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.

Tell me what you know about the monkeypox virus, its probable evolution and how it has evolved the ability to be passed from human to human. Monkeypox virus is a zoonotic pathogen belonging to the Orthopoxvirus genus, closely related to viruses such as smallpox (Variola virus). Originally identified in monkeys in 1958, the virus primarily infects rodents and other mammals in central and western Africa, occasionally transmitting to humans.

Virus Evolution and Transmission:

Historically, monkeypox outbreaks were relatively small and confined to rural African communities, primarily due to animal-to-human (zoonotic) transmission. However, recent outbreaks, particularly since 2022, have shown increased human-to-human transmission, indicating adaptive evolutionary changes.

Mechanisms of Evolution and Adaptation:

The monkeypox virus, like other viruses, evolves through mutations occurring during viral replication. These mutations are random, but natural selection favours variants that enhance the virus's ability to infect, replicate, and transmit between hosts. Mutations that facilitate greater transmissibility, replication efficiency, or immune evasion become more prevalent over time.

Recent Developments in Human Transmission:

Researchers have observed recent mutations in monkeypox that enhance its ability to spread between humans, primarily via prolonged direct contact, including skin-to-skin contact and contact with contaminated materials (e.g., bedding, clothing). Studies have identified genetic changes affecting virus surface proteins that interact with host cells, potentially improving the virus's ability to infect human cells and spread more efficiently.

Implications for Human Health:

Enhanced human-to-human transmissibility significantly raises public health concerns, as outbreaks can spread more quickly, potentially escalating into broader epidemics or pandemics. The recent international spread of monkeypox underscores the adaptive capacity of the virus and highlights the importance of surveillance, prompt containment measures, and targeted vaccination strategies.

Evolutionary Context:

The evolution of monkeypox toward improved human transmissibility exemplifies classic evolutionary principles:

• Mutation: Genetic variants arise randomly during viral replication.
• Natural Selection: Mutations beneficial to the virus (e.g., increased transmissibility) become dominant.
• Adaptation to Host Species: As viruses encounter new hosts (humans, in this case), selective pressure favours adaptations enhancing human infection and transmission.

In summary, the monkeypox virus exemplifies the evolutionary mechanisms of mutation and natural selection, demonstrating clearly how pathogens evolve enhanced capabilities for transmission, particularly when adapting to a new host species such as humans.

The Surrey University team have just published their findings in the journal Nature Medicine and explain it in a Surrey University news item:

Mpox could become a serious global threat, scientists warn

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Mpox has the potential to become a significant global health threat if taken too lightly, according to scientists at the University of Surrey.

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In a letter published in Nature Medicine, researchers highlight how mpox – traditionally spread from animals to humans – is now showing clear signs of sustained human-to-human transmission.

Mpox is a viral infection caused by a virus that belongs to the same family as smallpox. The virus can cause a painful rash, fever, and swollen glands and, in some cases, lead to more serious illness. Mpox usually spreads through close contact with an infected person or animal.

The most recent outbreaks show that intimate contact is now a significant way the virus spreads. That shift in how it’s transmitted is leading to longer transmission chains and lasting outbreaks.

Professor Dr Carlos Maluquer de Motes, lead author
Department of Microbial Sciences
University of Surrey, Guildford, UK.

The article notes that this change coincided with the rapid spread of clade IIb (a clade is a group of viruses that share a common ancestor) mpox viruses, but different clade I variants are now on the rise too. Researchers are also concerned because clade I viruses are thought to be more aggressive. These viruses appear to be accumulating specific genetic mutations – driven by enzymes in the human body – that may be changing viral properties, so the longer these viruses circulate amongst us, the higher the chances these mutations help mpox adapt to humans.

Although mpox was once mainly seen in Central Africa, the virus caused an outbreak worldwide in 2022 and is now causing outbreaks in multiple sub-Saharan countries. While it currently affects adults the most, the researchers stress that it has the potential to spread among other groups, including children, a group at greater risk of serious illness – although sustained transmission in children has not yet been reported.

Mpox control has to climb up the global health agenda. We have limited diagnostic tools and even fewer antiviral treatments. We urgently need better surveillance and local or regional capacity to produce what we need – otherwise, we are at risk of future epidemics.

Professor Dr Carlos Maluquer de Motes.

