Malevolent Designer News - How A Bacterium Is 'Intelligently Designed' To Spread Disease

Blacklegged tick, Ixodes scapularis

Bacteria hijack tick cell defenses to spread disease | WSU Insider

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.

This discovery was made by researchers at the College of Veterinary Medicine, Washington State University (WSU). Their findings have just been published in Proceedings of the National Academy of Sciences (PNAS) and are explained in lay terms in WSU Insider, the university's online news outlet.

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.

1. 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).
   
   
2. Disease in Humans
   • Caused mainly by Anaplasma phagocytophilum.
   • Known as Human Granulocytic Anaplasmosis (HGA).
   • Symptoms include:
     • Fever, chills, headache
     • Muscle aches
     • Malaise
     • Occasionally gastrointestinal symptoms (nausea, vomiting)
     • 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.
   
   
3. 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.
   
   
4. 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.
   
   
5. 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.
   
   
6. 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 disease

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Washington 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.

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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.

Publication:

K.A. Vosbigian,S.J. Wright,B.P. Steiert,K.L. Rosche,E.A. Fisk,E. Ramirez-Zepp,J.M. Park,E.A. Shelden,& D.K. Shaw
ATF6 enables pathogen infection in ticks by inducing stomatin and altering cholesterol dynamics
Proc. Natl. Acad. Sci. U.S.A. 122 (25) e2501045122, https://doi.org/10.1073/pnas.2501045122 (2025).

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.

K.A. Vosbigian,S.J. Wright,B.P. Steiert,K.L. Rosche,E.A. Fisk,E. Ramirez-Zepp,J.M. Park,E.A. Shelden,& D.K. Shaw
ATF6 enables pathogen infection in ticks by inducing stomatin and altering cholesterol dynamics
Proc. Natl. Acad. Sci. U.S.A. 122 (25) e2501045122, https://doi.org/10.1073/pnas.2501045122 (2025).

Copyright: ©2025 The authors.
Published by the National Academy of Sciences of the USA. Open access.
Reprinted under a Creative Commons Attribution 4.0 International license (CC BY 4.0)

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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The Malevolent Designer: Why Nature's God is Not Good

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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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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Malevolent Designer - How A Common Virus Sneaks Past Our Immune System And Causes Birth Defects

Scientists Uncover How a Common Herpes Virus Outsmarts the Immune System | School of Medicine | University of Pittsburgh.

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."

Refuting Creationism - Co-Evolution of Humans and Influenza Viruses - Just as the TOE Predicts

AI-generated image (ChatGPT4o)

H3N2 virus is a respiratory viral infection of the influenza A virus.

Large-scale immunity profiling grants insights into flu virus evolution | For the press | eLife

In a striking confirmation of evolutionary theory—and a clear rebuttal of several fundamental creationist claims—scientists have demonstrated a close correlation between population-level immunity and the evolution of influenza viruses to evade that immunity. The findings, reported in eLife, align perfectly with predictions made by evolutionary biology: as the immune landscape of a population shifts, so too does the genetic makeup of viruses in an ongoing evolutionary arms race.

Disappointingly for creationists hoping for signs that biomedical science is abandoning evolution in favour of supernatural explanations, there is no such evidence. Nowhere in the study is there a hint that scientists are retreating from evolutionary principles or embracing a non-falsifiable belief system involving mysterious, unexplained entities. On the contrary, the researchers are clear and unequivocal: their results reinforce the view that viral evolution is a dynamic, adaptive process shaped by natural selection in response to host immunity.

Even more troubling for proponents of Intelligent Design (ID) is the unavoidable implication that the viral mutations observed in this study constitute what William A. Dembski calls "complex specified information"—which he argues can only arise through the intervention of an intelligent designer. If one follows that line of reasoning, the logical (if deeply uncomfortable) conclusion is that this designer is actively modifying viruses to undermine the very immune systems it supposedly created to protect us. Such behaviour can hardly be described as intelligent and is incompatible with the benevolent deity so often associated with the Intelligent Design movement.

Malevolent Design - The Sneaky Way TB Keeps On Making Us Sick

Credit: Md Ariful Islam

Study discovers DNA switch that controls TB growth – and could help unlock its antibiotic resistance secrets | University of Surrey

If you're an omniscient, omnipotent, malevolent designer of parasites — such as the bacterium that causes tuberculosis in humans — then you're hardly going to let a little thing like the immune system (which you supposedly also designed to protect them) or even the development of medical science and antibiotics spoil your fun in causing random suffering, are you? Naturally, you'd equip your creation with mechanisms to overcome these obstacles.

