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.

Tell me all about the zika virus, its evolution and recent spread, please. Zika virus (ZIKV) is a mosquito-borne flavivirus primarily transmitted by Aedes mosquitoes, particularly Aedes aegypti. First identified in 1947 in a rhesus monkey in Uganda's Zika Forest, it was subsequently detected in humans in 1952 in Uganda and the United Republic of Tanzania. (who.int).

Evolution and Lineages

Zika virus (ZIKV) is an RNA virus. Specifically, it is a positive-sense, single-stranded RNA virus belonging to the Flavivirus genus within the Flaviviridae family. Other notable flaviviruses include dengue, yellow fever, and West Nile viruses.

Because ZIKV has an RNA genome, it mutates and evolves more rapidly than DNA viruses, which may have contributed to its recent spread and ability to cause large outbreaks.

Phylogenetic studies have identified two main lineages of ZIKV: African and Asian. The virus remained relatively obscure for decades, causing only sporadic human infections in Africa and Asia. However, in 2007, a significant outbreak occurred on Yap Island in Micronesia, marking ZIKV's first major emergence outside its traditional endemic areas. (academic.oup.com)

The Asian lineage is particularly notable for its role in the outbreaks in the Pacific and the Americas. Genetic analyses suggest that mutations in the virus may have enhanced its ability to infect humans and spread more efficiently, contributing to its rapid dissemination. (frontiersin.org).

Global Spread and Recent Developments

Following the Yap Island outbreak, ZIKV caused significant epidemics in the Pacific, including in French Polynesia in 2013. In 2015, Brazil reported its first case, leading to a large outbreak associated with severe birth defects, such as microcephaly, and neurological disorders like Guillain-Barré syndrome. The virus then spread throughout the Americas, prompting the World Health Organization to declare it a Public Health Emergency of International Concern in 2016. (who.int).

As of May 2024, ZIKV transmission persists in several countries, though generally at low levels since 2018. Recent data indicate that three additional countries have reported autochthonous mosquito-borne transmission, and two more have established *Aedes aegypti* populations without documented ZIKV transmission. (who.int).

In January 2025, new research revealed that ZIKV can manipulate human skin to emit chemical signals attracting more mosquitoes, potentially facilitating further spread of the virus. (sciencedaily.com).

Prevention and Control

Preventing ZIKV infection primarily involves controlling mosquito populations and minimizing exposure to mosquito bites. This includes using insect repellent, wearing protective clothing, and eliminating standing water where mosquitoes breed. Given the association between ZIKV infection during pregnancy and birth defects, pregnant women are advised to avoid travel to areas with active ZIKV transmission. (who.int).

Despite ongoing research, there is currently no specific antiviral treatment or vaccine for ZIKV. Efforts to develop a vaccine have faced challenges, including fluctuating transmission rates and limited funding.

Zika is still spreading. Why don’t we have a vaccine yet?

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

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Zika virus hijacks the skin of its human host to send out chemical signals that lure more mosquitoes to infect and spread the disease further, new research shows.

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Zika transmission has been reported more than 90 countries as the spread of the Aedes aegypti mosquito that carries the virus, as well as dengue and chikungunya, has increased over recent years as an effect of climate change and urbanisation. Yet surprisingly little is known about the factors that drive Zika transmission success.

A new study led by Liverpool School of Tropical Medicine and published in Communications Biology shows that Zika causes metabolic changes in human skin that essentially transforms it from a protective barrier to a magnet for mosquitoes.

Their research shows that the Zika virus alters gene and protein expression in dermal fibroblasts, the cell type responsible for maintaining structural integrity in the skin. These metabolic changes increase the production of certain chemicals emitted through the skin, known as volatile organic compounds (VOCs), that are attractive to mosquitoes and encourage them to bite. Their findings are supported by an extensive meta-proteome analysis, a technique that examines the overall effect of the interaction of different types of gene and protein within an organism.

Our findings show that Zika virus isn’t just passively transmitted, but it actively manipulates human biology to ensure its survival. As Zika cases rise and Aedes mosquitoes expand their range, understanding the mechanisms by which they gain a transmission advantage could unlock new strategies for combating arboviruses. This could include developing genetic interventions that disrupt the signal transmitted through the skin which seems to be so attractive to mosquitoes. The possibilities are as intriguing as they are urgent.

Dr Noushin Emami, co-corresponding author Department of Molecular Bioscience
Wenner-Gren Institute
Stockholm University, Stockholm, Sweden
And Vector Biology Department (VBD)
Liverpool School of Tropical Medicine (LSTM)
Liverpool, UK.