Abstract
The human interaction with mpox has changed across its entire endemic range, revealing the endemic and pandemic risk of monkeypox virus and the current knowledge gaps on its biology that hamper virus control.

Maluquer de Motes, Carlos; Ulaeto, David O.
Mpox poses an ever-increasing epidemic and pandemic risk
Nature Medicine (2025) DOI: 10.1038/s41591-025-03589-8

© 2025 Springer Nature Ltd.
Reprinted under the terms of s60 of the Copyright, Designs and Patents Act 1988.

That must be one of the shortest abstracts ever!

But its brevity does nothing to reduce the significance of this research to intelligent design creationists, who will struggle to explain why their putative intelligent designer is actively redesigning the monkeypox virus to make it better at infecting humans.

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:

Tell me all about Clostridium difficile including its evolutionary origins and pathology in humans. Clostridium difficile(now officially known as Clostridioides difficile) is a Gram-positive, anaerobic, spore-forming bacterium responsible for a range of gastrointestinal diseases collectively known as Clostridioides difficile infection (CDI). It's particularly notable as a healthcare-associated pathogen, often associated with antibiotic use.

Here's a detailed overview covering taxonomy, evolutionary origins, pathology, epidemiology, and treatment:

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Taxonomy and classification

• Kingdom: Bacteria
• Phylum:Bacillota (formerly Firmicutes)
• Class:Clostridia
• Order:Eubacteriales
• Family:Peptostreptococcaceae
• Genus:Clostridioides
• Species:Clostridioides difficile (formerly known as Clostridium difficile)

The reclassification from Clostridium to Clostridioides reflects genomic analyses showing distinct evolutionary divergence.

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Evolutionary origins

• Clostridioides difficile diverged from other members of the Clostridium genus millions of years ago, adapting uniquely to colonise and survive in the mammalian gastrointestinal tract.
• Genomic studies suggest it has undergone significant horizontal gene transfer, acquiring antibiotic resistance genes and virulence factors, enabling rapid adaptation to clinical environments.
• The evolutionary success of C. difficile has been significantly influenced by human activities, particularly widespread antibiotic use, which disrupts normal gut microbiota and creates an ecological niche favouring its growth and pathogenicity.

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Microbiology and transmission

• It is an obligate anaerobe, thriving without oxygen.
• Forms resilient spores that can survive harsh environmental conditions, resisting heat, disinfectants, and drying.
• Transmission is mainly faecal-oral, commonly via contaminated surfaces, healthcare workers’ hands, or medical equipment.
• Often colonises the human gut asymptomatically, especially in infants, though it can turn pathogenic under conditions of microbiota imbalance (dysbiosis).

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Pathogenesis in humans

C. difficile pathogenesis is primarily driven by its two major toxins:

• Toxin A (TcdA): an enterotoxin disrupting intestinal cell integrity, causing fluid secretion, inflammation, and diarrhoea.
• Toxin B (TcdB): a potent cytotoxin causing significant cellular damage and inflammation.

A third toxin, the binary toxin CDT, found in some strains (e.g., epidemic ribotype 027), may enhance virulence but is less consistently expressed.

Disease progression:

1. Antibiotic treatment disrupts normal gut microbiota.
2. Spores of C. difficile germinate into vegetative forms, multiply, and colonise the gut.
3. Toxins damage colonic epithelium, trigger inflammatory responses, and lead to disease manifestation.

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Clinical manifestations

In humans, the clinical spectrum ranges from mild diarrhoea to severe and life-threatening colitis:

• Mild to moderate CDI:Watery diarrhoea, abdominal cramping, fever, loss of appetite, nausea.
• Severe CDI:Profuse diarrhoea, dehydration, severe abdominal pain, pseudomembranous colitis (characteristic formation of pseudomembranes on the colon mucosa), toxic megacolon, bowel perforation, and sepsis, potentially fatal if untreated.

Risk factors include antibiotic exposure, advanced age, prolonged hospital stays, immunocompromise, proton-pump inhibitor usage, and inflammatory bowel disease.

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Epidemiology and public health impact

• CDI is primarily hospital -or healthcare-associated, although community-acquired infections have been increasingly documented.
• Epidemic strains (e.g., ribotype 027, also known as NAP1 or BI) emerged in the early 2000s, demonstrating increased virulence, toxin production, antibiotic resistance, and morbidity/mortality rates.
• Global incidence has been rising, influenced by antibiotic prescription practices and ageing populations, prompting greater vigilance in infection control.

