Mostly, our gut microbes are beneficial or at least neutral because we have co-evolved and reached an accommodation. One benefit we derive from their presence is that they make life difficult for potentially harmful organisms, if only by monopolising the available resources and occupying the niches in our gut.
There is a downside, of course, as in any evolved system, which is inevitably a compromise and can tip over into pathology under certain circumstances. But overall, because the disadvantages are more than compensated for by the benefits, the system has evolved and been maintained.
However, a newly discovered downside is that a Staphylococcus species may be implicated in one of the serious complications of diabetes mellitus (DM) — kidney fibrosis and ultimately kidney failure. The discovery was made by researchers at the University of Illinois Urbana-Champaign and Mie University in Japan, co-led by Professor Isaac Cann of Illinois and Professor Esteban Gabazza of Mie University. The bacterium is believed to produce corisin — a small peptide — which is found at high levels in patients with diabetic kidney fibrosis. The researchers have just published their findings, open access, in Nature Communications.
For creationists, this sort of discovery is always a problem, one they normally ignore or blame on “Eve’s sin,” revealing ID creationism for what it is — Bible literalism in a lab coat — which must retreat into mystical theology when faced with problems ID cannot address. Yet creationists also claim that their omniscient creator god is personally responsible for the design of organisms such as Staphylococcus. That would mean it knowingly endowed Staphylococcus with the genes to make corisin, along with all the harmful consequences.
Taking William A. Dembski’s “complex specified genetic information,” which supposedly produces a specific outcome, at face value, the staphylococcal genes are equally “proof” of intelligent design. And so we end up with an unresolved paradox for ID creationism: “complex specified” genes that do us harm, standing as evidence of malevolent design.
Creationists often imagine the human body as the handiwork of a supreme intelligence, carefully engineered for optimal function. Yet the reality revealed by biology is far messier. Our anatomy and physiology are riddled with compromises, inefficiencies, and vulnerabilities that make far more sense as the outcomes of evolutionary processes than as the products of intelligent design. I give multiple examples of the results of these sub-optimal evolutionary compromises in my book, The Body of Evidence: How the Human Body Refutes Intelligent Design. One striking example lies in the complex relationship between mother and foetus during pregnancy, where cooperation and conflict are locked in an evolutionary arms race.
In a paper published in the Proceedings of the National Academy of Sciences (PNAS), Associate Professor Kshitiz of the Department of Biomedical Engineering, University of Connecticut, together with postdoctoral fellows Yasir Suhail and Wenqiang Du, Gunter Wagner of Yale, and Junaid Afzal of the University of California San Francisco (UCSF), have shown how the interface between mother and foetus in the placenta is the product of evolutionary arms races—not the result of intelligent design, as creationists like to imagine.
Firstly, there is the need for the developing foetus to obtain an adequate supply of nutrients, which requires its placental cells to penetrate into the lining of the mother’s uterus.
Secondly, there is the need for the mother to defend herself against invasion by what her body recognises as a ‘foreign’ organism, part of her evolved immune response. Finally, there is the overarching evolutionary imperative of successful reproduction, which entails the birth of healthy offspring.
What the team discovered is that the inevitable evolutionary compromise involves the foetus’s placental cells producing a protein that suppresses the mother’s immune response. This suppression works only because the mother’s cells have evolved to cooperate, allowing the foetal protein to function.
In other words, the mother’s cells have evolved a strategy for permitting the foetus to dampen her immune system—an immune system that itself evolved in the ancestors of placental mammals. This situation can hardly be credited to the act of a supreme intelligence.
Parasite–host relationships are a nightmare for creationists. Their usual escape hatch is “The Fall”, but that undermines the Discovery Institute’s claim that intelligent design is science rather than Bible-literalist dogma in a lab coat. It also raises the obvious question: if parasites only appeared 6,000–10,000 years ago, how did they spread so quickly—and why do we find fossil evidence of parasitism millions of years old?
Creationists cope by dismissing science as a conspiracy, waving away radiometric dating, or pushing myths such as dinosaur fossils being “carbon-dated” [sic] to a few thousand years old. So creationism persists, despite the vast amount of evidence against it, by a combination of wilful ignorance, disinformation and a lack of critical thinking skills.
Now creationists must also ignore new research from Stockholm University, where scientists isolated bacterial DNA from the teeth of woolly and steppe mammoths. They showed these bacteria evolved into the ancestors of those infecting modern elephants—evidence of parasites a million years before “Creation Week”, and of co-evolution continuing right up to today’s elephants, the descendants of those mammoths.
