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 - More Brilliance from Creationism's Divine Malevolence

Dengue signs and symptoms

Source: CDC

Female mosquito taking a blood meal

Hijacking of plasmin by dengue virus for infection - NUS Faculty of Science | NUS Faculty of Science

If you're a creationists who follows the latest science (if there is such a thing), you must be bursting with admiration for the ingenuity of your beloved intelligent designer for the way its brilliance at making us sick and spreading more suffering in the world is being revealed by science.

In the last few days, I've reported on how HIV, the virus that causes AIDS, is designed to hijack our cell's metabolic processes to ensure its own survival, and how the zika virus that cause the serious birth defect, microcephaly, in children if their mothers become infected during pregnancy, is brilliantly designed to make our skin produce more of the scent that attracts mosquitoes, so ensuring it is spread as widely as possible.

Now we have a superb example of this skill in malevolent design revealed by researchers from the National University of Singapore (NUS) who have discovered how the dengue virus is designed to make sure as many people as possible are infected by it. And this is breath-taking in its ingenuity. It is spread by the divine malevolence's favourite insect vector - the mosquito.

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.

The Malevolent Designer - How Creationism Divine Malevolence Brilliantly Designed HIV to Kill Us With

Getty Images

HZI | Decoding HIV's tactics

This should thrill devotees of creationism's intelligent designer because it exposes what a brilliant job it did in designing the human immunosuppressive virus (HIV) that causes the acquired immune deficiency syndrome (AIDS). It was discovered by a group of researchers at the Helmholtz Institute for RNA-based Infection Research (HIRI) in Würzburg and the University of Regensburg, Germany.

They have discovered how HIV hijacks the internal machinery in our cells to ensure its own survival.

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 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.

Refuting Creationism - Even More Signs of The Divine Malevolence's Obsessive Compulsive Disorder?

AI-generated image (ChatGPT4o)

Over 160,000 new virus species discovered by AI - The University of Sydney

This is the second paper today to show the apparent obsession creationism's putative designer has with creating viruses, if you believe that superstition.

The first paper dealt with the discovery that there are some 600 different viruses to be found on a used toothbrush and on the shower heads in US bathrooms; this one reports on a discovery that makes that finding pale into insignificance. It is the discovery, using the machine learning of AI, of 161,979 new viruses!

This is just tip of the iceberg as the authors say the method just scratches the surface of biodiversity and opens up a world of discovery with millions more to be discovered.

Refuting Creationism - Is Creationism's Divine Malevolence Sufferring from Obsessive-Compulsive Disorder?

Northwestern microbiologists found more than 600 viruses on samples collected from used toothbrushes and shower heads.

AI-Generated graphic (ChatGPT4o)

Structural model at atomic resolution of bacteriophage T4

By Dr. Victor Padilla-Sanchez, PhD https://www.drvictorpadillasanchez.com
Own work, CC BY-SA 4.0, Link

Viruses are teeming on your toothbrush, showerhead - Northwestern Now

Creationism's putative creator is nothing if not obsessive.

One of its obsessions appears to be designing ever-more exquisite ways to kill its creation as almost nothing in nature exists that doesn't have something that lives on or in it, often killing it in the process or at least weakening it in some way.

Its most visible obsession seems to be with designing beetles of which there are some 500,000 species with more being discovered almost daily. It's highly likely that there may be as many as a million different beetles in the world, many of which catch and devour other arthropods.

But it's in the field of virology that we find another obsession with designing variations on a general theme. Not only are there literally hundreds of thousands of viruses but every species has multiple variants - look at the number of different variants of the SARS-CoV-2 virus that have emerged since the initial wave of the COVID-19 pandemic!

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 - 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 - 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?

Malevolent Design News - How Creationism's Favourite Malevolence Designed SARS-CoV-2 to Cause Long COVID

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One of creationism's putative major success in the last 100 years, has been its new (as of 2019) coronavirus, SARS-CoV-2 (Severe Acute Respiratory Syndrome – Corona Virus - 2.

