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.
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.
Christian superstition insists that every person conceived is a creation of their omniscient, omnipotent god who knows and has always known, exactly who is going to be born and has an oven-ready plan for their entire existence. Each baby conceived was exactly as the Christian god intended, down to the last detail of the DNA Exactly which sperm fertilizes which egg when, is part of the god's omniscient, perfect plan.
Leaving aside the absurdity of throwing millions of sperms at a single egg to produce that conception, when only a predetermined one was going to be the winner in order to produce the predetermined genome, when a single sperm would have been just as effective, we are left with the disturbing idea that any and all genetic defects were the intended outcome of that conception; the intention of a supposedly omnibenevolent god.
Now, it might, in fact it definitely is possible for a Christian to imagine some ultimate good will come from a child with a genetic defect, but what if a defect in the sperm causes harm not just to the baby, but to the mother? Are we to conclude that a mother whose life is put at risk by a defective sperm from her partner was the intended victim of an 'all-loving' god? What possible good can come from a mother's (and almost invariably her baby's) life being in danger from something beyond her control? What possible good can come from preeclampsia?
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.
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.
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!
One thing you can depend on with creationism's putative designer is that there will never be a simple solution when there is a more complicated way to solve the problem it just created, and just like William Heath-Robinson, it will try to use pre-existing structures that were designed for an entirely different function, like a pile of books under the legs of a ladder to make it tall enough, and every piece of string holding things together will have knots in it.
And when we look beneath the superficial resemblance of design in, for example, a living cell, we find all manner of if-it-works-it'll-do solutions to problems, like the solution to the problem of breaking DNA that a team of scientists, led by Kaspar Burger, from Julius-Maximilians-Universität Würzburg (JMU) in Bavaria, Germany, have discovered.
The problem arises of course because the method for replicating DNA as cells divide is poorly designed and unnecessarily complicated in the first place. If the putative designer had devised a more sensible method for replicating cells in multicellular organisms than that used for replicating single cells where the whole genome needs to be replicated, many of the problems of erroneous copying wouldn't arise because only a small subset of the genome is needed for specialised cells.
The human gut, like that of other mammals, birds and vertebrates in particular and the gut of many insects and worms, in fact any organism with a moth and an anus, is an ideal environment for a whole host of other organisms, most of which will have co-evolved with humans and have been with us since our ancestors were small insectivores, skulking in the dark of the night to avoid dinosaurs and predatory proto-birds.
They for a complex and dynamic ecosystem of competing and cooperating bacteria, viruses, fungi and protozoa which exists in a more or less stable balance of arms races, predation and symbiosis.
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.
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.
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.
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.
In the study, scientists performed a genetic analysis on the bones of 133 human individuals from late Neolithic megalithic graves near Warburg in North Rhine-Westphalia. The team discovered the genome of the bacterium Yersinia pestis in the bone samples of two independent individuals. Additionally, previously published genomic data from a bone sample of a Neolithic dog found in Ajvide (Sweden) suggested a potential infection route.
What was creationism's divine malevolence up to with one of its most successful pathogens with which if killed hundreds of millions and changes society - the Yersinia pestis bacterium which caused the waves of black death and plague that regularly spread across the world?
It seems to have been experimenting, possibly trying to either perfect its virulence or work out the best delivery system to ensure it got to and killed as many people as possible. Sometimes, entire villages were wiped out. Not far from where I currently live are a couple of former villages that disappeared during the black death - the village of Woodperry near Oxford is an example, surviving now only in the name 'Woodperry Road' and a farmhouse later built on the site.
But 5000 years ago, Y. pestis doesn't seem to have been anything like a virulent as it became in the 12th Century. According to a recent discovery, it was capable of killing the occasional neolithic farmer but not of becoming a major pandemic able to kill hundreds of thousands and depopulate vast areas.
So, what changed, and more to the point, which explanation would a creationist prefer; the one which blames their god or the one which attributes it to evolution, climate change and cultural changes in human society? One thing we can be sure of though is the Michael J. Behe's biologically nonsensical religious apologetic of 'genetic entropy', causing the bacterium to 'devolve' away from an assumed created perfection (as though that were remotely possible), can be ruled out, because whatever the changes were, it led to a massive increase in the number of Y. pestis organisms, so was indisputably beneficial to it - in other words, in classical terms, it evolved.
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.
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.