Incidentally, neither mammoths nor modern elephants are mentioned in the Bible, reflecting the parochial ignorance of its authors - a fact often overlooked in depictions of animals boarding Noah's Ark, which usually includes a pair of elephants!
The tRNA ensures the cohesion of the polymerase and the associated factors; without it, they would not arrange themselves in this way.
Image: Clemens Grimm.
Researchers at Julius Maximilian University of Würzburg (JMU) have discovered that poxviruses have developed a unique strategy to multiply rapidly after infecting a host cell. They achieve this by assembling a large protein complex with the help of a transfer RNA (tRNA) molecule. Remarkably, this is the first known example of a ‘chaperone’ function being carried out by a tRNA rather than a protein. Each component of the assembly plays a specific role in the production of new poxviruses. Crucially, the complex only functions when all parts are correctly assembled, and the tRNA is indispensable for this construction.
In other words, the tRNA provides the essential element of the complex, which some might describe—using the Discovery Institute’s own terms—as containing “complex specified information” and forming an “irreducibly complex” system essential to the virus’s success.
By that same logic, it follows that the viruses responsible for smallpox and mpox (monkeypox) must have been intelligently designed. This leaves creationists with an unenviable dilemma:
Accept the Discovery Institute’s definitions and admit their designer created deadly viruses — theologically awkward.
Claim another intelligence designs life, beyond their god’s control — even more awkward.
Abandon the Institute’s “evidence” for intelligent design — politically awkward.
The notion of intelligent design — the current flagship of creationism’s attempt to replace scientific realism with magical superstitions and Bible literalism dressed up as “alternative science” — contains a blatant paradox its advocates must ignore: the very same “logic” used to argue that the God of the Bible created living organisms can just as easily be used to argue that any such designer is a malevolent sadist who deliberately increases suffering in the world while ignoring countless ways to reduce it.
The theological problems this raises are never discussed in polite creationist circles, except for the lazy fallback of blaming everything on “The Fall.” But this move exposes intelligent design for what it really is — Bible-literalist religion in disguise. And that sits awkwardly against over half a century of insistence by the Discovery Institute that ID is not a religious idea, but rather a scientific one that should be taught in American public schools at taxpayer expense — a direct violation of the Establishment Clause and the U.S. Supreme Court’s ruling in Edwards v. Aguillard (1987).
The paradox lies in the fact that the very same so-called evidence — Michael J. Behe’s “irreducible complexity” and William A. Dembski’s “complex specified genetic information” — can be found in the genomes, structures, and processes of parasites and pathogens, making them devastatingly effective at exploiting and destroying their hosts. In fact, Behe himself has, probably without realising it, used precisely such examples. The bacterial flagellum he highlights enables E. coli to move efficiently through our gut, causing sometimes fatal food poisoning. And his example of resistance to anti-malarial drugs in Plasmodium parasites illustrate how evolution equips them to continue killing hundreds of thousands of children every year while condemning millions more to cycles of malarial fever.
Now, new research has highlighted another gruesome example. The bacterium Yersinia pestis — responsible for multiple waves of plague throughout the Middle Ages — has been shown to have evolved into its highly lethal form only in relatively recent human history. Beginning with the “Plague of Justinian” about 1,500 years ago, Y. pestis unleashed pandemics that killed between 30% and 50% of Europe’s population.
An interdisciplinary team at the University of South Florida (USF) and Florida Atlantic University (FAU), with collaborators in India and Australia, has now confirmed genomically that the Justinian plague was indeed caused by Y. pestis, as long assumed. Analysing DNA from plague victims buried in a mass grave at the ancient city of Jerash, Jordan — the epicentre of that pandemic — one group identified the culprit, while another team traced the bacterium’s evolutionary changes that made it one of history’s most notorious killers.
Here’s one of those discoveries in biological science that should have ID creationists jumping up and down yelling, "Told you so!". It’s news that the parasite that causes malaria shows both what they call 'irreducible complexity' and 'complex specified genetic information'. According to Discovery Institute fellows Michael J. Behe and William A. Dembski, that would mean it is intelligently designed and, by implication, designed to do exactly what it does — by the Christian God.
But, for reasons which can only be guessed at — and probably not a million miles from the fact that this conclusion would mean the Christian god is actively designing ways to kill people, particularly children, and especially in Africa — creationists tend to ignore it. After all, that’s the very antithesis of the compassionate, benevolent, loving god of the Bible.
