systems1. Bacteriophages also have the potential to affect bacterial pathogenesis, as exemplified by the cholera-toxin-encoding prophage CTXΦ (ref. 2). Moreover, bacteriophage predation is thought to limit the duration and severity of cholera epidemics and to affect individual patient outcomes3,4. Sampling of cholera patients has revealed that the O1 El Tor strains of Vibrio cholerae responsible for the ongoing seventh cholera pandemic (7PET) consistently co-occur with three lytic phages, ICP1, ICP2 and ICP3, with ICP1 being most frequently isolated5,6. Furthermore, the demonstration that a cocktail of ICP1, ICP2 and ICP3 can prevent cholera in animal infection models has led to renewed interest in using phages as a prophylactic treatment7. There is therefore an urgent need to understand the mechanisms by which V. cholerae defends against these and other viruses.
Since 1961, 7PET strains have spread out from the Bay of Bengal in a series of three distinct but overlapping waves8. Importantly, from wave 2 onwards, strains acquired SXT/R391 integrative and conjugative elements (SXT-ICE), which, in addition to carrying multiple antibiotic resistance genes, encode a variable anti-phage defence hotspot that in the globally dominant SXT-ICE harbours either BREX or restriction–modification systems active against ICP1–3 (refs. 8,9). In addition, a family of viral satellites, the phage-inducible chromosomal island-like elements (PLE), also occur sporadically and specifically parasitize ICP1 infection to mediate their own transmission10,11. Notably, these elements exemplify the co-evolutionary arms race of defence and counter-defence between bacterial hosts and their viral predators, with the emergence of resistant ICP1 phages that can overcome these defence mechanisms selecting for either alternative SXT-ICE carrying new defence systems or new PLE variants9,12. By contrast, how 7PET strains that lack SXT-ICE and PLE defend against these phages remains unknown. Given their ubiquitous nature and ability to shape epidemics, we hypothesized that these strains likely contained additional defence systems with activity against ICP1–3.
Adams, D.W., Jaskólska, M., Lemopoulos, A. et al.
West African–South American pandemic Vibrio cholerae encodes multiple distinct phage defence systems.
Nat Microbiol (2025). https://doi.org/10.1038/s41564-025-02004-9
Copyright: © 2025 The authors.
Published by Springer Nature Ltd. Open access.
Reprinted under a Creative Commons Attribution 4.0 International license (CC BY 4.0)
If one accepts the creationist framework, then these findings lead to a theological absurdity: that a supernatural designer not only created viruses capable of infecting bacteria but then also designed those bacteria with intricate means to resist the very infections it enabled. This implies a designer engaged in a self-defeating cycle of design, where each ‘solution’ immediately begets a new problem requiring yet another intervention. It raises the uncomfortable question of why such a being would create harmful pathogens at all, then equip them with tools to survive and proliferate—especially when this particular strain contributed to a major cholera epidemic in Latin America, causing widespread human suffering.
Moreover, both the cholera strain and the viruses that prey upon it meet the criteria that ID proponents like William Dembski and Michael Behe use to argue for design: they are allegedly ‘irreducibly complex’ and contain ‘complex, specified information’. Yet these features clearly evolved through natural arms races rather than through the intervention of a benevolent or rational designer. In evolutionary terms, they are understandable. In design terms, they are incoherent. Thus, this discovery not only undermines the central claims of ID creationism but highlights the explanatory power of evolution in accounting for biological complexity.
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