Within the framework of Intelligent Design creationism, that's precisely what this recent discovery should look like — at least to those creationists who don't simply ignore the obvious and pretend it isn't there. Scientists from the Universities of Surrey and Oxford have discovered that Mycobacterium tuberculosis uses a reversible process known as ADP-ribosylation to modify its DNA, controlling both replication and gene expression. This allows the bacterium to remain dormant for extended periods and reactivate when environmental threats, such as immune responses or antibiotics, have passed.

This presents a problem for creationists who insist on believing in a benevolent creator deity and simultaneously hold that features such as irreducible complexity and complex specified information are sure signs of intelligent design—claims promoted by Discovery Institute fellows Michael J. Behe and William A. Dembski. Since Mycobacterium tuberculosis displays these very characteristics, so either it was designed specifically to cause suffering, or those characteristics are not the reliable indicators of divine design that Behe and Dembski claim, and their entire argument collapses.

This discovery was recently published open access in The EMBO Journal, and further details are available in the University of Surrey press release:

Malevolent Design - How Creationism's Divine Malevolence is Helping Cholera Win An Arms Race Against A Virus

How cholera bacteria outsmart viruses - EPFL

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.

Adams, D.W., Jaskólska, M., Lemopoulos, A. et al. (2025).

Biological arms races represent one of those problematic areas in biology that Intelligent Design (ID) creationists tend to avoid — precisely because they undermine the notion of a single, supreme intelligence orchestrating the design of all living organisms. These arms races typically occur in predator–prey or parasite–host relationships, where the survival of one party depends on improving its ability to evade, resist, or defend against the other — while the other evolves countermeasures to overcome those defences. From the standpoint of a single, omniscient designer, this results in a paradox: today’s ‘solution’ to a problem becomes tomorrow’s new problem to be solved. Where, exactly, is the intelligence in that?

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.

Malevolent Designer News - How Monkeypox Is Being Redesigned to Infect More People

Mpox could become a serious global threat, scientists warn | University of Surrey

Science has just dealt creationism another body blow.

Researchers from the University of Surrey, UK, have demonstrated that the monkeypox virus has undergone a mutation that enhances its ability to spread more readily from person to person through direct contact. This increased transmissibility raises the concern of a potential global pandemic.

Since this mutation confers a benefit to the virus, it aligns with William A. Dembski's concept of 'specified complexity', which he uses to argue for intelligent design. By extension, Dembski’s argument suggests evidence of an intelligent designer, whom his intended audience typically identifies as the Christian God.

However, because the mutation has resulted in a greater prevalence of the mutated form of the virus compared to non-mutated forms, this clearly demonstrates evolution through natural selection. Consequently, it contradicts the notion of 'devolution' proposed by Michael J. Behe, who suggests that parasites and pathogens represent biological deterioration rather than adaptive evolution.

Therefore, the new variant of the monkeypox virus presents either evidence supporting creationism's deity — which would imply intentional creation of viruses specifically designed to cause illness—or clear evidence supporting evolution through natural selection.

Refuting Creationism - Students Discover How The Mammalian Immune System Evolved.

Nebraska undergrads uncover ancient secrets of human immunity | Nebraska Today

(C–F) Expanded views of the interaction interface between STAT2 CCD and IRF9 IAD for mouse (C), human (D), Hypanus sabinus (E), and Stegostoma tigrinum (F). The interactions are observed in the crystal structure of the mouse STAT2-IRF9 complex (PDB ID: 5OEN) [19.1]. For humans and the two cartilaginous fishes, the interactions are based on the modeled structures of the STAT2-IRF9 complex. The key residues involved in the interface are labeled. The phenylalanine (F) on the STAT2 protein is colored in green. The four residues forming the cleft on the IRF9 protein are colored in magenta. The corresponding sequences of the interface area and other details are found in Supporting Information S1: Figure S3.

Recent research conducted by undergraduate students at the University of Nebraska–Lincoln has provided compelling insights into the evolutionary development of the human immune system. Under the guidance of Professor Luwen Zhang, students Vanessa Hubing, Avery Marquis, and Chanasei Ziemann co-authored two significant studies published in the Journal of Medical Virology. Their work elucidates the progression of immune regulatory mechanisms in vertebrates, highlighting the transition to more complex systems with the evolution of jaws. Additionally, they explored how a pseudogene, potentially introduced into primate DNA via a retrovirus approximately 60 million years ago, may have enhanced ancestral immune responses.