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:
Ascaris lumbricoides (giant roundworm)
Trichuris trichiura (whipworm)
Ancylostoma duodenale and Necator americanus (hookworms)
Strongyloides stercoralis (threadworm)
Enterobius vermicularis (pinworm)
Wuchereria bancrofti and Brugia malayi (filarial worms)
Onchocerca volvulus (cause of river blindness)
Dracunculus medinensis (Guinea worm)
Toxocara spp (Toxocariasis)
Common Diseases Caused by Parasitic Nematodes in Humans
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.
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.
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.
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.
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.
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.
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.
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.
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 diseaseNew 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.
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 nematodes1,2,3 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 globally5,6, 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 parvum11,12. 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 leishmaniasis14,15. RNA virus infections have been identified in plant-parasitic nematodes16, parasitic flatworms17,18 and free-living nematodes17,19,20, 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. lumbricoides23,25. 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 parasites4,5,6,44,45. 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’ advantage14,15,47. 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.
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).
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?
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.
Immunofluorescence staining of human gastric cells grown in a microplate and infected with Chlamydia trachomatis. Blue: cell nuclei, green: C. trachomatis, grey: actin.
Image: Pargev Hovhannisyan / Universität Würzburg
Chlamydia doesn’t always cause symptoms, but when it does, these are some of the most common.
Chlamydia is a sexually-transmitted bacterial infection in which the bacteria are passed to a new victim during sexual intercourse. It caused few or no symptoms to begin with - usually nothing worse than mild itching - but if left untreated it can cause infertility and sometimes cancer. Fortunately, it can be treated successfully with antibiotics.
However, it is not unusual for people who have been successfully treated to develop a new infection with exactly the same strain as the previous infection, suggesting that the bacteria had somehow survived the antibiotic treatment although symptoms had disappeared, and traces of the bacteria had gone.
Researchers have now shown that chlamydia can take up residence in the gut where it can survive for some considerable time and develop increasing resistance to antibiotics with each course of treatment. The mechanism of this increasing resistance is a classic example of evolution as the antibiotic acts as an environmental selector which removes the non-resistant bacteria from the population gene pool, leaving the resistant form to become dominant in the gene pool.
The Annenberg Public Policy Centre of the University of Pennsylvania issued a warning today that, as the mpox virus (formerly known as the monkeypox virus) is making a significant comeback, both in the USA where it is making a resurgence, and in its homeland of Africa where a new, more deadly strain has recently evolved and spread to several states.
And, if you believe creationism's divine malevolence is responsible for designing these nasty little parasites, you will have to appreciate how it has been particularly sneaky with the virus, which is closely related to the variola virus that caused smallpox until smallpox was eradicated by a successful WHO vaccination campaign. This vaccination gave some incidental protection against the mpox virus but because smallpox has been eliminated, the vaccines are no longer given. This has allowed mpox to infect people, particularly those who were never vaccinated against smallpox and have never been exposed to the smallpox virus.
Cancer affects virtually all multicellular organisms, birds included. A new study highlights the trade-off between investment in reproduction and DNA maintenance. Birds laying larger numbers of eggs have less resources available to ensure the integrity of their DNA, leaving them more vulnerable to cancer.
Researchers at Arizona State University (ASU) have discovered a statistical link between the incidence of cancer in birds and their reproductive rates. As species, birds that lay more eggs are more liable to die of cancer.
The team attribute this to an evolutionary tradeoff between reproduction and survival. Those species which are more susceptible to cancer - which is a function of aging as the longer an individual lives the greater are its chances of developing a cancer - have evolutionary pressure to produce more offspring while young, where as those with a lower susceptibility can afford to expend less energy in reproducing and to spread it over a longer average lifespan.
This is easily understood as the result of an evolutionary process, as are cancers, which result from mistakes in cell replication, which is a sub-optimal, utilitarian process in multicellular organisms with specialised cells and tissues, resulting from inheriting the same mechanism that single-celled ancestors used so the whole genome is replicated in every cell, regardless of which genes those specialized cells will need.
If you've got money to invest, don't invest it all in one product. If that product fails you lose everything, so spread it around, that way you're reducing your risk and should have something left even if your main investment crashes. In other words, don't have all your eggs in one basket.
And Creationism's malevolent designer, who invested heavily in the SARS-CoV-2 virus as its preferred way to make people sick and die and to ruin national economies on a world-wide scale, understands that principle well. But the problem is, humans fought back and not only invented an effective vaccine that cut down the malevolence’s return on investment, but they also developed immunity which reduces the death toll down to a mere headache and feeling a bit lethargic for a few days.
Do you have any information on how many other species can also be infected with the SARS-CoV-2 virus?