Most Zika infections do not lead to disease, and those that do generally cause mild symptoms that last for 2-7 days.

Zika can occasionally cause more serious complications and can harm a developing baby if contracted by a pregnant woman.

This study was conducted in collaboration with Emami Lab at Stockholm University, alongside researchers from the Nature Research Centre in Vilnius, the University of Veterinary Medicine in Hanover, Molecular Attraction AB, Umeå University, Leibniz University Hannover, and the University of Greenwich.

Abstract
Transmission of Zika virus (ZIKV) has been reported in 92 countries and the geographical spread of invasive virus-borne vectors has increased in recent years. Arboviruses naturally survive between vertebrate hosts and arthropod vectors. Transmission success requires the mosquito to feed on viraemic hosts. There is little specific understanding of factors that may promote ZIKV transmission-success. Here we show that mosquito host-seeking behaviour is impacted by viral infection of the vertebrae host and may be essential for the effective transmission of arboviruses like ZIKV. Human skin fibroblasts produce a variety of metabolites, and we show that ZIKV immediately alters gene/protein expression patterns in infected-dermal fibroblasts, altering their metabolism to increase the release of mosquito-attractive volatile organic compounds (VOCs), which improves its transmission success. We demonstrate that at the invasion stage, ZIKV differentially altered the emission of VOCs by significantly increasing or decreasing their amounts, while at the transmission stage of the virus, all VOCs are significantly increased. The findings are complemented by an extensive meta-proteome analysis. Overall, we demonstrate a multifaceted role of virus-host interaction and shed light on how arboviruses may influence the behaviour of their vectors as an evolved means of improving transmission-success

Introduction
The human body comprises around 40 trillion (3.7 × 10¹³) cells¹, which produce an enormous variety of metabolites including volatile organic compounds (VOCs). The qualitative and quantitative changes in VOC profiles reflect the optimum status of healthy cells. The skin is the body’s largest organ, serving multiple essential functions, including acting as a physical barrier for protection, a site for sensory perception, and a centre for vitamin synthesis. The release of VOCs through the skin, which contributes to the distinct odours of the human body, is a familiar part of our daily experience². These VOCs include a large number of volatiles that can be listed as carboxylic acids, aldehydes, alcohols or ketones³. Dermal fibroblasts are the main cell type present in skin connective tissue (dermis)⁴. These mesenchymal/stromal cells derived from the embryonic mesoderm, reside in the dermal layer of skin. They produce extracellular matrix proteins to strengthen the dermal compartment and interact with epidermal cells⁵.

Zika virus (ZIKV) had not been widely known until a series of outbreaks occurred with severe clinical complications that made it a matter of global public health concern. The emergence of ZIKV followed a typical pattern of a vector-borne disease being introduced into a new ecosystem and host population and spreading rapidly with severe implications for human health. ZIKV is a mosquito-borne virus belonging to the genus Flavivirus and is transmitted to humans by mosquitoes of the genus Aedes. Both Aedes aegypti and Aedes albopictus are the primary vectors for ZIKV transmission in nature⁶. Vector-mediated transmission of ZIKV is initiated when a blood-feeding female Aedes mosquito injects the virus into the skin of its mammalian host, followed by infection of a wide range of permissive cells. Indeed, skin cells, including dermal fibroblasts were found to be permissive to ZIKV infection. Infection of skin fibroblasts rapidly resulted in the presence of high RNA copy numbers and a gradual increase in the production of ZIKV particles over time, indicating an active viral replication stage. In humans, the incubation period from mosquito bite to symptom onset is ≈3–12 days⁷. Accumulating data indicate that ZIKV alters the biochemical processes of the infected cells by modifying glucose^8,9 and fatty acid¹⁰ metabolism. However, no published data has yet revealed any changes in the composition of infected cell volatome. While Zhang and colleagues¹¹ demonstrated that flaviviruses can manipulate host skin microbiota to produce an odour that attracts mosquitoes, the specific role of infected human skin cells in manipulating mosquitoes’ behaviour remains unclear.

Mosquitoes have made themselves at home in new geographical regions throughout recent years, bringing with them some historically exotic diseases. Epidemiologic and laboratory studies have implicated various Aedes spp. mosquitoes as ZIKV vectors¹¹. In mosquitoes, it appears that the viral load is initially high on the day of feeding, but then decreases to undetectable levels for about ten days. After this incubation period, the viral content increases again by day 15 and remains high from days 20 to 60. This is important because it suggests that it takes about 10 days for the virus to reach the salivary glands of the mosquito where it can potentially be transmitted to humans⁷. There is currently no specific treatment or vaccine available to mitigate or prevent ZIKV infection. Prevention measures, particularly conventional vector control, are currently the priority while we await these and other advances in control of the substantial harm caused by this virus. The World Health Organization has issued recommendations on this matter¹².