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Diagnosis

• Clinical suspicion (recent antibiotics use, hospitalisation, symptoms) prompts laboratory testing.
• Laboratory tests typically include:
  • Stool toxin assays(enzyme immunoassays, ELISA, PCR for toxin genes)
  • Glutamate dehydrogenase (GDH) antigen testfor rapid screening
  • Culture: Used less frequently due to longer turnaround time, but necessary for strain typing and antibiotic susceptibility.

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Treatment and management

1. Initial management:
   • Discontinue or alter antibiotics that predispose to CDI.
   • Restore fluids and electrolytes.
2. Medical therapies:
   • Oral vancomycin or fidaxomicin:Recommended first-line treatments for severe or recurrent CDI.
   • Metronidazole:Less preferred now due to reduced efficacy, recommended only if vancomycin or fidaxomicin unavailable.
3. Recurrent CDI management:
   • Faecal Microbiota Transplantation (FMT):Restores normal microbiota and has shown high efficacy (>85%) in preventing recurrence.
4. Monoclonal antibodies (Bezlotoxumab):Target toxin B, reducing recurrence risk.
5. Infection control measures:
   • Strict hand hygiene (soap and water preferred over alcohol rub due to spore resistance).
   • Environmental cleaning with sporicidal disinfectants (e.g., chlorine-based agents).

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Prevention and ongoing research

• Improved antibiotic stewardship to reduce CDI risk.
• Ongoing vaccine development aimed at toxin neutralisation.
• Research continues into probiotic formulations and other microbiota-directed therapies for prevention and treatment.

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Summary

• Clostridioides difficile is a rapidly evolving bacterium whose success is closely tied to human interventions, especially antibiotic use.
• Pathogenicity stems from toxin production causing severe inflammation and colonic injury.
• CDI remains a significant public health concern globally, demanding continued attention to prevention, effective treatment protocols, and infection control measures.

Understanding its evolutionary dynamics, microbiology, and host interactions is critical in managing and mitigating its clinical impact.

C. diff uses toxic compound to fuel growth advantage

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The findings of a new research study increase understanding of the molecular drivers of C. diff infection and point to novel therapeutic strategies aimed at a pathogen that causes about half a million infections in the U.S. each year.

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The pathogen C. diff — the most common cause of health care-associated infectious diarrhea — can use a compound that kills the human gut’s resident microbes to survive and grow, giving it a competitive advantage in the infected gut.

A team led by investigators at Vanderbilt University Medical Center has discovered how C. diff (Clostridioides difficile) converts the poisonous compound 4-thiouracil, which could come from foods like broccoli, into a usable nutrient. Their findings, published March 25 in the journal Cell Host & Microbe, increase understanding of the molecular drivers of C. diff infection and point to novel therapeutic strategies.

C. diff causes about half a million infections in the U.S. each year, according to the Centers for Disease Control and Prevention. Factors that increase risk of C. diff infection include antibiotic use, age over 65, and recent stays in hospitals and other health care facilities.

Like other pathogens, C. diff must acquire nutrients to survive and grow.

We’re interested in trying to understand the nutrients that C. diff needs during infection, and how what you eat influences what C. diff eats in your gut.

Matthew Munneke, first author
Department of Pathology, Microbiology, and Immunology
Vanderbilt Institute for Infection, Immunology, and Inflammation
Vanderbilt University Medical Center, Nashville, TN.

The group focused on nucleotides — the building blocks of DNA and RNA — which are a class of nutrients that hasn’t been well studied for C. diff .

The researchers found that C. diff must acquire a certain type of nucleotides (pyrimidines) to cause infection, and they discovered an enzyme they named TudS (thiouracil desulfurase) that C. diff uses to salvage the pyrimidine nucleotide uracil from a related compound: 4-thiouracil.

They showed that 4-thiouracil gets incorporated into RNA and is toxic to resident gut microbes that do not have the TudS enzyme. In C. diff , however, TudS modifies and detoxifies 4-thiouracil, making it available as a nutrient. The researchers demonstrated that TudS contributes to C. diff “fitness” in mice fed 4-thiouracil and in a novel MiniBioreactor model that contains a community of bacteria isolated from human feces with added 4-thiouracil.