Instead, they quietly sidestep the inconvenient reality that examples of their supposed 'proof of intelligent design' are found just as often in parasites and pathogens as in their hosts. This is precisely what evolutionary biology predicts: a host–parasite relationship invariably leads to an evolutionary arms race, producing sophisticated and complex systems that equip the parasite to survive in the host and to infect new victims.
And, true to form, we now have another such example in the major cause of malaria, Plasmodium falciparum, which killed some 569,000 people in Africa in 2023:
Key Facts:
Globally in 2023, there were an estimated 263 million malaria cases and 597,000 malaria deaths in 83 countries.
The WHO African Region carries a disproportionately high share of the global malaria burden.
In 2023, the WHO African Region was home to 94% of malaria cases (246 million) and 95% (569,000) of malaria deaths (432,400 children under 5).
Children under 5 accounted for about 76% of all malaria deaths in the Region.
It gets tedious repeating this point so often, but so long as creationists keep using what they claim is irreducible complexity and/or complex specified genetic information as evidence for intelligent design, they need to be reminded that the same argument can also be used as evidence of their putative designer’s malevolence.
Creationists, of course, ignore the fact that parasites are no less “designed” than humans and have structures and processes that are “irreducibly complex” and depend on “complex specified information” in order to succeed in their environments. Yet their existence, and how they interact with and even manipulate their hosts, inevitably increases suffering in the world – a theological problem that creationist disinformation organisations such as the Discovery Institute avoid like the plague.
Parasite–host relationships also inevitably involve evolutionary arms races – the antithesis of intelligence if both “sides” are supposedly designed by the same designer.
So, to keep reminding them: if their justification for designating their god as the designer of living systems holds true, then it is also justification for designating the same god as the cause of suffering. Here is another example of a parasite that falls within their definition of an organism “designed” to do what it does and to participate in an arms race with its host in order to do so. This concerns the discovery that the parasitic worm Schistosoma mansoni, which causes schistosomiasis, is able to suppress neurons in the skin to evade detection as it burrows into its victim’s body (usually the leg).
A major stumbling block that non-biologist Christian fundamentalist theologian William A. Dembski has blundered into is that his so-called ‘proof of intelligent design’ (i.e., the Christian god) also, by the same reasoning, constitutes evidence for malevolent design — something found in virtually every genome of every parasite and pathogen. This presents CDesign proponentsists with a fatal paradox: either their ‘proof of intelligent design’ also proves the existence of an evil designer, or ‘complex specified information’ is not the definitive evidence for design they like to claim it is.
A classic example — and another blow to creationist reasoning—has just been described in a study by researchers from the Swiss universities of Basel and Zurich. They have recovered and analysed the genome of the virus responsible for the 1918–1920 ‘Spanish flu’ pandemic, which killed more people than were killed in the First World War. In fact, the term ‘Spanish flu’ is a misnomer; the virus is now believed to have originated in a U.S. military base in Kansas and was brought to Europe by American soldiers.
The Swiss team discovered that from the outset, the virus appears to have been pre-adapted for infectivity and immune evasion. They identified three key mutations that remained unchanged as the virus evolved over the course of the pandemic. Two of these mutations made the virus resistant to an antiviral component of the human immune system, while the third enabled it to bind more effectively to receptors on the surface of human cells, allowing it to enter and infect them more readily. These mutations were so effective that victims frequently died within hours of the onset of symptoms.
According to creationist superstition, humans were specially created by a perfect, anthropophilic, omnibenevolent creator god. If that were true, it would be reasonable to expect humans to be perfectly designed—free from defects or anything likely to cause long-term suffering.
However, the facts do not support this view. For example, as humans age, they increasingly suffer from a condition known as inflammaging — low-grade, chronic inflammation that contributes to a range of health problems, including heart disease, strokes, diabetes, cancer, and osteoarthritis.
Properly understood, this should give creationists cause for concern. The same designer god apparently gave some other primates—most notably, certain species of lemur—the ability to avoid this consequence of ageing. In fact, these lemurs even show a reduced tendency toward inflammatory conditions as they grow older.
This raises a serious question for Intelligent Design creationists: if the same designer god was capable of creating such a mechanism for lemurs, why did it not see fit to bestow the same gift upon its supposed favourite creation—humans? Or are these inflammatory conditions intended to cause suffering and disease as we age?