To further understand this complex issue, this study aims to demonstrate how ZIKV manipulate vector behaviour by altering gene/protein expression in human dermal fibroblasts at different stages of infection. These changes lead to an increased release of mosquito-attractive VOCs, ultimately enhancing transmission success. Here, we describe how ZIKV infection of human host cells provoked the modified feeding behaviour of its tiger mosquito vector in a manner that plausibly results in enhanced transmission success.

Obviously, to creationism's intelligent designer who designed mosquitoes to drink human blood and so spread several nasty parasites and viruses, and gave them the ability to detect and home in on the scents we give off, it was a simple matter to design the zika virus to enhance those scents to attract more mosquitoes and have the virus spread as widely as possible, to maximise the number of children born with microcephaly. At least, since that is about all the zika virus does, we have to assume that wehoever designed it, designed it with that specific function in mind.

And William Dembski insists that whatever a DNA/RNA sequence produces it must have been intelligently specified to produce that outcome. The malice of this designer knows no bounds apparently. That's if you believe what creationists claim.

If you believe what science says, it's easy to see how genes mutating and being selected for when they convey an advantage can produce this sort of host-parasite arms race over time, especially if it only takes a few tweaks of the RNA sequence to manipulate one of our genes, and suddenly, lots more mosquitoes are homing in and spreading the new variant far and wide.

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.

Malevolent Designer News - How An Oral Bacteria Aggrevates Rheumatoid Arthritis

AI-generated image (ChatGPT4o)

Colorized image of a colony of Actinobacillus actinomycetemcomitans

Derren Ready/Wellcome Images
CC BY-NC-ND 3.0

Shedding Light on How Oral Bacteria Can Aggravate Rheumatoid Arthritis｜Tokyo Medical and Dental University, National University Corporation

Not content with the suffering that gum disease and dental caries cause, creationism's divine malevolence used at least one of the pathogens behind those problems to increase suffering a little more by aggrevating rhuematoid arthritis.

That's the inevitable conclusion honest creationist, who rejects the notion of evolution in which pathogenic parasites evolve naturally without intent, malevolent, benign or indifferent, should be drawing from the evidence from a Tokyo Medical and Dental University team of researchers led by Tokuju Okano and Toshihiko Suzuki of the Department of Bacterial Pathogenesis recently published in the International Journal of Oral Science.

This is not the first instance of creationism's divine malevolence multi-tasking its pathogens: in 2017 a team of researchers from The Chinese University of Hong Kong found a link between five oral bacteria, Peptostreptococcus stomatis, Streptococcus anginosus, Parvimonas micra, Slackia exigua and Dialister pneumosintes and the incidence of stomach and eosphageal cancer.

The oral bacterium which has been found to be aggrevating rheumatoid arthritis is Aggregatibacter actinomycetemcomitans.

Malevolent Design - How A Human Mouth Bacterium Is 'Designed' For Super-Fast Proliferation

Corynebacterium matruchotii

Public domain

Open Wide: Human Mouth Bacteria Reproduce through Rare Form of Cell Division | Marine Biological Laboratory

Cellular elongation at the tips of the filamentous bacteria Corynebacterium matruchotii.

Credit: Chimileski et al (2024).

Most cells, either single-celled organisms like bacteria or the eukaryote cells of multicellular organisms, reproduce by simple division into two daughter cells. Under favourable conditions, this means a cell can produce a population of descendants that grows exponentially 1 → 2 → 4 → 8 → 16 → 32→64 … etc. (population = 2ⁿ; where n= the number of generations)

But the trick a bacterium, Corynebacterium matruchotii, that is only found in the human mouth uses is to divide into multiple new cells at each generation. For example, assuming it splits into 10 daughter cell at each generation, its growth rate from a single founder cell will be 1 → 10 → 100 → 1000 → 10,000 → 100,000 → 1,000,000 … etc., (population = 10ⁿ). But scientists have found it can do better than that, producing up to 14 new cells at each generation.

In 6 generations in favourable conditions, Corynebacterium matruchotii can produce 1 million or more offspring, against an 'ordinary' bacteria's 64, so rapidly out-pacing any other bacteria. C. matruchotii is an essential component of the plaque that quickly develops on teeth. It appears to have no other known function.