We think that 4-thiouracil metabolism is beneficial to C. diff because it acts as a nutrient to fuel the bacteria, and it also may inhibit neighboring bacteria, which would give C. diff a further competitive advantage within the gut environment.

Matthew Munneke

The TudS enzyme may represent a novel therapeutic target for treating C. diff infections. It is not present in many resident gut microbes (or in human cells), so an antimicrobial targeting it to kill C. diff might help preserve the healthy gut microbiota, he noted.

The researchers also showed that adding C. diff TudS to a probiotic strain of E. coli blunted C. diff ’s fitness advantage in an in vitro model.

It might be possible to use a probiotic with this enzyme to diminish C. diff ’s ability to thrive in the gut and push it out.

Matthew Munneke

F
Although the researchers showed that 4-thiouracil is present in the human gut, the source of this compound is unclear. Livestock that consume a diet rich in cruciferous vegetable family members (such as kale and other leafy greens, broccoli and cauliflower) have elevated levels of 4-thiouracil, and it is present in broccoli, both suggestive that a dietary source may contribute to the presence of 4-thiouracil in the human gut.

More research is needed to understand the source of 4-thiouracil, but if it comes from the diet, that could inform dietary interventions for C. diff infection.

Matthew Munneke

It’s not time to give up eating cruciferous vegetables though. In the healthy gut, some resident microbes contain a TudS-related enzyme and can likely convert 4-thiouracil into nutrients. These microbes may be missing in the C. diff -infected gut, Munneke said.

Other VUMC authors of the Cell Host & Microbe paper are Catherine Shelton, PhD, Darian Carroll, PhD, Nicole Kirchoff, PhD, Martin Douglass, PhD, M. Wade Calcutt, PhD, Katherine Gibson-Corley, DVM, PhD, Maribeth Nicholson, MD, MPH, and Mariana Byndloss, DVM, PhD. Collaborators at the University of Florida and Baylor College of Medicine contributed to the studies.

Highlights

• Pyrimidine nucleotide synthesis is critical for Clostridioides difficile infection
• A thiouracil desulfurase (TudS) enables C. difficile to utilize 4-thiouracil (4-TU)
• TudS prevents 4-TU toxicity and incorporation into RNA by converting it to uracil
• 4-TU is present in the human gut and confers a fitness advantage to C. difficile

Summary
Nucleotides are essential building blocks for major cellular macromolecules and are critical for life. Consequently, bacterial pathogens must acquire or synthesize nucleotides during infection. Clostridioides difficile is the most common hospital-acquired gastrointestinal infection, and nutrient acquisition is critical for pathogenesis. However, the impact of nucleotide metabolism on C. difficile infection remains unclear. Here, we discover that 4-thiouracil (4-TU), a pyrimidine analog present in the human gut, is toxic to commensal bacteria. 4-TU hijacks the uracil salvage pathway for incorporation into RNA through the uracil phosphoribosyltransferase activity encoded by PyrR and Upp. C. difficile can salvage 4-TU as a pyrimidine source through the enzymatic action of a thiouracil desulfurase (TudS), thereby contributing to C. difficile fitness in mice fed 4-TU or MiniBioreactor models of infection containing exogenous 4-TU. Collectively, these results reveal a molecular mechanism for C. difficile to utilize a poisonous pyrimidine analog in the vertebrate gut to outcompete commensal microbes.

Graphical abstract

Munneke, Matthew J.; Yuan, Yifeng; Preisner, Eva C.; Shelton, Catherine D.; Carroll, Darian T.; Kirchoff, Nicole S.; Dickson, Ken P.; Cantu, Jose O.; Douglass, Martin V.; Calcutt, M. Wade; Gibson-Corley, Katherine N.; Nicholson, Maribeth R.; Byndloss, Mariana X.; Britton, Robert A.; de Crécy-Lagard, Valérie; Skaar, Eric P.
A thiouracil desulfurase protects Clostridioides difficile RNA from 4-thiouracil incorporation, providing a competitive advantage in the gut Cell Host & Microbe (2025) DOI:10.1016/j.chom.2025.03.001.

© 2025 Elsevier.
Reprinted under the terms of s60 of the Copyright, Designs and Patents Act 1988.

Of course, as anyone with even a basic grasp of evolutionary biology knows, all aspects of parasitic organisms and their ability to survive and thrive in hostile environments can be readily explained by the Theory of Evolution, which remains unrivalled in its ability to account for the observable evidence.