The discovery that some lemurs appear to have been specially favoured by a creator god—if we accept the ID creationist premise for the sake of argument—was made by a team of researchers led by Elaine Elizabeth Gomez Guevara, a biological anthropologist in the Department of Evolutionary Anthropology at Duke University, Durham, USA. As a scientist and biologist, however, she attributes the differences between lemurs and humans to evolution — not to indifference or malevolence on the part of a designer god.
News, in The Conversation that the latest variant of the Sars-CoV-2 virus that causes COVID-19, XFG, could soon become the dominant variant worldwide, prompted me to ask ChatGPT to construct a family tree for the known variants of the virus, to illustrate the basic principles of evolution that creationists continue to deny.
Construct a family tree of known SARS-CoV-2 variants and explain how this illustrates evolution in progress.
Explanation: Evolution in Progress
This tree diagram represents a simplified phylogenetic tree of SARS-CoV-2, showing how the virus has evolved since it first emerged in Wuhan in late 2019.
Here we have yet another example demonstrating that, if we apply Discovery Institute fellow William A. Dembski's criteria for proving intelligent design — namely the presence of complex specified genetic information — then we must conclude that creationism's supposed intelligent designer is, in fact, a malevolent force devising ever more sophisticated ways to inflict suffering on the world.
Once again, honest creationists are left with a stark dilemma: either complex specified information is indeed evidence of design, in which case the designer is malevolent, or it is not, in which case a central tenet of Intelligent Design creationism collapses. The dishonest ones, of course, will simply dismiss the evidence, likely misrepresent the science, and continue to bear false witness against scientists. In neither case should we expect creationists to admit that the theory of evolution fully accounts for the appearance of "malevolent" design, arising naturally without conscious intent or divine interference.
It’s a curious paradox that people who claim to worship the God of the Bible as an omnibenevolent, anthropophilic being are so often willing to see that deity cast in the role of a malevolent agent—so long as they can reject the theory of evolution. This strongly suggests that their opposition to evolution is not primarily theological, but political.
The latest example comes from the tick-borne pathogen Anaplasma, which causes anaplasmosis and contributes to Lyme disease. This bacterium hijacks the cellular machinery of ticks to ensure its own survival and transmission to new hosts, including humans. Although Dembski has famously avoided providing a rigorous, testable definition of "complex specified genetic information," any such definition would surely encompass genetic adaptations that promote survival and reproduction.
What information do you have on Anaplasma and the tick that transmits it?
Anaplasma is a genus of bacteria that includes several species capable of causing disease in humans and animals. The most medically relevant species is Anaplasma phagocytophilum, which causes anaplasmosis—a tick-borne disease that affects both humans and various mammals.
Overview of Anaplasma
Anaplasma are obligate intracellular bacteria in the family Anaplasmataceae.
They primarily infect white blood cells (especially neutrophils in the case of A. phagocytophilum).
Disease is often seasonal, peaking during the months of high tick activity (late spring to early autumn in temperate zones).
In severe cases: respiratory failure, organ failure, neurological symptoms
Incubation period: ~5–14 days after a tick bite.
Treatment: Responds well to doxycycline, especially if started early.
If untreated, it can lead to complications, especially in the elderly or immunocompromised.
Tick Vectors
The primary vector in the United States is the blacklegged tick (Ixodes scapularis), also called the deer tick.
In Europe, the main vector is the castor bean tick (Ixodes ricinus).
These are the same ticks that transmit Lyme disease (Borrelia burgdorferi) and Babesia (babesiosis), leading to frequent co-infections.
Hosts and Reservoirs
Main animal reservoirs include:
White-tailed deer
Rodents
Small mammals
Ticks acquire the bacteria when feeding on an infected host and then transmit it during subsequent feedings.
Biological Strategy of the Pathogen
Recent research (such as the 2025 WSU referenced) shows that Anaplasmacan:
Hijack the tick's cellular defence mechanisms, particularly its oxidative stress response, allowing the bacteria to survive within the tick's gut.
Manipulate the cell death pathways of tick cells, suppressing apoptosis (programmed cell death) to extend the viability of the cells it infects.
Modify gene expression in the tick to enhance its own survival and transmission potential.
These mechanisms qualify as highly sophisticated biological strategies—precisely the sort of adaptations that Intelligent Design proponents would struggle to explain without appealing to either special pleading or malevolent intent.