In some ways, C. matruchotii behaves more like fungal hyphae, growing at the tip to produce a long thin filament. It is this filament that then simply splits up into small sections, each of which becomes a new cell.

The filamentous bacteria C. matruchotii splitting into multiple cells at once, a rare kind of cell division called multiple fission.

Credit: Scott Chimileski, MBL

In 2020 a team of researchers showed how plaque is a highly structured and organised colony of different microorganisms which almost seems to be designed to allow Streptococcus mutans to get on with its job of dissolving the tooth enamel and causing caries. Creationists dogma insists that anything with a complex, organised structure must be intelligently designed because, so they assert, complexity and order can’t arise from disorder without intelligent intervention.

This latest discovery shows how the beginnings of this organised colony are established very quickly.

Malevolent Designer News - The Parasitic Nematodes 'Designed' To Carry Viruses

Ecuadorian whipworms, Trichuris trichiuria

Image: Mark Taylor

Virus RNA (red) in a B. malayi

Quek, S., Hadermann, A., Wu, Y. et al (2024)

Nematodes May Cause Disease Indirectly, via the Viruses They Carry

Not content with a whole range of parasitic worms to cause suffering, creationism's divine malevolence has also designed them to carry a payload of viruses to make their victims suffer even more.

This is the inescapable conclusion an honest creationist (if there is such a thing) would need to reach if he/she made an honest assessment of the facts just published by a team of researchers from the Centre for Neglected Tropical Diseases, Liverpool School of Tropical Medicine (LSTM), Liverpool, UK and the Global Health Institute, University of Antwerp, Antwerp, Belgium, in the journal Nature Microbiology.

This research team have identified a wide variety of viruses infecting nematodes and, most worryingly, the parasitic nematodes responsible for diseases in humans, so it is entirely possible that the diseases associated with infection by these nematodes could actually be caused by the viruses they carry. Related nematodes also show signs of virus-nematode co-evolution over millions of years in the form of a global distribution of nematode-virus associations.

Their research is explained in a press release from LSTM:

Tell me all about parasitic nematodes and the diseases they cause in humans, please. Parasitic nematodes (roundworms) are a diverse group of organisms that infect humans, animals, and plants. They can be found in various environments, from soil to water, and have adapted to parasitize a wide range of hosts. These nematodes can cause various diseases in humans, ranging from mild discomfort to severe and life-threatening conditions.

Overview of Parasitic Nematodes

Parasitic nematodes are classified under the phylum Nematoda. They are elongated, cylindrical, and non-segmented worms. Some of the most common parasitic nematodes that infect humans include:

1. Ascaris lumbricoides (giant roundworm)
2. Trichuris trichiura (whipworm)
3. Ancylostoma duodenale and Necator americanus (hookworms)
4. Strongyloides stercoralis (threadworm)
5. Enterobius vermicularis (pinworm)
6. Wuchereria bancrofti and Brugia malayi (filarial worms)
7. Onchocerca volvulus (cause of river blindness)
8. Dracunculus medinensis (Guinea worm)
9. Toxocara spp (Toxocariasis)

Common Diseases Caused by Parasitic Nematodes in Humans

1. Ascariasis
   • Causative agent: Ascaris lumbricoides
   • Symptoms: Often asymptomatic, but heavy infections can cause abdominal pain, malnutrition, growth retardation in children, intestinal obstruction, and respiratory issues (due to larval migration through the lungs).
   • Transmission: Ingestion of eggs from contaminated soil, water, or food.
   • Geographical distribution: Common in tropical and subtropical areas with poor sanitation.
   
   
2. Trichuriasis (Whipworm Infection)
   • Causative agent: Trichuris trichiura
   • Symptoms: Asymptomatic in mild cases, but heavy infections can cause diarrhea, rectal prolapse, anemia, growth retardation in children, and malnutrition.
   • Transmission: Ingestion of eggs from contaminated soil, food, or water.
   • Geographical distribution: Widespread in tropical regions, especially in areas with poor sanitation.
   
   
3. Hookworm Infections
   • Causative agents: Ancylostoma duodenale and Necator americanus
   • Symptoms: Anemia (due to blood loss in the intestines), abdominal pain, diarrhea, weight loss, and fatigue. Skin itching and rash can occur where larvae penetrate the skin.
   • Transmission: Larvae penetrate the skin, usually through bare feet when walking on contaminated soil.
   • Geographical distribution: Common in warm, moist climates, particularly in sub-Saharan Africa, Southeast Asia, and South America.
   