In contrast, intelligent-design creationists struggle to explain why an allegedly omniscient and omnibenevolent designer would deliberately create parasitic organisms. They must also explain why such a designer would equip these organisms with adaptations specifically to out-compete beneficial microbes in our microbiome, solely enabling parasites to replicate more effectively and cause greater suffering.

To date, I have yet to encounter any persuasive explanation for parasites or parasite-host arms races that could reasonably be attributed to the purposeful actions of a supremely intelligent and benevolent designer.

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:

Malevolent Designer News - How The SARS-CoV-2 Virus Steals Proteins From Our Immune System To Protect Itself

AI-Generated image

ChatGPT4o

AI-Generated depiction of SARS-CoV-2 virus coated in stolen proteins.

ChatGPT4o

SARS-CoV-2 “steals” our proteins to protect itself from the immune system

Although COVD-19 has been mostly brought under control by medical science and the vaccination campaign, it still kills thousands of people a year, but nowhere near the volume of deaths during the initial wave when world-wide health services came close to collapse and economies were on the point of ruin.

But there is still much to learn about why it was so virulent and successful.

To an admirer of creationism’s divine malevolence it must have seemed like a triumph of design, as it filled hospitals, killed millions and wrecked economies, helped by its supporters in the evangelical Christian churches who opposed measures to mitigate the worse effect of the virus, and then opposed the vaccination campaign with lies, scare tactics and the most infantile conspiracy theories imaginable, to help ensure the virus got to as many people as possible.

Now, a team of researcher from the Medical University of Vienna together with colleagues from the Medical University of Innsbruck have discovered how the virus protects itself from the immune system creationists believe their putative intelligent designer designed to protect us from the virus’s and other pathogens it designs to make us sick, would grace the pages of another 'intelligent design' polemic by Michael J. Behe and his Deception Institute. It depends on several components of a system being present in a classic 'irreducibly complex' system that creationists wave around as 'proof' that the locally-popular creator god is real because they can't understand how it could have evolved.

Malevolent Design - How Sleeping Sickness Parasites Are 'Designed' to Evade Our Immune System

Trypanosoma brucei

Sleeping sickness

Discovery Illuminates How Sleeping Sickness Parasite Outsmarts Immune Response | Johns Hopkins | Bloomberg School of Public Health

Trypanosoma brucei is a blood-borne eukaryote parasite that should leave believers in an intelligent designer, open-mouthed in admiration for its inventive genius. Christian fundamentalist creationists of the white supremacist persuasion should also admire the racist that, through T. brucei, has managed to keep large parts of Africa technologically under-developed due to the difficult in maintaining herds of domestic animals where the vector of these parasites - the tsetse fly - is common.

As a vector, the tsetse fly is a triumph of malevolent design which I mentioned in my popular book, The Unintelligent Designer: Refuting the Intelligent Design Hoax, but it would have been all for nothing without the nasty little T. brucei to cause sleeping sickness in humans and the debilitating disease "nagana" in cattle.

What creationist admires of the divine malevolence they believe designs these things should now be marveling at is the sheer brilliance of the design by which it manages to evade the immune system, which they believe was created by the same designer god which now regards his design as a problem to be overcome oh parasites like T. brucei can continue making Africans and their cattle sick.

Malevolent Designer News - Stand By For The Next Move In The Mpox Arms Race

Colorized transmission electron micrograph of mpox virus particles (light green) found within VERO E6 cells (teal).

NIAID Integrated Research Facility
Fort Detrick, Maryland.

Mpox virus particles

Mpox Vaccine Is Safe and Generates a Robust Antibody Response in Adolescents | NIAID: National Institute of Allergy and Infectious Diseases

As Medical science announces success in the search for a vaccine against the mpox virus currently spreading misery and suffering around the globe, we can be as sure as can be that creationism’s divine malevolence is working on a variant with an inbuilt way to evade the antibodies the vaccine produces, in just the same way it did with COVID-19 - if you believe a magic designer is behind these things, the way intelligent [sic] design creationists do.

Malevolent Design - How Chlamydia Is 'Designed' to Cause Maximum Sufferring.

Chlamydia pneumoniae

AI-generated image (ChatGPT4o)

Schematic representation of how a C. pneumoniae cell infects a human cell. The bacterium injects the protein SemD (green) into the cell, which activates the cell protein N-WASP, which in turn initiates vesicle formation.