Yes, many other species can be infected with the SARS-CoV-2 virus, the virus responsible for COVID-19 in humans. Research has identified several animals that can be naturally or experimentally infected. Here is an overview of some of the species known to be susceptible to SARS-CoV-2:
Domestic Animals:
Cats: Both domestic and big cats (like lions and tigers in zoos) have been infected. Cats can also transmit the virus to each other.
Dogs: Some dogs have tested positive, but they generally show no or mild symptoms.
Ferrets: Highly susceptible and can transmit the virus to other ferrets.
Mink: Infected minks have been found on farms, with some cases leading to large outbreaks and human infections.
*Wildlife:
Big Cats: Lions, tigers, snow leopards, and cougars in zoos have contracted the virus.
White-tailed Deer: Studies have shown that these deer can be infected and spread the virus among themselves.
Non-Human Primates: Various species of monkeys, such as rhesus macaques, cynomolgus macaques, and marmosets, can be infected and exhibit symptoms similar to humans.
Laboratory Animals:
Hamsters: Both Syrian and Chinese hamsters are susceptible and can transmit the virus.
Mice: Wild-type mice are generally not susceptible, but genetically modified mice expressing the human ACE2 receptor can be infected.
Rabbits: Some susceptibility has been observed, although with mild or no symptoms.
Tree Shrews: Can be infected and are used in research studies.
Farm Animals:
Pigs: Some studies have shown low susceptibility with no significant symptoms.
Cows** and **Chickens: Generally considered not susceptible based on current evidence.
The list of species continues to evolve as more research is conducted. Surveillance and studies are ongoing to better understand the range of susceptible species, their role in the transmission of the virus, and the potential implications for human and animal health.
By the divine malevolence was crafty and hedged its bets by designing the virus so it also infects wild animals so it can build up a nice little nest egg with which to launch another big raid on the futures market which could pay dividends in terms of human lives and increased suffering. All it need do is give the virus a little tweak and we could have another pandemic to rival the 2020 one all over again.
We have known about the zoonotic abilities of the virus for some time - after all it is believed to have evolved in another species before transferring to humans in 2019, but a team of Virginia Tech researchers have discovered that it may be more widespread in the wild animal populations, especially those near human habitation, than was previously thought.
Their results are published, open access in the journal Nature Communications and are explained in a Virginia Tech news release:
The virus that causes COVID-19 is widespread in wildlife, Virginia Tech scientists find Six of 23 common wildlife species showed signs of SARS-CoV-2 infections in an examination of animals in Virginia, as revealed by tracking the virus’s genetic code.
SARS-CoV-2, the virus responsible for COVID-19, is widespread among wildlife species, according to Virginia Tech research published today in Nature Communications. The virus was detected in six common backyard species and antibodies indicating prior exposure to the virus were found in five species with rates of exposure ranging from 40 to 60 percent depending on the species.
Genetic tracking in wild animals confirmed both the presence of SARS-CoV-2 and the existence of unique viral mutations with lineages closely matching variants circulating in humans at the time, further supporting human-to-animal transmission, the study found.
The highest exposure to SARS CoV-2 was found in animals near hiking trails and high-traffic public areas, suggesting the virus passed from humans to wildlife, according to scientists at the Fralin Biomedical Research Institute at VTC, the Department of Biological Sciences in Virginia Tech’s College of Science, and the Fralin Life Sciences Institute.
The findings highlight the identification of novel mutations in SARS-CoV-2 in wildlife and the need for broad surveillance. These mutations could be more harmful and transmissible, creating challenges for vaccine development.
The scientists stressed, however, that they found no evidence of the virus being transmitted from animals to humans, and people should not fear typical interactions with wildlife.
Investigators tested animals from 23 common Virginia species for both active infections and antibodies indicating previous infections. They found signs of the virus in deer mice, Virginia opossums, raccoons, groundhogs, Eastern cottontail rabbits, and Eastern red bats. The virus isolated from one opossum showed viral mutations that were previously unreported and can potentially impact how the virus affects humans and their immune response.
The virus can jump from humans to wildlife when we are in contact with them, like a hitchhiker switching rides to a new, more suitable host. The goal of the virus is to spread in order to survive. The virus aims to infect more humans, but vaccinations protect many humans. So the virus turns to animals, adapting and mutating to thrive in the new hosts.
Professor Carla Finkielstein, Co-corresponding author
Professor of biological sciences
Department of Biological Sciences
Virginia Tech, Blacksburg, VA, USA.