   
4. Strongyloidiasis
   • Causative agent: Strongyloides stercoralis
   • Symptoms: Often asymptomatic, but can cause abdominal pain, diarrhea, skin rash, and severe life-threatening hyperinfection syndrome, especially in immunocompromised individuals.
   • Transmission: Larvae penetrate the skin from contact with contaminated soil.
   • Geographical distribution: Tropical and subtropical regions, but also occurs in temperate areas.
   
   
5. Enterobiasis (Pinworm Infection)
   • Causative agent: Enterobius vermicularis
   • Symptoms: Perianal itching, irritability, sleep disturbances, and sometimes abdominal pain.
   • Transmission: Ingestion of eggs from contaminated hands, surfaces, or food.
   • Geographical distribution: Worldwide, particularly in temperate regions; commonly affects children.
   
   
6. Lymphatic Filariasis (Elephantiasis)
   • Causative agents: Wuchereria bancrofti, Brugia malayi, Brugia timori
   • Symptoms: Lymphedema (swelling of limbs), elephantiasis (thickening of the skin and underlying tissues), and hydrocele (swelling of the scrotum).
   • Transmission: Mosquito bites (primarily Culex, Anopheles, and Aedes species).
   • Geographical distribution: Sub-Saharan Africa, Southeast Asia, the Pacific, and parts of the Americas.
   
   
7. Onchocerciasis (River Blindness)
   • Causative agent: Onchocerca volvulus
   • Symptoms: Severe itching, skin rash, depigmentation, and nodules under the skin. Can lead to visual impairment or blindness if the eyes are affected.
   • Transmission: Blackfly bites (genus Simulium).
   • Geographical distribution: Sub-Saharan Africa, with some cases in Latin America and Yemen.
   
   
8. Dracunculiasis (Guinea Worm Disease)
   • Causative agent: Dracunculus medinensis
   • Symptoms: Painful blister and ulcer, often on the lower limbs. The emerging worm can cause secondary infections.
   • Transmission: Ingestion of water contaminated with infected copepods (small crustaceans) that harbor larvae.
   • Geographical distribution: Historically widespread in Africa and Asia, now largely confined to a few countries due to eradication efforts.
   
   
9. Toxocariasis
   • Causative agents: Toxocara canis and Toxocara cati
   • Symptoms: In visceral larva migrans (VLM), symptoms may include fever, cough, abdominal pain, and eosinophilia; in ocular larva migrans (OLM), it may cause visual impairment or blindness.
   • Transmission: Ingestion of eggs from contaminated soil or food, or from contact with infected animal feces.
   • Geographical distribution: Worldwide, especially in areas where pets are not regularly dewormed.

Diagnosis and Treatment

Diagnosis of parasitic nematode infections typically involves stool examinations for eggs or larvae, blood tests for antibodies or microfilariae, or skin snips in the case of onchocerciasis. Advanced imaging or biopsies may be required for some infections.

Treatment often involves anti-parasitic medications such as albendazole, mebendazole, ivermectin, diethylcarbamazine, and praziquantel, depending on the type of nematode and the severity of the infection.

Prevention and Control

• Improving sanitation: Proper disposal of human feces and access to clean water.
• Personal hygiene: Handwashing, wearing shoes, and using protective clothing.
• Mass drug administration (MDA): In endemic areas to reduce transmission, especially for lymphatic filariasis and onchocerciasis.
• Vector control: Reducing the population of mosquitoes and blackflies.
• Public health education: Raising awareness about transmission and prevention methods.

Would you like more information on any specific nematode or disease?

Newly discovered viruses in parasitic nematodes could change our understanding of how they cause disease

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New research shows that parasitic nematodes, responsible for infecting more than a billion people globally, carry viruses that may solve the puzzle of why some cause serious diseases.

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A study led by Liverpool School of Tropical Medicine (LSTM) used cutting-edge bioinformatic data mining techniques to identify 91 RNA viruses in 28 species of parasitic nematodes, representing 70% of those that infect people and animals. Often these are symptomless or not serious, but some can lead to severe, life-changing disease.

Nematode worms are the most abundant animals on the planet, prevalent in all continents worldwide, with several species infecting humans as well as agriculturally and economically important animals and crops. And yet in several cases, scientists do not know how some nematodes cause certain diseases.

The new research, published in Nature Microbiology(link is external)(opens in a new tab), opens the door to further study of whether these newly discovered viruses – only five of which were previously known to science – could contribute to many chronic, debilitating conditions. If a connection can be proven, it could pave the way for more effective treatments in the future.