Ecological and Public Health Impact
Geographic spread is increasing, partly due to climate change, which expands the habitat range of ticks.
Public health monitoring is challenged by co-infections and misdiagnosis (HGA is often confused with Lyme disease or viral infections).
Preventative strategies include tick checks, repellents, and public awareness campaigns.
Bacteria hijack tick cell defenses to spread diseaseWashington State University researchers have discovered how the bacteria that cause anaplasmosis and Lyme disease hijack cellular processes in ticks to ensure their survival and spread to new hosts, including humans.
Based in the College of Veterinary Medicine, the team found that the bacteria can manipulate a protein known as ATF6, which helps cells detect and respond to infection, to support its own growth and survival inside the tick. The findings, published in the journal Proceedings of the National Academy of Sciences, could serve as a launching point for developing methods to eliminate the bacteria in ticks before they are transmitted to humans and other animals.
Most research has looked at how these bacteria interact with humans and animals and not how they survive and spread in ticks. What we have found could open the door to targeting these pathogens in ticks, before they are ever a threat to people.
Kaylee A. Vosbigian, lead author
Department of Veterinary Microbiology and Pathology
College of Veterinary Sciences
Washington State University, Pullman, WA, USA.
Vosbigian and her advisor, Dana Shaw, the corresponding author of the study and an associate professor in the Department of Veterinary Microbiology and Pathology, focused their research on Ixodes scapularis, also known as the black-legged tick, which is responsible for spreading both Anaplasma phagocytophilum and Borrelia burgdorferi, the causative agents of anaplasmosis and Lyme disease. Both diseases are becoming increasingly common and can cause serious illness in humans and animals.
The team discovered that when ATF6 is activated in tick cells, it triggers the production of stomatin, a protein that helps move cholesterol through cells as part of a normal cellular processes. The bacteria exploit this process against their tick hosts, using the cholesterol — which they need to grow and build their own cell membranes but cannot produce themselves — to support their own survival and success.
Stomatin plays a variety of roles in the cell, but one of its key functions is helping shuttle cholesterol to different areas. The bacteria take advantage of this, essentially stealing the cholesterol they need to survive.
Kaylee A. Vosbigian
When the researchers blocked the production of stomatin, restricting the availability of cholesterol, bacterial growth is significantly reduced. The researchers believe this shows targeting the ATF6-stomatin pathway could lead to new methods for interrupting the disease cycle in ticks before transmission occurs.
As part of the study, Vosbigian also developed a new research tool called ArthroQuest, a free, web-based platform hosted by WSU that allows scientists to search the genomes of ticks, mosquitoes, lice, sand flies, mites, fleas and other arthropod vectors for transcription factor binding sites — genetic switches like ATF6 that control gene activity.
There aren’t many tools out there for studying gene regulation in arthropods. Most are built for humans or model species like fruit flies, which are genetically very different from ticks.
Kaylee A. Vosbigian
Using ArthroQuest, the team found that ATF6-regulated control of stomatin appears to be prevalent in blood-feeding arthropods. Since the hijacking of cholesterol and other lipids is common among arthropod-borne pathogens, the researchers suspect many may also exploit ATF6.
We know many other vector-borne pathogens, like Borrelia burgdorferi and the malaria-causing parasite Plasmodium, rely on cholesterol and other lipids from their hosts. So, the fact that this ATF6-stomatin pathway exists in other arthropods could be relevant to a wide range of disease systems.
Assistant Professor Dana K. Shaw, corresponding author.
Department of Veterinary Microbiology and Pathology
College of Veterinary Sciences
Washington State University, Pullman, WA, USA.
Significance
Infection dynamics for tick-borne pathogens like Anaplasma have primarily been studied in mammals. Comparatively less is known about tick–pathogen interactions. We found that Anaplasma activates the stress response receptor, ATF6, in ticks. Activated ATF6 functions as a transcriptional regulator. Using a custom script in R, we identified stomatin as an ATF6-regulated target that supports Anaplasma by modulating cholesterol trafficking. Our custom tool “ArthroQuest” revealed that the ATF6-regulated nature of stomatin is unique to arthropods. Given that lipid hijacking is common among arthropod-borne microbes, ATF6-mediated induction of stomatin may be exploited in many vector–pathogen relationships. In addition, our findings predict that there are many ATF6-regulated genes unique to ticks, highlighting that there is still much to be uncovered.