SARS CoV-2 infections were previously identified in wildlife, primarily in white-tailed deer and feral mink. The Virginia Tech study significantly expands the number of species examined and the understanding of virus transmission to and among wildlife. The data suggests exposure to the virus has been widespread in wildlife and that areas with high human activity may serve as points of contact for cross-species transmission.
This study was really motivated by seeing a large, important gap in our knowledge about SARS-CoV-2 transmission in a broader wildlife community. A lot of studies to date have focused on white-tailed deer while what is happening in much of our common backyard wildlife remains unknown.
Assistant Professor Joseph R. Hoyt, co-corresponding author
Assistant professor of biological sciences
Department of Biological Sciences
Virginia Tech, Blacksburg, VA, USA.
The research team collected 798 nasal and oral swabs across in Virginia from animals either live-trapped in the field and released, or being treated by wildlife rehabilitation centers. The team also obtained 126 blood samples from six species. The locations were chosen to compare the presence of the virus in animals in sites with varying levels of human activity, from urban areas to remote wilderness.
The study also identified two mice at the same site on the same day with the exact same variant, indicating they either both got it from the same human, or one infected the other.
Researchers are not certain about the means of transmission from humans to animals. One possibility is wastewater, but the Virginia Tech scientists believe trash receptacles and discarded food are more likely sources.
I think the big take home message is the virus is pretty ubiquitous. We found positives in a large suite of common backyard animals.
Dr Amanda R. Goldberg, first author
Department of Biological Sciences
Virginia Tech, Blacksburg, VA, USA.
While this study focused on the state of Virginia, many of the species that tested positive are common backyard wildlife found throughout North America. It is likely they are being exposed in other areas as well, and surveillance across a broader region is urgently needed, Hoyt said.
The virus is indifferent to whether its host walks on two legs or four. Its primary objective is survival. Mutations that do not confer a survival or replication advantage to the virus will not persist and will eventually disappear. We understood the critical importance of sequencing the genome of the virus infecting those species. It was a monumental task that could only be accomplished by a talented group of molecular biologists, bioinformaticians, and modelers in a state-of-the-art facility. I am proud of my team and my collaborators, their professionalism, and everything they contributed to ensure our success.
Professor Carla Finkielstein.
The Roanoke lab was established in April 2020 to expand COVID-19 testing.
Scientists should continue surveillance for these mutations and not dismiss them, the scientists said. More research is needed about how the virus is transmitted from humans to wildlife, how it might spread within a species, and perhaps from one species to another.
This study highlights the potentially large host range SARS-CoV-2 can have in nature and really how widespread it might be. There is a lot of work to be done to understand which species of wildlife, if any, will be important in the long-term maintenance of SARS-CoV-2 in humans.
Assistant Professor Joseph R. Hoyt.
But what we’ve already learned is that SARS CoV-2 is not only a human problem and that it takes a heck of a multidisciplinary team to address its impact on various species and ecosystems effectively.
Professor Carla Finkielstein.
The team will continue its research supported by a $5 million grant from the U.S. Department of Agriculture’s Animal and Plant Health Inspection Service.
Other authors on the paper include:
Kate Langwig, associate professor, Department of Biological Sciences, Fralin Life Sciences Institute
James Weger-Lucarelli, assistant professor, Department of Biomedical Sciences and Pathobiology, Virginia-Maryland College of Veterinary Medicine
Anne Brown, associate professor, Department of Biochemistry
Amanda Goldberg, former postdoctoral associate, Department of Biological Sciences
Jeffrey Marano, graduate research assistant, Department of Biological Sciences
Pallavi Rai, graduate research assistant, Department of Biomedical Sciences and Pathobiology, Virginia-Maryland College of Veterinary Medicine
Kelsi King, graduate research assistant, Genetics, Bioinformatics, and Computational Biology
Amanda Sharp, graduate research assistant, Genetics, Bioinformatics, and Computational Biology
Christopher Kailing, graduate research assistant, Department of Biological Sciences
Macy Kailing, graduate research assistant, Department of Biological Sciences
Members of the Virginia Tech Molecular Diagnostics Laboratory: Katherine L. Brown, Alessandro Ceci, Russell Briggs, Matthew G. Urbano, Clinton Roby
Details of the carrier species appear in the team's open access paper on Nature Communications:
Abstract
Pervasive SARS-CoV-2 infections in humans have led to multiple transmission events to animals. While SARS-CoV-2 has a potential broad wildlife host range, most documented infections have been in captive animals and a single wildlife species, the white-tailed deer. The full extent of SARS-CoV-2 exposure among wildlife communities and the factors that influence wildlife transmission risk remain unknown. We sampled 23 species of wildlife for SARS-CoV-2 and examined the effects of urbanization and human use on seropositivity. Here, we document positive detections of SARS-CoV-2 RNA in six species, including the deer mouse, Virginia opossum, raccoon, groundhog, Eastern cottontail, and Eastern red bat between May 2022–September 2023 across Virginia and Washington, D.C., USA. In addition, we found that sites with high human activity had three times higher seroprevalence than low human-use areas. We obtained SARS-CoV-2 genomic sequences from nine individuals of six species which were assigned to seven Pango lineages of the Omicron variant. The close match to variants circulating in humans at the time suggests at least seven recent human-to-animal transmission events. Our data support that exposure to SARS-CoV-2 has been widespread in wildlife communities and suggests that areas with high human activity may serve as points of contact for cross-species transmission.