This is a truly exciting discovery and could change our understanding of the millions of infections caused by parasitic nematodes. Finding an RNA virus in any organism is significant, because these types of viruses are well-known agents of disease. When these worms that live inside of us release these viruses, they spread throughout the blood and tissues and provoke an immune response. This raises the question of whether any of the diseases that these parasites are responsible for could be driven by the virus rather than directly by the parasitic nematode.

Professor Mark J. Taylor, co-corresponding author
Professor of Parasitology
Centre for Neglected Tropical Diseases
Department of Tropical Disease Biology
Liverpool School of Tropical Medicine, Liverpool, UK.

Parasitic nematodes including hookworms and whipworms can cause severe abdominal problems and bloody diarrhoea, stunted development and anaemia. Infection with filarial worms can lead to disfiguring conditions such as lymphoedema or ‘elephantiasis’, and onchocerciasis, or ‘river blindness’, that leads to blindness and skin disease.

This is a truly exciting discovery and could change our understanding of the millions of infections caused by parasitic nematodes.

The study authors propose that these newly identified viruses may play a role in some of these conditions. For example, Onchocerciasis-Associated Epilepsy (OAE) that occurs in children and adolescents in Sub-Saharan Africa has recently been associated with onchocerciasis, but it is not known why this causes neurological symptoms such as uncontrollable repeated head nodding, as well as severe stunting, delayed puberty and impaired mental health.

One of the viruses in the parasites that cause onchocerciasis identified in the new study is a rhabdovirus – the type that causes rabies. The authors of the study suggest that if this virus is infecting or damaging human nerve or brain tissue, that could explain the symptoms of OAE.

The full extent and diversity of the viruses living in parasitic nematodes, how they impact nematode biology and whether they act as drivers of disease in people and animals now requires further study.

The illuminating discovery of these widespread yet previously hidden viruses was first made by Dr Shannon Quek, a Postdoctoral Research Associate at LSTM and lead author of the new study, who had initially been using the same data mining method to screen for viruses within mosquitoes that spread disease, before deciding to investigate nematodes.

As a child [in Indonesian], I saw a lot of people infected with these diseases and I suffered from the dengue virus on three occasions. That got me interested in tropical diseases. Diseases caused by parasitic nematodes are very long-term, life-long illnesses that persistently affect people. It has a significant impact on people's quality of life, their economic outputs and mental health.

There are a lot of studies about the microbiomes of mosquitoes, and how the bacteria that lives inside can block the spread of viruses, which might stop vector-borne diseases like dengue. This interplay between organisms in the same host led me to think - what else might be inside parasitic nematodes as well? Which after my discovery will now be the focus of our research.

Dr Shannon Quek, lead author
Centre for Neglected Tropical Diseases
Department of Tropical Disease Biology
Liverpool School of Tropical Medicine, Liverpool, UK.

The study also involved researchers from University of Antwerp and KU Leuven, Belgium, Brock University, Canada, University of Queensland, Australia, University of Buea, Cameroon and the University of Energy and Natural Resources, Ghana.

Abstract
Parasitic nematodes have an intimate, chronic and lifelong exposure to vertebrate tissues. Here we mined 41 published parasitic nematode transcriptomes from vertebrate hosts and identified 91 RNA viruses across 13 virus orders from 24 families in ~70% (28 out of 41) of parasitic nematode species, which include only 5 previously reported viruses. We observe widespread distribution of virus–nematode associations across multiple continents, suggesting an ancestral acquisition event and host–virus co-evolution. Characterization of viruses of Brugia malayi (BMRV1) and Onchocerca volvulus (OVRV1) shows that these viruses are abundant in reproductive tissues of adult parasites. Importantly, the presence of BMRV1 RNA in B. malayi parasites mounts an RNA interference response against BMRV1 suggesting active viral replication. Finally, BMRV1 and OVRV1 were found to elicit antibody responses in serum samples from infected jirds and infected or exposed humans, indicating direct exposure to the immune system.