Abstract
How tick-borne pathogens interact with their hosts has been primarily studied in vertebrates where disease is observed. Comparatively less is known about pathogen interactions within the tick. Here, we report that Ixodes scapularis ticks infected with either Anaplasma phagocytophilum (causative agent of anaplasmosis) or Borrelia burgdorferi (causative agent of Lyme disease) show activation of the ATF6 branch of the unfolded protein response (UPR). Disabling ATF6 functionally restricts pathogen survival in ticks. When stimulated, ATF6 functions as a transcription factor, but is the least understood out of the three UPR pathways. To interrogate the Ixodes ATF6 transcriptional network, we developed a custom R script to query tick promoter sequences. This revealed stomatin as a potential gene target, which has roles in lipid homeostasis and vesical transport. Ixodes stomatin was experimentally validated as a bona fide ATF6-regulated gene through luciferase reporter assays, pharmacological activators, RNA interference transcriptional repression, and immunofluorescence microscopy. Silencing stomatin decreased A. phagocytophilum colonization in Ixodes and disrupted cholesterol dynamics in tick cells. Furthermore, blocking stomatin restricted cholesterol availability to the bacterium, thereby inhibiting growth and survival. Taken together, we have identified the Ixodes ATF6 pathway as a contributor to vector competence through Stomatin-regulated cholesterol homeostasis. Moreover, our custom, web-based transcription factor binding site search tool “ArthroQuest” revealed that the ATF6-regulated nature of stomatin is unique to blood-feeding arthropods. Collectively, these findings highlight the importance of studying fundamental processes in nonmodel organisms.
The North American deer tick, Ixodes scapularis, can transmit up to seven different pathogens that impact human and animal health including Anaplasma phagocytophilum (causative agent of anaplasmosis) and Borrelia burgdorferi (causative agent of Lyme disease) (1). The continuous rise in reported cases of tick-borne disease (2–10) underscores the need for novel intervention strategies. Although the intricacies of mammalian host–pathogen interactions have been well studied, comparatively little is known about tick–pathogen interactions.
Recently we have shown that A. phagocytophilum and B. burgdorferi activate the unfolded protein response (UPR) in ticks, which influences microbial colonization and persistence in the arthropod (11, 12). The UPR is a cellular response network that is initiated by three endoplasmic reticulum (ER) transmembrane receptors IRE1α, PERK, and ATF6. Each branch of the UPR initiates a signaling cascade and coordinates gene expression networks by activating specific transcription factors. We have shown that the IRE1α-TRAF2 pathway leads to microbe-restricting immune responses in arthropods by activating the NF-κB-like molecule, Relish (11). We have also demonstrated that stimulating PERK activates the antioxidant transcription factor, Nrf2, which facilitates pathogen persistence in ticks (12). Out of the three UPR receptors, ATF6 is the least understood (13). When activated, site-1 and site-2 proteases cleave the cytosolic portion of ATF6, which allows it to translocate to the nucleus and act as a transcriptional regulator (nATF6) (14). The role of ATF6 has never been explored in arthropod vectors.
Here, we demonstrate that Ixodes ATF6 is activated by tick-borne pathogens and supports A. phagocytophilum colonization in ticks. To determine how ATF6 impacts vector competence, we used protein modeling and a custom transcription factor binding site query to probe the ATF6 regulatory network in I. scapularis. Gene ontology (GO) and Reactome analyses identified Stomatin, a lipid homeostasis and vesical transport protein, as a potential gene regulated by ATF6 in ticks. Using pharmacological manipulations, RNA interference (RNAi), quantitative fluorescent assays, and immunofluorescence microscopy, we found that Stomatin supports pathogen colonization in ticks by facilitating cholesterol acquisition by the bacterium. These findings demonstrate that stomatin is induced during the arthropod-phase of the pathogen life cycle to enable survival and persistence in the vector.
Programs that predict transcription factor regulatory networks are generally restricted to model organisms, leaving out many arthropod vectors. We used our custom R script to develop a publicly available, web-based tool termed “ArthroQuest” that currently allows users to query 20 different arthropod vector genomes, in addition to Drosophila and humans. Queries with ArthroQuest revealed that the ATF6-regulated nature of stomatin appears to be unique to arthropods. Given that lipid hijacking and cholesterol incorporation is common in many arthropod-borne microbes (15), ATF6-mediated induction of stomatin may be a shared phenomenon among many vector–pathogen relationships that is exploited for the survival and persistence of transmissible pathogens.