Credit: HHU/Fabienne Kocher.

Universität Düsseldorf: Original or copy: How Chlamydia manipulate the host cell

The problem of parasites for creationists is one that, despite the best efforts of apologists like Michael J Behe of the Deception Institute, just won't go away.

Sadly, Behe shot himself in the foot with his original claim to have proven 'intelligent [sic] design in living organisms with his choice of the bacterial flagellum in E. coli, where he persuaded his willing audience that these nasty little pathogens had been intelligently designed - and by unspoken assumption, designed by the locally-popular god.

Now creationists wave his 'proof' of design as evidence for their creator god because only their god is capable of creating living organisms.

But, with characteristic double-think, creationists also argue that their god is omnibenevolent, so something else must have created parasites like E. coli, and, courtesy again of Michael J. Behe, they cite 'Sin' causing 'genetic entropy' and the absurd idea of 'devolution' this supposedly causes, as the cause of parasites and pathogens (but not the bacterial flagellum, obviously!).

The problem with that notion is that they need to do their double-think trick one more time and believe that a trait with improves a pathogens ability to live and reproduce in its host makes it somehow less perfect that one without that trait. So, in the creationist's world, an improvement is a move away from perfection!

But, with a cult that appears to believe learning is a move away from the 'perfection' of pristine ignorance (from whence comes expertise in all aspects of science), that's probably not too difficult a feat of mental gymnastics for a creationist to perform.

Malevolent Design - How Bacteria Are 'Designed' With a Protective Coat

Bacterial cell wall structure

AI generated (ChatGPT40)
With apologies for the spelling!

Study unveals a novel protective mechanism in bacterial cell wall

Structure of gram-negative cell envelope

By Jeff Dahl - Own work, CC BY-SA 4.0, Link

Here's a conundrum for creationists who have fallen for the Deception Institute's biologically nonsensical excuse for parasites - that they weren't designed by the only entity capable of designing living organisms, but by a process of 'devolution' [sic] from an initial created perfection caused by 'genetic entropy'. This excuse was hastily cobbled together by Michael J Behe when he realised his 'intelligent [sic] design' notion was making creationism's putative creator look like a pestilential malevolence, especially after Behe had gone to such lengths and scuppered his academic credentials with how 'irreducibly-complex-therefore-magically-created' E. coli flagellum, then his claim that resistance to antimalarial drugs in Plasmodium falciparum must have been designed.

The problem was that having produced an excuse for parasites that was designed to appeal to religious fundamentalists, Behe inadvertently abandoned any pretense that creationism is science not religion, by incorporating Christian fundamentalism in his excuse - initial created perfection followed by 'genetic entropy' caused by 'Sin', which depends on a belief in 'The Fall' and original sin.

Although Behe insists he's not a Christian fundamentalist YEC, his books invariably appeal to, and reinforce the prejudices of, those who are, and feed their insatiable demand for validation from the science they despise and continually attack as biased/Satanic/lies/flawed, etc.

But now we have research that shows how bacteria are 'designed' with a protective cell wall which helps them resist enzymes which would otherwise destroy them. Defensive structures and processes cannot logically be described as 'devolutionary', they therefore either evolved naturally, or, if you reject evolution in favour of intelligent [sic] design, were intelligently designed to make the bacteria better at making us sick, i.e., with malevolent intent.

Malevolent Design News - Researchers Show Another Of The Devine Malevolence's Nasties - HIV's Little Brother HTLV-1

HTLV-1 virus-like particle

© Nature Structural & Molecular Biology/Obr et al.

A viral close-up. HTLV-1 virus-like particles with a close-up view of the building blocks forming the viral lattice.

© Nature Structural & Molecular Biology/Obr et al.

ISTA | A Viral Close-Up

Not content with increasing the suffering and misery in the world with its brilliantly designed Human Immunosuppressive Virus (HIV), creationism's favourite pestilential malevolence also produced a related virus, Human T-lymphotropic virus type 1 (HTLV-1).

HIV is a deadly, (normally) sexually-transmitted retrovirus which medical scientists has managed to bring under control, but not cure or eradicate or even produce a vaccine against. What they have produced are anti-retroviral drugs which prevent the virus replicating so it doesn't kill its victims and, more importantly it isn't passed on to sexual partners.