These findings offer robust evidence supporting the theory of evolution by demonstrating the gradual and adaptive changes in genetic material that have led to sophisticated immune functions in humans. The identification of a pseudogene's integration into primate DNA and its subsequent role in immunity exemplifies natural selection's influence on genetic composition over millions of years. Such evidence challenges creationist perspectives by providing concrete examples of evolutionary processes shaping complex biological systems, underscoring the dynamic nature of genetic evolution in response to environmental pressures.

During the course of evolution, these factors have evolved as additional layers of complexity to improve and refine a system which, as the product of an unplanned, utilitarian evolutionary process was a suboptimal compromise between the tendencies to over-react to some infections and fail to respond to others. An intelligently-designed sytem would need no such regulatory mechanisms. This is how we can tell that such overly-complex systems were not intelligently designed.

Malevolent Designer News - How C. difficile is Designed to Kill Off Competition in Our Gut

C. diff uses toxic compound to fuel growth advantage VUMC News

Like all organisms, and particularly pathogenic parasites that colonise our intestines, Clostridioides difficile (C. diff) must compete with other organisms for nutrients. This competition inevitably fuels evolutionary arms races.

For devotees of creationism’s ‘intelligent designer’, C. diff might appear to be a cunning response to medical science's successful use of antibiotics against bacterial pathogens. This is because C. diff is equipped with multiple antibiotic-resistance genes, allowing it to thrive in hospital environments. It often infects patients who are already vulnerable due to other health conditions or compromised immunity, making it a significant medical challenge.

Furthermore, if one follows William A. Dembski's reasoning, the ‘complex specified information’ in C. diff’s genome, which grants it a competitive edge, must logically be attributed to an intelligent designer. Michael J. Behe’s attempt to absolve his version of an intelligent designer by blaming ‘sin’, ‘genetic entropy’, or alleged ‘devolution’ fails here. A mutation that clearly provides an adaptive advantage cannot logically be termed a ‘devolution’ from a supposedly more ‘perfect’ ancestral state.

If creationism’s intelligent designer intended to kick people when they were down, it could hardly have done better than designing C. diff.

How C. diff competes for resource in our gut by waging chemical warfare against the other gut biota is the subject of a paper in the journal Cell Host & Microbe by researchers at Vanderbilt University Medical Center (VUMC). Their findings are described in VUMC News:

Refuting Creationism - How Chimpanzees Have Evolved For Different Parasites, Including Malaria

Mother and baby chimpanzee in Uganda.

Kevin Langergraber, The Ngogo Chimpanzee Project.

Chimpanzees are genetically adapted to local habitats and infections such as malaria | UCL News - UCL – University College London

It can't be easy making a living as a creationist grifter when science continually undermines your claims, exposing your misrepresentation of evolutionary biology and eroding your credibility — even among the faithful supporters you count on to pay for confirmation of their biases. It must be a relief that your target will rarely, if ever fact check your claims, making them easy victims of your disinformation.

So, you can take comfort in the fact that none of your marks will read this piece of research that shows how chimpanzees are closely related to humans and have evolved over time to adapt to a number of different environments, much the way the ancestors of modern humans adapted when their environment changed from forest to savannah, some 6 million years ago.

Included in the study is how chimpanzees, who have been suffering from malaria for much longer than humans, humans having acquired their most deadly species of the plasmodium parasites from chimpanzees only some 300,000 years ago and possibly as recently as 50,000 years ago, have evolved resistance to the parasite so they now show almost no signs of infection.

Malevolent Designer News - How Tuberculosis Is Protected During Airborne Transmission

This article is best read on a laptop, desktop, or tablet

Scientists have discovered a family of genes that becomes essential for survival specifically when the tuberculosis pathogen is exposed to the air, likely protecting the bacterium during its flight.

Image: iStock; MIT News.

Study: Tuberculosis relies on protective genes during airborne transmission | MIT News | Massachusetts Institute of Technology

Imagine you're the designer of a nasty little pathogen that is designed to make people sick and die, but you have a problem. The organism needs to get from one victim to the next in order to spread and make as many people sick as possible, but, as an obligate pathogen, it is designed to life in the moist warm interior of its victims, so is not very good at living outside, where it needs to be, if only briefly, to get into its next victim.

Quite a problem, eh?

But not something beyond creationism's divine malevolence, it seems, because, if you accept creationists' argument for the moment, the parasitic organism that causes tuberculosis is specially designed to survive while in transit, so to speak.