This discovery poses a significant problem for proponents of Intelligent Design (ID) creationism because it challenges one of their core assertions: that complex specified information (CSI) within genetic material is a reliable indicator of an intelligent, purposeful designer. If we accept this premise, then we are compelled to ask why such intelligence would devote itself to crafting mechanisms that cause suffering, disease, and death—such as the ability of Anaplasma to hijack tick cell defences and ensure its own propagation at the expense of both ticks and mammalian hosts, including humans.
The usual ID response is to insist that their designer is benevolent — typically equated with the God of the Bible. But here, we are faced with a biological system so well-adapted to spreading infection that it must either be acknowledged as a product of evolutionary processes or attributed to a designer with malevolent intent. This is not a fringe example; it is one of many cases where nature reveals a level of intricate adaptation that ID advocates would normally cite as evidence for design, were it not so profoundly disturbing.
What this ultimately reveals is the theological inconsistency at the heart of ID creationism. The refusal to acknowledge the explanatory power of evolution, even when confronted with examples like Anaplasma, indicates that ID is not a scientific theory but a religious or ideological stance. The selective application of their own criteria — applauding "design" in butterflies but ignoring it in parasites — exposes the intellectual dishonesty behind the movement. Evolution, by contrast, provides a consistent and naturalistic framework that explains both the beautiful and the brutal features of the living world — without invoking a morally compromised designer.
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This book presents the reader with multiple examples of why, even if we accept Creationism's putative intelligent designer, any such entity can only be regarded as malevolent, designing ever-more ingenious ways to make life difficult for living things, including humans, for no other reason than the sheer pleasure of doing so. This putative creator has also given other creatures much better things like immune systems, eyesight and ability to regenerate limbs that it could have given to all its creation, including humans, but chose not to. This book will leave creationists with the dilemma of explaining why evolution by natural selection is the only plausible explanation for so many nasty little parasites that doesn't leave their creator looking like an ingenious, sadistic, misanthropic, malevolence finding ever more ways to increase pain and suffering in the world, and not the omnibenevolent, maximally good god that Creationists of all Abrahamic religions believe created everything. As with a previous book by this author, "The Unintelligent Designer: Refuting the Intelligent Design Hoax", this book comprehensively refutes any notion of intelligent design by anything resembling a loving, intelligent and maximally good god. Such evil could not exist in a universe created by such a god. Evil exists, therefore a maximally good, all-knowing, all-loving god does not.
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The Unintelligent Designer: Refuting The Intelligent Design Hoax
ID is not a problem for science; rather science is a problem for ID. This book shows why. It exposes the fallacy of Intelligent Design by showing that, when examined in detail, biological systems are anything but intelligently designed. They show no signs of a plan and are quite ludicrously complex for whatever can be described as a purpose. The Intelligent Design movement relies on almost total ignorance of biological science and seemingly limitless credulity in its target marks. Its only real appeal appears to be to those who find science too difficult or too much trouble to learn yet want their opinions to be regarded as at least as important as those of scientists and experts in their fields.
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According to creationists, humans are the designer’s special creation, and the Universe, Earth, and all life upon it were created solely for our benefit.
If that were the case, one might reasonably expect human design to be uniquely perfect—free from disease and physical defects. Yet, paradoxically, we are more prone to cancer than our closest evolutionary relatives, the other great apes. Recent research from the UC Davis Comprehensive Cancer Center suggests that this heightened cancer susceptibility may be linked to the very mutation that enabled us to develop our comparatively large brains.
The theory of evolution, of course, precisely predicts these kinds of suboptimal trade-offs and their consequences. As an undirected, uncaring process, evolution is concerned solely with reproductive success—not with long-term health, perfection, or ideal design.
Intelligent (sic) Design creationists have painted themselves into a corner.
Two of their most prominent arguments—irreducible complexity (Michael J. Behe) and complex specified information (William A. Dembski)—are intended to demonstrate the involvement of an intelligent designer in the natural world. But when these same criteria are applied to harmful parasitic organisms, such as the common herpesvirus (cytomegalovirus), which is the leading infectious cause of birth defects in the United States, the implication is that this virus too is the product of intentional design by the same creator that ID proponents insist is responsible for all life.
Within the framework of Intelligent Design creationism, the conclusion is inescapable: their designer deity—typically equated with the omniscient, omnibenevolent god of the Christian Bible—knowingly and deliberately created a pathogen that causes immense suffering. If ID logic is followed consistently, their deity is not a benevolent creator but a malevolent force that engineers disease and deformity with full foreknowledge of the consequences.
The only escape from this theological and philosophical bind is for ID creationists to refute their own criteria—to claim that irreducible complexity and complex specified information are compelling proof of design when found in beneficial biological systems, but somehow irrelevant or invalid when found in destructive pathogens. In doing so, they are forced to hold two mutually exclusive beliefs simultaneously.
In reality, these hallmarks of design touted by ID advocates are common outcomes of natural evolutionary processes — especially arms races between host defences and parasitic invaders. These processes are inherently unguided and wasteful, which in itself refutes the idea of intelligent planning.
Another striking example of this evolutionary struggle has just been published in Nature Microbiology by researchers from the University of Pittsburgh School of Medicine and the La Jolla Institute for Immunology. Their study sheds light on how the herpesvirus has evolved sophisticated strategies to evade the immune system — a feature that ID logic would classify as evidence of "design."
The human genome compacted inside cells eight hours after infection.
Credit: Esther González Almela and Álvaro Castells García
(Top) Cropped representative STORM-PAINT images of EdC-AF647 labeled hDNA (magenta), immunolabeled H3 (green), and their merge in mock and HSV-1 infected A549 cells. Scale bar: 2 µm. (Bottom) Zoomed-in regions are shown inside yellow boxes. Scale bar: 200 nm.
One of the many problems with Intelligent Design (ID) creationism is its complete failure to account for evolutionary arms races.
According to leading ID proponents like William A. Dembski and Michael J. Behe, living organisms and their parasites — including viruses — must have been intelligently designed because they are supposedly “irreducibly complex” and exhibit “complex specified information”. But if that were true, it would mean the same designer is deliberately crafting both parasites and the defence mechanisms their hosts use to fend them off — hardly the mark of a supremely intelligent creator.
A further problem, and one that creationists prefer to ignore, is theological: designing pathogens like viruses is fundamentally incompatible with the notion of a benevolent creator. In fact, it suggests a malevolent intelligence — one more concerned with maximising suffering than promoting life and maximising happiness. So, when science uncovers yet another example of a virus behaving with surgical precision and apparent ingenuity, ID creationists find themselves in a bind. Is irreducible complexity and complex specified genetic information not evidence of intelligent design after all? Or must they admit that the designer is, at best, morally indifferent — or worse, actively malevolent?
The latest headache for the ID camp comes courtesy of the Herpes simplex virus — the one responsible for cold sores. Researchers at the Centre for Genomic Regulation (CRG) in Barcelona, Catalunya, Spain, with colleagues in Guangdong Provincial People’s Hospital, Guangdong, China, have discovered that the virus can radically reorganise a host cell’s genetic architecture — and it does so using the host's own cellular machinery. Their findings have just been published open access in Nature Communications.
Hot on the heels of the news that the putative intelligent designer behind creationism apparently devised a method to prevent the spread of cancer cells through the body—then handed it to the sea cucumber, a group of species not especially prone to cancer—comes another remarkable revelation.
It now appears that this same designer, if we accept the claims of ID creationists, has also developed a highly effective mechanism for disabling the SARS-CoV-2 virus that causes COVID-19. And once again, rather than bestowing this gift upon humans, the species most affected by the virus, the designer gave it to llamas — creatures not exactly known for their vulnerability to coronaviruses.
The mechanism in question involves relatively simple molecules known as single-domain antibodies, or VHHs—also referred to as nanobodies. These are much smaller than the conventional antibodies produced by most animals, including humans. They work by binding tightly to the virus’s spike proteins, effectively neutralising it by preventing it from prising open host cells and initiating infection. Even more impressively, these nanobodies appear to be broadly effective against a wide range of SARS-related coronaviruses.
While creationists might marvel at the ingenuity of such a designer, they would be hard-pressed to explain — or more likely, would simply ignore — why this supposedly anthropophilic intelligence chose not to equip humans with such a defence. Instead, it stood idly by as millions suffered and economies collapsed, despite having the ‘cure’ readily available.
This unique llama-specific mechanism was discovered by a team of researchers led by Prof. Xavier Saelens and Dr. Bert Schepens at the Flemish Institute for Biotechnology (Vlaams Instituut voor Biotechnologie) – University of Ghent (VIB-UGent) Center for Medical Biotechnology.