Sadly for creationists, they have been denied the excuse of 'genetic entropy' and 'devolution' to absolve their favourite sadist of responsibility for HIV because they have also jubilantly declared it to be a 'gay plague' sent by their 'loving' god to punish homosexuals for behaving how it designed them to behave.

HTLV-1 is not nearly so deadly as HIV when left untreated, but, being closely related to it, it uses the same modus operandi as HIV and in some cases causes cancer and neurodegenerative disease that can be more deadly and debilitating than HIV treated by anti-retroviral drugs.

Malevolent Designer News - Why Cholera is So Good at Killing Us

Vibrio cholerae

AI generated image (ChatGPT4o)

Vibrio cholerae

AI generated image (ChatGPT4o)

News - Experts discover the deadly genetics of cholera, which could be key to its prevention - University of Nottingham

Although good hygiene and safe drinking water have most brought cholera under control in developed societies, it is still a major kill, especially of children, in poor and technologically under-developed countries.

It was a cholera outbreak of 1849 in Soho, London, the John Snow famously showed was statistically linked to drinking water from a well in Broad Steet, eventually persuading the authorities to remove the pump handle from the well, so ending the epidemic, that Snow conformed the Germ Theory of disease and founded modern epidemiology.

The cause was later shown to be a leaking septic tank which was contaminating the water in the well, and more remotely to a baby which caught cholera elsewhere whose nappy (diaper) was washed into the sewer, introducing the Vibrio cholerae into the septic tank.

I was born and brought up in North Oxfordshire in a rural community where, a generation earlier, cholera had been the single most common cause of death of children. A perusal of the parish burial registers shows regular patterns of epidemics causing a sudden increase in child deaths.

Even in technologically advanced countries, natural disasters such as earthquakes and floods, and man-made conflicts such as those currently in Gaza and Ukraine can destroy the infrastructure and quickly lead to conditions in which cholera can further devastate an already weakened population.

It would be an especially despicable malevolence that designed an organism to exploit people in those situation to ensure there was even more suffering, but those subscribing to the intelligent design hoax are unwittingly attributing exactly that to their putative designer god.

Malevolent Designer News - How A Parasitic Wasp Targets Adult Fruit Flies

Syntretus perlmani grub emerging from the side of a fruit fly

Scale bar: 1mm

Newly-discovered parasitoid wasp, Syntretus perlmani. Scale bar: 1mm.

Moore, L.D., Chris Amuwa, T., Shaw, S.R. et al. (2024)

New species of wasp ‘hidden in plain sight’ discovered by MSU researchers | Mississippi State University

The world of parasites is a world that creationists need to turn a blind eye to (and not one blinded by a parasitic worm) because it contains abundant examples of how an intelligence that designed parasites can only be regarded as some sort of malevolent sadist who designs ways to make living things suffer, often horribly and in especially ghoulish ways - the sort of ways that only a sick mind could dream up.

Creationist cult leaders are also probably reticent about discussing parasites, given their parasitic lifestyle, but that’s a different matter.

Within the world of parasites, there are fewer better examples of the casual cruelty that characterises it than those of the many parasitoid wasps that lay their eggs in the living bodies of their host species, where their larvae feed on the body of the host, often only killing it at the last moment and sometimes manipulating its victim or reanimating its dead body to protect the parasites within it.

Very many of these parasitoid wasps attack the larvae of other insects and gain the protection of the eventual cocoon their host makes before dying, so the wasp's reproductive cycle is linked to that of its host species.

Malevolent Designer News - Creationism's Favourite Pestilential Malevolence Is Improving Its Delivery System

Invasive Asian tiger mosquito, Aedes albopicus

Aedes albopicus

Photo by James Gathany/CDC

Study identifies areas of Europe at risk from dengue fever | UK Centre for Ecology & Hydrology

For devotees of creationism's putative intelligent [sic] designer, news that it is using a new, improved mosquito to deliver dengue fever to more people, including those in the densely populated continent of Europe, will be greeted with admiration for its creative genius.

Those with a more rational, adult understanding of the evidence will see this news as a natural consequence of environmental change and exactly the sort of thing evolution can produce, precisely as the Theory of Evolution predicts.

The news is that climate change has enabled the Asian tiger mosquito, Aedes albopictus, to extend its range into Europe and with it the virus that causes dengue fever or which the tiger mosquito is a vector.