Main
Humans and animals are frequently infected with multiple species of parasitic nematodes^1,2,3 and suffer from chronic, lifelong infections and exposure to continuous reinfection⁴. Such infections impose a substantial health burden on billions of people, impacting their health, quality of life and economic productivity. Medically important parasitic nematodes infect over one billion people, resulting in up to 7.53 million disability-adjusted life years globally⁵. Prominent examples include intestinal species such as Ascaris lumbricoides and Trichuris trichiura⁴, which infect an estimated 511 and 412 million people, respectively⁵, as well as the hookworms Necator americanus, Ancylostoma duodenale and Ancylostoma ceylanicum, which collectively infect up to 186 million people globally⁵. Infected individuals can suffer from severe abdominal discomfort, bloody diarrhoea, stunted development and anaemia. Other examples include the filarial nematodes Wuchereria bancrofti and Brugia malayi, the causative agents of lymphatic filariasis that infect up to 96 million people globally^5,6, and Onchocerca volvulus, which infects up to 21 million people⁵. In the case of O. volvulus, recent estimates indicate that 14.6 million are afflicted with skin disease and 1.15 million with blindness⁷. Furthermore, there has been increasing recognition of a disease known as onchocerciasis-associated epilepsy (OAE), occurring in children and adolescents in onchocerciasis meso- and hyperendemic foci across sub-Saharan Africa⁸. This condition manifests as a variety of epileptic seizures, including uncontrollable repeated head nodding (‘nodding syndrome’), as well as severe stunting, delayed puberty and impaired mental health (Nakalanga syndrome)⁹. OAE has been epidemiologically linked to infection with O. volvulus¹⁰, but the pathogenesis has yet to be identified⁸.

A variety of viruses can be found infecting several human parasitic protozoa, including Plasmodium vivax, Trichomonas vaginalis and Cryptosporidium parvum^11,12. Viruses infecting Leishmania sp. have been studied in great detail¹³ and can increase disease severity, parasite prevalence and potentially the incidence rates of both drug resistance and mucocutaneous leishmaniasis^14,15. RNA virus infections have been identified in plant-parasitic nematodes¹⁶, parasitic flatworms^17,18 and free-living nematodes^17,19,20, although the impact of viral infections on the biology of the worms is largely unknown.

Here we analysed the transcriptomes of 41 parasitic nematode species infecting humans and animals and discovered 91 virus or virus-like genomic sequences across 28 species. We further characterize the viruses infecting B. malayi and O. volvulus, describing their genomic diversity, geographic spread, phylogeny, abundance throughout different developmental stages, tissue tropism, localization and vertebrate host serology. Finally, we show that an RNA interference (RNAi) response is induced in B. malayi against BMRV1, providing evidence for active viral replication.

[…]

Discussion
We reveal an abundant and diverse RNA virome spanning 14 different viral orders and 24 families within parasitic nematodes. Of the 91 viruses discovered, only 5 have been previously reported, including 3 from A. suum and A. lumbricoides^23,25. Our survey is probably an under-representation of the true extent and diversity of the parasitic nematode RNA virome owing to a variety of factors including variations in sample preparation resulting in discarded viral reads and the restricted number, or lack, of transcriptomes for several important parasites. Nevertheless, our analysis supports a conserved global spread of virus–nematode associations across multiple continents in the case of the viruses of A. suum and A. lumbricoides, and O. volvulus, suggesting an ancient and stable co-evolution. This is perhaps best exemplified by members of the Trichinellidae (Supplementary Fig. 1), which show a close evolutionary relationship, as well as phylogenetic clustering of diverse virus sequences from different species and orders of parasitic nematodes.

The parasitic nematodes identified with viruses include several important human parasitic nematodes, A. lumbricoides, T. trichiura, O. volvulus, B. malayi, A. ceylanicum and Trichinella spiralis, which cause substantial public health issues, with over 1.5 billion people infected with one or more such parasites^4,5,6,44,45. Several other species cause an even greater global burden in the livestock industry⁴⁶, with 15 economically important parasites (A. suum, Dictyocaulus viviparous, Haemonchus contortus, Ostertagia ostertagi, Oesophagostomum dentatum, Teladorsagia circumcinta, Trichuris suis plus 8 Trichinella spp.) of cattle, sheep and pigs, harbouring 37 previously unreported viruses.

The full extent and diversity of the parasitic nematode RNA virome, how it impacts nematode biology and whether they act as drivers or modulators of disease pathogenesis remain critical knowledge gaps. Indeed, in the parasite Toxocara canis, which causes neurotoxocariasis, components of the TCLA virus have been reported to be highly expressed in infective larvae (18% of expressed sequence tags) before entry into a vertebrate host (for example, humans and dogs)²⁹, with human infections eliciting antibody responses against several TCLA virus proteins²⁹, indicating potential roles in transmission and infectivity. Alternatively, extrapolation from the most well-characterized RNA viruses of Leishmania sp. protozoan parasites suggests potential roles of nematode viruses in disease pathology and progression. Both Leishmania virus 1 (LRV1) and T. vaginalis virus induce hyperinflammatory immunity, which drives disease pathogenesis and subverts host immunity to the parasites’ advantage^14,15,47. We show that BMRV1 and OVRV1 elicit antibody responses from the host showing direct exposure to the immune system, and we speculate that this suggests the potential to modulate host immunity to the parasite and cross-reactive immunity to other RNA viruses.
[…]

Fig. 4: Representative FISH microscopy images of B. malayi showing localization of virus RNA within nematode tissues, alongside the Wolbachia endosymbiont as a technical control.

Virus RNA stained red; Wolbachia stained green; DAPI nuclear stain blue. a–e, Note the different levels of viral infection in microfilariae (a), localization of the viral stain in male testes (b) and the hypodermal cells near the male spicule (c). Virus signal within adult female reproductive tracts appears between developing eggs within the paired uteri of adult females, with early embrys in the left uteri and ‘pretzel-stage’ microfilariae in the right (d), with the developing eggs casting a ‘shadow’ in between virus staining, visible in 3D images of female uteri (e). f–j, In older adults (>12 months), we observed ‘epicuticular inflations’ often with an intense viral signal (f), typically occurring near the head (g) or tail regions of the nematodes. They can appear as single separate inflations at different nematode orientations, either next to internal organs (h) or the hypodermal chords (i), or as a continuous inflation along the nematode flank (j). Scale bars measure 20 µm (a,b,h,i) or 50 µm (d,g). Gridlines in three-dimensional 𝓏-stack figures (c,e,f,j) measure 40 µm by 40 µm. A total of 15 adult male and female parasites were processed in separate experiments. Parasites with epicuticular inflations were typically between 12 and 19 months at the time of sampling, with jird animal hosts being 15–22 months of age, respectively. Parasites without were typically 3–6 months of age, with the jird animal hosts being 6–9 months of age.

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Fig. 5: Validation of OVRV1 using RT-PCR, western blot and representative IFA staining of O. volvulus nodules with anti-OVRV1 glycoprotein antibodies.

Anti-OVRV1 glycoprotein antibodies stained green; DAPI nuclear stain blue. a, RT-PCR experiments show that OVRV1 can be amplified only from reverse-transcribed RNA, from both O. volvulus (lane 1, n = 1) and O. ochengi (lanes 2–4, n = 3). b, Western blots against the OVRV1 glycoprotein show different molecular weight bands occurring depending on the life cycle stage of O. volvulus (n = 3). All IFA images include the DAPI nuclear stain (blue). c,d, Images of the paired uteri from adult O. volvulus females show virus stains surrounding and entering developing embryos within the uteri (solid arrow), while surrounding but not within the early embryos (hollow arrow). Developing embryos can show either complete infection rates (c) or a much smaller proportion (d). e, Mature microfilariae released from the female, located within surrounding nodule tissues, stain heavily for OVRV1 glycoprotein. f,g, Intense antibody staining is observed surrounding the nematode rachis, where eggs are first formed (solid arrows). The heavily stained rachis is either surrounded by early-stage eggs with green staining surrounding them (f) or without surrounding eggs (g). h,i, Cellular inflations containing intense antibody staining are observed on the external face of the adult female uterine walls (solid arrows). j,k, Male O. volvulus are frequently observed to be infected, with viral stains occurring in different tissues (j), as well as surrounding and entering the male testes (k). Parasites were obtained from sections of fixed O. volvulus nodules from human patients (n = 8 nodules).

Quek, S., Hadermann, A., Wu, Y. et al.
Diverse RNA viruses of parasitic nematodes can elicit antibody responses in vertebrate hosts. Nat Microbiol (2024). https://doi.org/10.1038/s41564-024-01796-6

Copyright: © 2024 The authors.
Published by Springer Nature. Open access.
Reprinted under a Creative Commons Attribution 4.0 International license (CC BY 4.0)

So, if you reject the evolutionary explanation of these viruses-nematode associations in favour of a creationist 'intelligent [sic] design' explanation you must assume the designer intended the consequences of its design since it is axiomatic of the creationist cult that the designer is a perfect, omniscient god for whom the consequences of its design must have been known in advance and so were designed with that function in mind.

And of course we can dismiss the childish nonsense about 'genetic entropy; causing 'devolution' [sic] because these viruses are clearly gaining an advantage in infecting the nematodes because that gives them easy access to their vertebrate hosts, and anything which conveys an advantage is evolution, not 'devolution'. Only someone ignorant of evolution would fall for such biologically nonsensical excuse for parasites, as any biologist worthy of the term would have known before he came up with it.

So, the question remains unanswered by creationists - is this an example of malevolent design, or of evolution?