Exactly how it does it has recently been discovered by researchers at the Massachusetts Institute of Technology (MIT) and their collaborators. The key to its survival is a family of genes that were previously believed to be non-essential because they had no effect when injected into a potential host but have now been shown to be essential for survival outside a host's body.

Malevolent Designer News - How a Fungus Makes Its Host Destroy Its Own Brain

Beauveria bassiana on unidentified insect.

© Lisa Bennett (CC-BY 4.0)

Fungus ‘hacks’ natural immune system causing neurodegeneration in fruit flies - University of Birmingham

If we are to believe creationists, their god created insects such as fruit flies, Colorado beetles, etc., and then set about devising ways to kill them with, amongst other pathogens, fungi that infect them and destroy them from inside.

One of the problems this supposedly intelligent designer had to overcome was the immune system it had given the insects in order to protect them from the pathogens it was designing to kill them.

According to an open access paper just published in PLOS Biology by a team led by Professor Alicia Hidalgo from School of Biosciences, The University of Birmingham, one species of parasitic fungus, Beauveria bassiana, cleverly turns its host's immune system against its host, making it destroy its own brain. Although this fungus does not affect mammals, so poses no threat to humans, the team warns that it is possible that another fungus could use a similar technique against mammals, including humans.

Malevolent Design - How Sudan Virus is Cleverly Designed to Kill 50% of Its Victims

Cryo-EM structure of Sudan ebolavirus glycoprotein complexed with its human endosomal receptor NPC1

New Study Reveals How Sudan Virus Binds to Human Cells | Midwest Antiviral Drug Discovery (AViDD) Center

It's shaping up to be a thrilling month for devotees of creationism's divine malevolence as science finds out just how brilliantly its nasty little parasites are designed to make us sick and increase the suffering in the world, although quite why any normal person would worship a hate-filled sadistic psychopath is even more of a mystery than the mechanism by which it designs and creates organisms.

The latest is the details of how the Sudan virus (a variant of Ebola with a 50% 'success' rate in terms of deaths of its victims) has an improved method of binding to our cells to gain entry and start the killing process. Like Ebola, it binds to receptors on the cell surface, but because it has just 4 different amino acids in its coat proteins, it binds much more efficiently - a factor which probably contributes to its high kill rate.

Malevolent Design - How Zika Is Designed to Spread Maximum Suffering.

Zika manipulates the skin to make it more attractive to mosquitoes

Illustration of Zika virus in blood

Kateryna Kon/Science Photo Library

Zika uses human skin as ‘mosquito magnet’ to spread virus further | LSTM

January was something of a joyous month for devotees of creationism's divine malevolence. Following closely behind the news of how it brilliantly designed HIV to use our cells defences against us so making it better at infecting and killing us, we have news of another breathtakingly brilliant design of a nasty little pathogen - the zika virus that causes microcephaly in children if their mothers become infected during pregnancy.

This news is that it turns our skin into a living 'magnet' to attract the vector that spreads it - mosquitos - so ensuring it gets transmitted to as many victims as possible. It does it by altering a gene and protein expression in dermal fibroblasts, causing the skin to produce odours that are attractive to mosquitoes. In effect, calling them to come and feed.

Before creationists start bleating unscientific and biologically non-sensical nonsense about 'genetic entropy' and devolution allowed by 'sin' I should point out that no mutation that conveys a benefit on an organism can be regarded as 'devolutionary'. It is classic evolution by natural selection. And, as per William Dembski's gibberish about 'specified complexity', any complex DNA or RNA sequence that codes for a specific function must be regarded as 'specified complexity', using his argument, so must have been specified by a magic designer, according to his misuse of statistics and probability. Or perhaps a creationist could explain why such a highly specific function of converting a human gene to make special mosquito-attracting scents, is not an example of Dembski's 'specified complexity'.

So, how was this, in creationist terms, intelligently designed virus, discovered to have this touch of brilliance in its design? That was the result if a new study by an international team led by Liverpool School of Tropical Medicine. Their findings are published, open access, in Communications Biology.

Malevolent Design - The Sneak Tactics of Toxoplasma gondii

Toxoplasma gondii.

Image by Michael Holmes

Toxoplasma gondii parasite uses unconventional method to make proteins for evasion of drug treatment

Here we are with yet another example of an organism that, if there is a designer behind it, that designer can only be described as malevolent and determined to maximise the suffering and misery in the world.