According to the WHO, as of 11 August 2024, there have been 775,917,102, cases worldwide (increasing at about 40,000 new cases per week) with 7,058,381 deaths (increasing at about 900 per week), despite the fact that 13.64 billion doses of COVID vaccine have been administered.

Creationism Refuted - How We Inherrited Part Of Our Anti-Viral Immune Response From A Microbial Ancestor

Credit: Pedro Leão.

A comparison of immune proteins called viperins from Asgard archaea (left) and from a group of more complex life that includes humans, called eukaryotes (right). The three-dimensional shapes (a.k.a. structures) are strikingly similar, suggesting they also function similarly.

Credit: Pedro Leão.

Next Time You Beat a Virus, Thank Your Microbial Ancestors | College of Natural Sciences

Multicellular organisms are collections of specialised eukaryote cells, which are themselves collections of prokaryote cells that have been around for several billion years before getting together to form more complex cells.

And those prokaryote cells - bacteria and archaea - had had to cope with viruses which arose as soon as there were replicating assemblages of DNA for them to parasitize and co-opt the replication mechanism to make more copies of themselves.

The result was one of the first evolutionary arms races as the prokaryotes evolved ways to prevent themselves being parasitised and viruses evolved ways to overcome the microbes defences.

And, or course, the later eukaryote, complex cells that were to form the multicellular organisms inherited these antiviral defences and carried on the arms race with viruses, so it makes sense to find some of the remnants of these microbial defences, probably modified, inside our own cells, and forming a first line of defences.

This is a simple prediction of the Theory of Evolution and the resulting descent with modification from a common ancestor from billions of years ago.

What information do you have on the anti-viral proteins, Asgard Viperin and Eukaryote Viperin? Asgard Viperin and Eukaryote Viperin are both antiviral proteins that play crucial roles in the innate immune response, particularly in targeting and neutralizing viral infections. They belong to a broader family of proteins called Viperin (virus inhibitory protein, endoplasmic reticulum-associated, interferon-inducible). Viperin is a well-known antiviral protein that is highly conserved across various species, including archaea, bacteria, and eukaryotes. Here's a breakdown of what is known about Asgard Viperin and Eukaryote Viperin:

1. Asgard Viperin
   • Origin: Asgard Viperin is derived from the Asgard archaea, a group of microorganisms that are thought to be closely related to the last common ancestor of archaea and eukaryotes. These archaea were discovered in deep-sea hydrothermal vent environments and are considered important in studying the evolution of complex life forms.
   • Function: Asgard Viperin has been identified as an antiviral protein that provides insights into the ancient mechanisms of immune defense. Its function is similar to that of Viperin in eukaryotes, where it inhibits viral replication by targeting viral components or the cellular machinery viruses depend on for replication.
   • Structure and Mechanism: Like other Viperins, Asgard Viperin is likely to have a radical SAM (S-adenosylmethionine) domain, which is critical for its antiviral activity. This domain allows the protein to produce a reactive radical species, which can interfere with viral processes, such as the synthesis of nucleotides that viruses require for replication.
   • Evolutionary Significance: The discovery of Asgard Viperin highlights the ancient origins of antiviral defense mechanisms. It suggests that the strategies used by modern eukaryotic cells to combat viruses may have deep evolutionary roots.
2. Eukaryote Viperin
   • Origin: Eukaryote Viperin is found in eukaryotic organisms, including humans. It is one of the interferon-stimulated genes (ISGs) that are upregulated in response to viral infection. This protein is highly conserved across various species, from simple eukaryotes like algae to complex organisms like mammals.
   • Function: In eukaryotes, Viperin is a key player in the innate immune response. It exerts its antiviral effects through multiple mechanisms, depending on the type of virus. For example:
     • Inhibition of Viral Replication: Viperin can interfere with the replication of viruses by altering lipid metabolism or disrupting the assembly of viral particles.
     • Interaction with Cellular Machinery: It can inhibit viral RNA polymerase, thereby preventing the replication of RNA viruses.
     • Modulation of Immune Response: Viperin can enhance the production of other antiviral molecules and modulate the signaling pathways involved in the immune response.
   • Mechanism of Action: The radical SAM domain is crucial for the antiviral activity of Viperin in eukaryotes. This domain facilitates the formation of a radical species that can interfere with the function of viral proteins or the host cell machinery that viruses exploit.
   • Clinical Relevance: Understanding the role of Viperin in the immune response has significant implications for developing antiviral therapies. Since Viperin is involved in the response to a wide range of viruses, enhancing its activity could be a potential strategy for treating viral infections.

Comparative Insights

• The study of Asgard and Eukaryote Viperin provides valuable insights into the evolution of antiviral defense mechanisms. The presence of similar antiviral proteins in both archaea and eukaryotes suggests that these defense strategies are ancient and have been conserved throughout evolution.
• While both Asgard and Eukaryote Viperin share functional similarities, their specific roles and mechanisms may differ due to the differences in their cellular environments and the types of viruses they encounter.

Research Significance

• The discovery and study of Asgard Viperin contribute to our understanding of the origin of eukaryotic cells and their immune systems. It also opens up new avenues for research into the evolution of antiviral defenses and the development of new antiviral strategies based on ancient mechanisms.

Understanding these proteins, particularly in the context of their evolutionary history and their function in modern organisms, is crucial for advancing our knowledge of immune responses and the development of antiviral therapies.

And this is precisely what researchers in the College of Natural Science at The University of Texas at Austin have found. They have shown that the proteins Asgard Viperin from the Asgard archaea and the Eukaryote viperin, possessed by eukaryotes including humans are structurally (and functionally) very similar.

Next Time You Beat a Virus, Thank Your Microbial Ancestors

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Two of our key defenses against viruses have persisted for billions of years, arising before complex life.

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When you get infected with a virus, some of the first weapons your body deploys to fight it were passed down to us from our microbial ancestors billions of years ago. According to new research from The University of Texas at Austin, two key elements of our innate immune system came from a group of microbes called Asgard archaea.

Specifically, viperins and argonautes, two proteins that are known to play important roles in the immune systems of all complex life — from insects to plants to humans — came from the Asgard archaea. Versions of these defense proteins are also present in bacteria, but the versions in complex life forms are most closely related to those in Asgard archaea, according to the new scientific study published in the journal Nature Communications.

This research bolsters the idea that all complex life, called eukaryotes, arose from a symbiotic relationship between bacteria and Asgard archaea.

It adds more support to the fact that the Asgards are our microbial ancestors. It says that not only did eukaryotes get all these rich structural proteins that we’ve seen before in Asgards, now it’s saying that even some of the defense systems in eukaryotes came from Asgards.

Associate Professor Brett J. Baker, senior author
Associate professor of integrative biology and marine science
Department of Integrative Biology
University of Texas at Austin, Austin, TX, USA.

The researchers identified for the first time a large arsenal of defense systems in archaea that were previously known only in bacteria.

When viperins detect foreign DNA, which might indicate a dangerous virus, they edit the DNA so that the cell can no longer make copies of the DNA, which stops the virus from spreading. When argonautes detect foreign DNA, they chop it up, also halting the virus. Additionally, in more complex organisms, argonautes can block the virus from making proteins in a process called RNA silencing.

Viral infections are one of the evolutionary pressures that we have had since life began, and it is critical to always have some sort of defense. When bacteria and archaea discovered tools that worked, they were passed down and are still part of our first line of defense.

Assistant Professor Pedro Leão, lead author
Department of Microbiology - RIBES
Radboud University, Nijmegen, The Netherlands.

The researchers compared proteins involved in immunity across the tree of life and found many closely related ones. Then they used an AI tool called ColabFold to predict whether ones that had similar amino acid sequences also had similar three-dimensional shapes (aka structures). (It’s the shape of a protein that determines how it functions.) This showed that variations of the viperin protein probably maintained the same structure and function across the tree of life. They then created a kind of family tree, or phylogeny, of these sister amino acid sequences and structures that showed evolutionary relationships.

A family tree of immune proteins called viperins from different organisms. Versions of viperin found in complex life forms, called eukaryotes (green), fit within the group of viperins from Asgard archaea (purple).

Credit: University of Texas at Austin.

Finally, the researchers took viperins from Asgard archaea genomes, cloned them into bacteria (so the bacteria would express the proteins), challenged the bacteria with viruses, and showed that Asgard viperins do in fact provide some protection to the modified bacteria. They survived better than bacteria without the immune proteins.

This research highlights the integral role cellular defenses must have played from the beginning of both prokaryotic and eukaryotic life. It also inspires questions about how our modern understanding of eukaryotic immunity can benefit from unraveling some of its most ancient origins.

Emily Aguilar-Pine, co-author Department of Integrative Biology
University of Texas at Austin, Austin, TX, USA.

It’s undeniable at this point that Asgard archaea contributed a lot to the complexity that we see in eukaryotes today, so why wouldn’t they also be involved in the origin of the immune system? We have strong evidence now that this is true.

Assistant Professor Pedro Leão

Other authors, all from UT, are Mary Little, Kathryn Appler, Daphne Sahaya, Kathryn Currie, Ilya Finkelstein and Valerie De Anda.

This work was supported by the Simons and Moore foundations (via the Moore-Simons Project on the Origin of the Eukaryotic Cell) and The Welch Foundation.

Abstract
Dozens of new antiviral systems have been recently characterized in bacteria. Some of these systems are present in eukaryotes and appear to have originated in prokaryotes, but little is known about these defense mechanisms in archaea. Here, we explore the diversity and distribution of defense systems in archaea and identify 2610 complete systems in Asgardarchaeota, a group of archaea related to eukaryotes. The Asgard defense systems comprise 89 unique systems, including argonaute, NLR, Mokosh, viperin, Lassamu, and CBASS. Asgard viperin and argonaute proteins have structural homology to eukaryotic proteins, and phylogenetic analyses suggest that eukaryotic viperin proteins were derived from Asgard viperins. We show that Asgard viperins display anti-phage activity when heterologously expressed in bacteria. Eukaryotic and bacterial argonaute proteins appear to have originated in Asgardarchaeota, and Asgard argonaute proteins have argonaute-PIWI domains, key components of eukaryotic RNA interference systems. Our results support that Asgardarchaeota played important roles in the origin of antiviral defense systems in eukaryotes.

Introduction
Organisms across the tree of life contain complex defense systems (DS) to battle viral infections^1,2,3. Over the past decade, dozens of new DS have been identified and characterized in bacteria, sparking a debate about a potential link between these systems and the origins of innate immune mechanisms in eukaryotes. More recently, protein components of bacterial NLR (Nucleotide-binding domain leucine-rich repeat), CBASS (Cyclic oligonucleotide-based antiphage signaling system), viperins (virus-inhibitory protein, endoplasmic reticulum-associated, interferon (IFN)-inducible), argonautes, and other DS have been shown to exhibit homology with proteins involved in the eukaryotic immune system⁴. Most of the research on prokaryotic defense systems has focused on bacteria, with archaea representing <3% of the genomes in these studies^5,6,7. Thus, very little is known about the diversity or evolution of these systems in archaea.

Recently, diverse novel genomes have been obtained belonging to the archaea most closely related to eukaryotes, commonly referred to as “Asgard” archaea, the phylum Asgardarchaeota⁸. In addition to being sister lineages to eukaryotes, these archaea also contain an array of genes that are hallmarks of complex cellular life involved in signal processing, transcription, and translocations, among other processes⁹. The Asgard archaea are descendants of the ancestral host that gave rise to eukaryotic life. One newly described order, the Hodarchaeales (within the Heimdallarchaeia class), shared a common ancestor with eukaryotes⁸. Here, we characterize defense systems in archaea and show that Asgard archaea have a broad array of these DS. We also show that Asgards contributed to the origins of innate immune mechanisms in eukaryotes.

Fig. 2: Evolutionary history and anti-phage activity of Asgard viperins.

A Phylogenetic analysis of viperins. Viperins phylogeny revealed ancestral links of eVip (eukaryotic viperin) with asVip (asgard viperin) (nodes marked in red), particularly those within the Heimdallarchaeia class (including Kariarchaeaceae (2), Heimdallarchaeaceae (3) and Hodarchaeales (5)). The size of the dots on the nodes is proportional to bootstrap values ranging between 60 and 100. B Structure-based homology of viperins. Consistent with the sequence homology-based phylogenetic tree, the eVip structure appears to have been inherited from asVip (red node). The darker green color represents reference sequences predicted experimentally. The size of the dots at the center of the nodes is proportional to bootstrap values ranging between 50 and 100. C Superposition of an eVip structure, predicted by X-ray diffraction (green), and the structural models of an asVip, archaeal viperin (arVip), and bacterial viperin (from left to right). The yellow color in the models emphasizes the high conservation of the viperin catalytic site across the tree of life. The information regarding bacteria, archaea, asgard archaea and eukaryotes in panels (A–C) are represented by the pink, blue, purple and green color respectively. D Anti-T7 phage activity of asVip in E. coli. Nine asVip (asVip 26,11,20,25,16,12,17,23,8) exhibited anti-viral activity as indicated by the p-values (*p < 0.05; **p < 0.01). E Anti-T7 phage activity of asVip after codon optimization for their expression in E. coli. One asVip from a Hodarchaeales organism provided protection against viral infection (asVip 19). The center line of each box plot denotes the median; the box contains the 25^th to 75^th percentiles. Black whiskers mark the 5th and 95^th percentiles. pVip34 is a prokaryotic viperin selected as a positive control from Bernheim et al.¹³. Each experimental condition includes, on average, 53 plaques pooled from three biological replicates. A two-tailed t-test was used to calculate statistical significance in figures (E, D).

Fig. 3: Evolutionary history of Asgard argonaute proteins.

A Phylogeny of long type argonaute proteins from archaea, bacteria, and eukaryotes with cyclases as outgroup (grey). B Structure-based homology of argonautes. C Structural alignment of asAgo5 and 4OLA (eAgo) MID and PIWI domains (left), and the graphic model of the corresponding alignments (right). Salmon regions on the alignment highlight strong conservation (low RMDS values). Red amino acids in the structural alignment, and their respective models represent the 4OLA conserved functional residues in MID and PIWI. The information regarding bacteria, archaea, asgard archaea and eukaryotes are represented by the pink, blue, purple and green color respectively. The size of the dots on the nodes is proportional to bootstrap values ranging between 70 and 100.

Leão, P., Little, M.E., Appler, K.E. et al.
Asgard archaea defense systems and their roles in the origin of eukaryotic immunity.
Nat Commun 15, 6386 (2024). https://doi.org/10.1038/s41467-024-50195-2

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

A highly-conserved antiviral protein across all eukaryote cells speaks loudly of common ancestry. The fact that a very similar protein is found in an "Asgard" archaea is strongly supportive of the theory that the fist eukaryote cells were alliances of bacteria and archaea and that the "Asgard" archaea contributed antiviral protection on this early eukaryote, showing common ancestry extending back beyond the first eukaryotes.

Of course, the less intelligent creationists will now be chanting 'Common Ancestry', but the more intelligent cultists would realise that that would mean the first eukaryote cells arose after Adam and Eve, because these antiviral proteins wouldn't have been needed until after 'Sin' had allowed viruses to 'devolve' by 'genetic entropy' (© Michael J. Behe), unless they don't understand how having an arms race with oneself is not the sign of an intelligent designer.