Introduction
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent of coronavirus disease 2019 (COVID-19), has resulted in over 771 million human cases and over six million deaths worldwide1. As SARS-CoV-2 becomes endemic in humans, one of the greatest threats to public health is the resurgence of more virulent and transmissible variants. The considerable pathogen pressure imposed by the pandemic has caused concern as to whether SARS-CoV-2 will spill into wildlife populations, establish a sylvatic cycle, and potentially serve as a source for new variants.
Transmission of SARS-CoV-2 to captive animals has been well documented2,3,4, but detections in free-ranging wildlife are currently limited to only a few species including white-tailed deer (Odocoileus virginianus5,6,7), feral mink (Neovison vison8), and Eurasian river otters (Lutra lutra9). Experimental infections and modeling of the functional receptor for SARS-CoV-2 (angiotensin-converting enzyme 2: ACE2) have shown that numerous wildlife species may be competent hosts10,11,12,13,14,15. However, it remains unexplored whether a diversity of wildlife species are infected in natural settings, where exposure to SARS-CoV-2 is likely to be indirect and at a lower exposure dose.
Since the emergence of SARS-CoV-2 in 2019, numerous variants have been detected in humans and animals. Many variants that have become dominant have mutations that increase their infectivity in humans16, and may also impact the virus’s ability to infect new wildlife species. SARS-CoV-2 collected from white-tailed deer have included lineages circulating in humans, caused by human-to-deer transmission5, but have also included lineages with unique mutations suggestive of deer-to-deer transmission17. This implies that only minimal adaptation may be needed for transmission to occur among deer following initial human-to-animal transmission events18. Other human peridomestic species, such as deer mice (Peromyscus maniculatus)12,13 and skunks (Mephitis mephitis)14 have been shown to be capable of viral shedding in laboratory settings11. Collectively, these studies raise important questions about the extent of human-to-wildlife transmission and the ability of other wildlife species to sustain transmission.
Establishment of SARS-CoV-2 infections in wildlife communities could result in novel mutations that increase virulence, transmissibility, or confer immune escape, negatively impacting both human and wildlife populations. Furthermore, as SARS-CoV-2 adapts to not only human hosts, but potentially a wide diversity of wildlife species, SARS-CoV-2 evolution may become more unpredictable19. This could present several challenges for human health, including concerns related to vaccine development targeting human-specific lineages, and novel impacts to pathogenicity and transmissibility of the virus.
Here, we examine how widespread SARS-CoV-2 exposure has been in wildlife communities between May 2022 and September 2023. We used quantitative reverse transcription polymerase chain reaction (RT-qPCR) to examine 789 nasopharyngeal/oropharyngeal samples from 23 species sampled across Virginia and Washington D.C., USA and documented the presence of SARS-CoV-2 RNA in six of these species. In addition, we analyzed 126 serum samples from six species collected before and after the arrival of SARS-CoV-2 and detected neutralizing antibody titers in five of the six species. Finally, we detected an effect of urbanization and human use on seropositivity in animals, and examined genomic data associated with positive samples.
Goldberg, A.R., Langwig, K.E., Brown, K.L. et al. Widespread exposure to SARS-CoV-2 in wildlife communities.Nat Commun 15, 6210 (2024). https://doi.org/10.1038/s41467-024-49891-w
The fact that this virus is so capable of infecting other species is a cause for concern because the wider it spreads and the more species it come into contact with, the greater the chance of it crossing over to new species, and the more species it infects, the greater the probability of new variants evolving that can transfer back into humans with unpredictable consequences.
Creationists must be very proud of the devious nastiness of their favorite malevolence.