It is, of course, another example of a nasty little parasite which, if you subscribe to the creationist view that complexity 'proves' design, has been designed to ensure we are as vulnerable to is as possible by helping it evade the immune system and other mechanisms, supposedly designed by the same designer god to protect us from the parasites it designs to harm us.

This example is the parasite Toxoplasma gondii, which is notorious for manipulating its natural victims, which are felines and their prey species. For example, mice infected with T. gondii lose their fear of cats so they get eten and the parasite gets into its primary host; infected chimpanzees develop a liking for the smell of leopard urine.

Humans are not the natural secondary host, but the parasite readily infects us as we catch it from cats. It is thought that about one third of humans are infected. Once infected it is impossible to get rid of from the body because, even if antibodies are produced by our immune system, the parasites go into a dormant state as cysts which can form in any organs of the body, including the brain.

Malevolent Design - How Malaria Is Being Redesigned to Keep On Killing Children

Photomicrograph of a blood smear contains a macro- and microgametocyte of the Plasmodium falciparum parasite

Photo Credit: CDC/Dr. Mae Melvin - This media comes from the Centers for Disease Control and Prevention's Public Health Image Library (PHIL) #2704, Public Domain, Link

Study uncovers first evidence of resistance to standard malaria treatment in African children with severe malaria

In another twist of the arms race with human medical science Plasmodium falciparum, the malevolently designed parasite that causes malaria and kills hundreds of thousands of children a year, mostly in Africa, has developed resistance to Artemisinin. Scientists were already aware that resistance had arisen in cases of uncomplicated malaria, but this is the first such incidence of resistance in the more severe form of the disease.

Indiana University School of Medicine researchers, in collaboration with colleagues at Makerere University in Uganda have discovered a case of complicated malaria in a child in Uganda.

Mallevolent Design - How Salmonella Sneaks Past Our Defences To Make Us Sick

Salmonella infects the small intestine and alters the colon environment

Intestinal lumen

New study shows how salmonella tricks gut defenses to cause infection

There is a simple paradox at the heart of creationism that I have never even seen an attempt to resolve. It all comes from two beliefs: there is only one designer god capable of designing living organisms and that designer god designed us complete with our immune system with which we can attempt to resist attack by pathogens, and that pathogens are not the work of this design, but are the result of 'genetic entropy' and 'devolution' since Adam & Eve let 'sin' into the world. The fact that Michael J. Behe, who invented that excuse, has let slip that ID Creationism is Bible literalism in a lab coat seems to be lost on his followers who still dutifully insist that it is a scientific alternative to evolution and should be taught in school science class (presumably now with the tale of Adam & Eve taught as real history and 'sin' as a real force in science).

The paradox is, did the designer god give Adam & Eve an immune system, or did it design an upgrade when 'sin' allowed pathogens to exist? If the former, it was anticipating and planning for the so-called 'fall'; if the latter, it lacked foresight so is not omniscient.

But however creationists resolve this paradox they still have to explain why the 'intelligently designed' immune system doesn't work very well and why whatever is designing pathogens seems to be able to overcome it.

The nonsense about 'sin', 'the fall', etc., is trivially easy to refute because any improvement in a parasite's ability to parasitise its host can't possibly be regarded as a devolution from some assumed initial perfection because an improvement can't be worse that what it's an improvement on. The whole nonsense of 'devolution' is biological gobbledygook, intelligently designed to appeal to scientifically illiterate simpletons who want to fit the Bible superstition somewhere in the reasoning without bothering too much about the logic or the biology.

So, the paradox boils down to why an intelligent designer would be having an arms race with itself so the parasites it creates can continue to parasitise the victims it creates complete with their immune system it created to stop them. Creationists normally flee in terror at the mere mention of arms races, which is why you'll never see them discussed in the cult literature apart from where pathogens are waved aside as 'caused by sin', blah, blah, blah...
So, it would be refreshing indeed to see a genuine attempt by an intelligent design creationist try to give some rational explanation, and hopefully without giving away the fact that ID creationism is merely Christian fundamentalism in disguise, for the discovery by a new UC Davis Health study that shows how the Salmonella bacteria, a major cause of food poisoning, can invade the gut even when protective bacteria are present.

As an added embarrassment for creationists, Salmonella is closely related to Escherichia coli (E.coli) that they usually cite Michael J. Behe as 'proving' it must have been designed by their god because its flagellum is 'irreducibly complex'.

First a little AI background information about Salmonella, where it came from and what it does to us: