The U.S. Department of Agricultures (USDA) Animal and Plant Health Inspection Service (APHIS) has found that SARS-CoV-2, the virus causing COVID-19, has widely spread within the U.S. white-tailed deer population, possibly transmitted from humans to deer, where it mutated and potentially transmitted back to humans. The findings are part of a study involving the surveillance of over 11,000 white-tailed deer.
White-tailed deer (Odocoileus virginianus) in 2022, 12.2% were carrying the virus and 31% showed signs of previous exposure.
If you're a malevolent designer and you just had a major triumph with a nasty little virus that killed millions, made many more times that sick, and wrecked economies worldwide, but the human victims hit back with a vaccine that protects them, what do you do?
We'll, if you're creationism's favourite sadist, you don't just give up and allow your victims to win; you have a long-term plan to teach the upstarts a lesson.
Using the fact that immunity to your virus is short-lived because you designed their immune systems that way, you store your nasty little virus away somewhere where there is no vaccine-induced immunity and you can experiment with better, more deadly and more infectious versions of it and wait until your human victims no longer have enough immunity to resist the new, improved, version, then you transfer it back into the human population and sit back to enjoy the suffering again!
And what better than a wild species that humans regularly hunt for food, but which don't need to meet the food-hygiene regulations with which humans normally protect themselves from infections in domesticated species.
In China, this could be practically any species, but in North America, what better species is there than the white-tailed deer, which is regularly hunted for meat?
This, of course, is the sort of thinking an honest, troobuleeving creationist (if there is such a thing) would have to believe, because the evidence is that white tailed deer are a reservoir species harbouring the SARS-CoV-2 and providing an environment in which to mutate and evolve.
This evidence comes from the United States Department of Agriculture’s (USDA) Animal and Plant Health Inspection Service (APHIS) which has just released the results of its first year of sampling white-tailed deer (Odocoileus virginianus) for active infection of SARS-CoV-2, the virus that causes COVID-19. These studies show that SARS-CoV-2 is likely to have spread widely within the U.S. white-tailed deer population.
According to a USDA APHIS news item:
Creationism's divine malevolence excelled itself with the SARS-CoV-2 virus that caused the COVID-19 pandemic, killing millions, making hundreds of millions more sick either in the short term with the initial infection, or long-term with the long-lasting aftereffects experienced by some victims with 'long-COVID'. It managed to achieve a stunning over three-quarters of a billion cases worldwide with nearly 7 million deaths, as of 18 May 2023, not to mention the bankrupted business and ruined national economies.
But human science having hit back with a vaccine produced in record time, it then had to go into an arms race of new, resistant variants to keep it ahead of science. The most successful of those, Omicron, resulted in unprecedented peaks of cases although deaths were relatively low due to the vaccines.
And now, not to be outdone by humans, it has produced the latest variant, a version of Omicron (Omicron XBB.1.16) that epidemiologists have named Arcturus.
Should we be concerned, that Arcturus can evade the immunity conveyed by vaccines, regular booster vaccines and natural immunity due to previous infections? Here is how Manal Mohammed, a Senior Lecturer and Medical Microbiology at the University of Westminster, UK sees it. Her article is reprinted from The Conversation under a Creative Commons licence, reformatted for stylistic consistency:
Arcturus: what to know about the new COVID variant, omicron XBB.1.16
A new COVID variant XBB.1.16, or “Arcturus”, has now been identified in at least 34 countries including the UK.
Arcturus is a subvariant of omicron and was first detected in India in January 2023.
As of April 17, the latest date up to which the UK Health Security Agency (UKHSA) has reported data on this variant in the UK, 105 cases of Arcturus had been sequenced across England. Five Britons who tested positive for Arcturus have died.
It’s important to note that only a small portion of COVID infections undergo genetic sequencing, so it’s likely there are many more cases of Arcturus. The UKHSA recently reported that the variant is making up 2.3% of sequences in the UK.
Meanwhile, Arcturus has been steadily rising in the US in recent weeks, accounting for more than 10% of new confirmed COVID cases as of the end of April.
But the variant has been most dominant in India, which had recorded 61% of global sequences of Arcturus as of mid-April. It has driven a huge increase in cases in India over the past month. The country was recording more than 10,000 COVID cases each day with Arcturus making up about two-thirds of all cases. Fortunately this wave now appears to be on the decline.
Nonetheless, Arcturus has been classified as a variant of interest by the World Health Organization. So what do we know about this variant, and should we be worried?
XBB.1.16 is a descendant of XBB, a recombinant omicron strain, meaning it contains genetic material from two different variants. Specifically, XBB is a mixture of two BA.2 sublineages: BA.2.10.1 and BA.2.75.
XBB has shown increased transmissibility relative to earlier variants, probably because it appears to be better at evading existing immunity from vaccination and prior infections.
Arcturus is very closely related to XBB.1.5, also known as Kraken.
Compared with its parent strain XBB, Arcturus has three additional mutations in the spike protein: E180V, F486P and K478R. This is a protein on the surface of SARS-CoV-2 (the virus that causes COVID) which allows it to bind to and infect our cells.
Arcturus is understood to be the most contagious subvariant yet, and these additional mutations might explain why.
The typical symptoms of COVID include fever, cough, runny nose and loss of sense of taste or smell. However, doctors in India have reported conjunctivitis symptoms in children infected with Arcturus, which has not generally been seen in earlier COVID waves.
What about vaccine protection?
COVID vaccines target the spike protein of SARS-CoV-2. As such, mutations in the spike protein may affect how well the vaccines work.
There is no data yet on vaccine efficacy against Arcturus. However, a recent study found that among people who had been vaccinated or previously infected, the antibody responses generated against closely related strains XBB and XBB.1 were significantly lower than against other variants.
So XBB subvariants could threaten current COVID vaccines and therapeutics. But importantly, it’s likely vaccines still offer good protection against severe disease.
While further studies are needed to confirm how Arcturus responds to vaccines, scientists are continuing work on new vaccines that could offer stronger protection against emerging variants.
The continued evolution of omicron
Although omicron was first detected in late 2021 it continues to evolve resulting in new subvariants. Arcturus is one of some 600 detected to date.
This is to be expected in a highly vaccinated population. New variants naturally evolve to evade existing defences. Those strains with a competitive advantage – namely greater transmissibility and capacity to escape our immune response – will dominate. Arcturus may yet fuel a rise in cases in the UK and elsewhere.
However, there is no great cause for concern. While scientists will continue to monitor Arcturus, there’s no evidence at this stage to suggest it’s more severe than previous variants. In addition, we have good protection now from vaccines and natural infection.
That said, the continued evolution of COVID and the emergence of new strains such as Arcturus is a reminder that the virus is still with us. For those eligible for further boosters, it’s important to keep these up to date.
Manal Mohammed, Senior Lecturer, Medical Microbiology, University of Westminster
Published by The Conversation. Open access. (CC BY 4.0)
I'm still waiting for an intelligent reply explaining why creationists would rather we thought of their putative designer god as a pestilential malevolence forever designer new and better ways to make its creation suffer, than have people accept that the theory of evolution explains the origins of parasites like the SARS-CoV-2 coronavirus as a natural process, without the intervention of a supernatural deity - which would let their favourite genocidal monster off the hook.
Endogenous retroviruses have long been a bugbear for creationists in that they show convincing evidence of evolutionary phylogeny and common ancestry, so this paper which reveals the recent entry into the genome of the African rhinoceroses but not the Asian rhinoceroses, shows that the African rhinos share a common ancestor more recently than they share a common ancestor with the Asian species. That African ancestor became infected after it split from the common ancestor of the African and Asian rhinos.
The research team was led by Alex D. Greenwood of the Department of Wildlife Diseases, Leibniz Institute for Zoo and Wildlife Research (IZW), Berlin, Germany.
First, a little about ERV's:
Endogenous retroviruses (ERVs)
Endogenous retroviruses (ERVs) are remnants of ancient retroviral infections that have become permanently integrated into the genome of the host organism. They are found in the genomes of most vertebrates, including humans. ERVs are considered "endogenous" because they are passed from generation to generation and are inherited in a Mendelian fashion, just like other genes.
The life cycle of a retrovirus involves the reverse transcription of its RNA genome into DNA, which is then integrated into the host genome. Occasionally, retroviruses infect germ cells (cells that give rise to eggs or sperm) and their DNA is inserted into the genome of the offspring. Over time, these integrated viral sequences can become fixed in the population and passed on to future generations.
ERVs provide evidence for evolution in several ways:
Shared ERVs among species: ERVs are found in the genomes of different species, and the presence of the same ERV at the same genomic location in different species suggests a common ancestor. For example, scientists have identified a specific retroviral sequence called "HERV-K" that is present in the genomes of humans, chimpanzees, and other primates. The shared presence of this ERV provides strong evidence for a common evolutionary history.
ERV distribution and phylogenetic relationships: The distribution of ERVs across different species can be used to construct phylogenetic trees, which illustrate the evolutionary relationships between species. By comparing the presence or absence of specific ERVs in different genomes, scientists can infer the evolutionary history and relatedness of species. This approach has been used to study the evolutionary relationships between primates and other mammals.
ERVs as "molecular fossils": ERVs can act as "molecular fossils" that provide insights into ancient viral infections and evolutionary events. By studying the DNA sequences of ERVs, scientists can gain information about the timing of viral integration events and the evolutionary relationships between different ERVs. This information helps reconstruct the evolutionary history of the host species.
Functional remnants of ERVs: Although most ERVs have accumulated mutations over time and lost their ability to produce functional viral particles, some ERVs retain functional elements. These functional remnants can have important roles in the regulation of gene expression and embryonic development. For example, certain ERVs have been co-opted by the host organism to play a role in placenta formation in mammals. This co-option of ERV sequences for new functions illustrates the process of exaptation, where existing genetic material is repurposed for novel functions during evolution.
chatGPT3, "Tell me all about endogenous retroviruses (ERV's), how they enter the genome and why they are evidence for evolution, with references, please.
[Response to user question] Retrieved from https://chat.openai.com
The press release from the Leibniz Institute for Zoo and Wildlife Research explains the research and its significance:
Rhinoceros belong to a mammalian order called odd-toed ungulates that also include horses and tapirs. They are found in Africa and Asia. Until recently, evidence suggested that throughout their evolutionary history, gammaretroviruses such as Murine leukemia virus had not colonised their genomes, unlike most other mammalian orders. The colonisation process is called retroviral endogenisation and has resulted in most mammalian genomes being comprised of up to ten percent retroviral like sequences. An analysis of modern and extinct rhino genomes headed by the German Leibniz Institute for Zoo and Wildlife Research (Leibniz-IZW) now found that African rhinos have dozens of gammaretroviruses in their genomes absent from the genomes of Asian rhino species, such as the Sumatran and Javan rhino, and that the African black rhino has two related groups, one missing from the white rhinos. The restriction of gammaretroviruses to African rhinos and the close relatedness of the viruses to rodent viruses, particularly those of African rodents, suggests that African rhinos were infected by an exogenous viral variant and their genomes colonised in Africa. The work is published in the scientific “Journal of Virology”.
We had data from several rhino species where we kept finding large portions of gammaretroviruses. When we used much newer and more complete reference genomes from modern and extinct rhinos we found that only African rhinos had been colonised
Dr Kyriakos Tsangaras, lead author
Department of Life and Health Sciences
University of Nicosia, Nicosia, Cyprus
This ultimately comes down to lack of high-quality reference sequences of wildlife. While things have improved a lot since the first human genome was sequenced, you miss things such as viral history when the databases lack so many species or high-quality reference genomes from many species. It is really another example of why we need more genome reference sequences from wildlife because we don’t know what other things we are missing and which conclusions we draw about presence and absence of sequences that may turn out to be a consequence of too little information.
Professor Alex Greenwood, Senior author
Head of the Wildlife Disease Department.
Leibniz Institute for Zoo and Wildlife Research
Berlin, Germany
Retroviruses such as the causal agent of aids, HIV-1, are unique among viruses in that they have to integrate into the DNA of the host as part of their replication cycle. If this happens in the germline in spermatocytes or oocytes, they can become a part of the host genome that is inherited by the following generation and then are present in every cell of offspring bodies. This evolutionary process has happened so often that on average up to ten per cent of the mammalian genome is made up of retroviruses or their remnants. A previous study of available genomes from horses and their relatives suggested that they, along with rhinos and tapirs, had not been invaded by gammaretroviruses, a group of viruses related to mouse and bird viruses that have successfully colonised most mammalian genomes.
Together with colleagues from Australia and Germany the scientific team found that in fact two different viral groups had colonised African rhinos. One of them had only colonised the black rhino (Diceros bicornis) and not the white rhino (Ceratotherium simum) and was evolutionarily younger than the one shared by both. As both groups are restricted to African rhinos the study suggests that the African rhino lineage was infected and their genomes colonised in Africa, and that is why the respective gammaretroviruses are not found in Asian rhinoceros and other rhino relatives.
More detail is given in the team's paper in the Journal of Virology, which sadly lies behind a paywall. However, the abstract is freely available:
ABSTRACT
High-throughput sequences were generated from DNA and cDNA from four Southern white rhinoceros (Ceratotherium simum simum) located in the Taronga Western Plain Zoo in Australia. Virome analysis identified reads that were similar to Mus caroli endogenous gammaretrovirus (McERV). Previous analysis of perissodactyl genomes did not recover gammaretroviruses. Our analysis, including the screening of the updated white rhinoceros (Ceratotherium simum) and black rhinoceros (Diceros bicornis) draft genomes identified high-copy orthologous gammaretroviral ERVs. Screening of Asian rhinoceros, extinct rhinoceros, domestic horse, and tapir genomes did not identify related gammaretroviral sequences in these species. The newly identified proviral sequences were designated SimumERV and DicerosERV for the white and black rhinoceros retroviruses, respectively. Two long terminal repeat (LTR) variants (LTR-A and LTR-B) were identified in the black rhinoceros, with different copy numbers associated with each (n = 101 and 373, respectively). Only the LTR-A lineage (n = 467) was found in the white rhinoceros. The African and Asian rhinoceros lineages diverged approximately 16 million years ago. Divergence age estimation of the identified proviruses suggests that the exogenous retroviral ancestor of the African rhinoceros ERVs colonized their genomes within the last 8 million years, a result consistent with the absence of these gammaretroviruses from Asian rhinoceros and other perissodactyls. The black rhinoceros germ line was colonized by two lineages of closely related retroviruses and white rhinoceros by one. Phylogenetic analysis indicates a close evolutionary relationship with ERVs of rodents including sympatric African rats, suggesting a possible African origin of the identified rhinoceros gammaretroviruses.
IMPORTANCE:Rhinoceros genomes were thought to be devoid of gammaretroviruses, as has been determined for other perissodactyls (horses, tapirs, and rhinoceros). While this may be true of most rhinoceros, the African white and black rhinoceros genomes have been colonized by evolutionarily young gammaretroviruses (SimumERV and DicerosERV for the white and black rhinoceros, respectively). These high-copy endogenous retroviruses (ERVs) may have expanded in multiple waves. The closest relative of SimumERV and DicerosERV is found in rodents, including African endemic species. Restriction of the ERVs to African rhinoceros suggests an African origin for the rhinoceros gammaretroviruses.
Tsangaras K, Mayer J, Mirza O, Dayaram A, Higgins DP, Bryant B, Campbell-Ward M, Sangster C, Casteriano A, Höper D, Beer M, Greenwood AD (2023) Evolutionarily young African rhinoceros gammaretroviruses. J VIROL 97, e0193222. https://doi.org/10.1128/jvi.01932-22.
To any normal person, evidence like this would confirm evolutionary divergence, firstly between the African and Asian rhinoceroses, then, later between the African rhinoceroses.
It would also show that the scientists are in no doubt that evolution is the fundamental explanation for their findings, with no hint that they believe magic and supernatural magicians were involved, like creationist frauds fool their dupes into believing they increasingly are. Indeed, why would they? What rational, educated adult, with a mental age greater than about 9, believes in magic or supernatural magicians and thinks they should play any part in scientific explanations of real-world evidence?
If you've bought into the Creation Cult's intelligent [sic] design notion, it's probably best to ignore articles like this that might cause you to doubt the competence of your putative designer, but you're probably used to ignoring evidence that refutes creationism or you wouldn't have fallen for the intelligent [sic] design hoax in the first place.
Nevertheless, it discoveries such as this by Danish Scientists led by Shiraz A. Shah, of Copenhagen University Hospital, Herlev-Gentofte, Gentofte, Denmark, together with colleagues from France and Canada, that highlight the way arms races can lead to ludicrous levels of complexity of which any even half-competent designer would be rightly ashamed.
It comes about because the human gut, especially that of babies, is an ideal, warm, moist, and nutrient-rich environment for micro-organisms, so is teeming with bacteria, protozoa, and viruses, some of which are harmless but some of which parasitize both the microbes and the human cells of the gut.
One incidental benefit that creationists will point to is that the presence of these organisms probably helps train the developing babies’ immune system so it is more effective in later life, so the presence of these organisms can be beneficial.
But hold on! What are they 'training the immune system' for? They are training it to protect us from the very bacteria that the supposedly intelligent designer designed to harm us. At least, since it is supposedly omniscient, it knew what its bacteria and viruses would do when it designed them, so we must assume it designed them for that purpose.
And, if we accept that it designed bacteria to train our immune system, why did it then design the viruses that kill these beneficial bacteria?
But whatever it was thinking of, if 'thinking' is the appropriate term, the result is a baby’s gut teeming with more than 200 different families of virus, many of which were unknown prior to this study. The team's findings are published, open access, in the journal Nature Microbiology.
The research and its significance is explained in a University of Copenhagen news release:
Distribution of endogenous MCP clusters across 462 genomes from 238 protist species. MCP clusters (25% identity across 30% length, 73 clusters) are shown as inner circles scaled in size according to the number of MCPs in each cluster. Numbers refer to the MCP cluster number assigned, with the larger viral groups labeled. MCP clusters are connected to the eukaryotic species (based on NCBI taxonomy) they are found in. Clusters with a more diverse host range are drawn closer to the center of the plot.
Q. What is the difference between an evolved organism, and one allegedly designed by creationism's putative intelligent designer?
A. Nothing! They both look like no intelligence was involved in their design, because they will both have masses of waste, ludicrous complexity, and no ultimate purpose, other than making more copies of themselves.
Although creationists have been programmed to point to complexity as evidence of design, it is actually evidence of bad (or no) design, because good, intelligent design is minimally complex.
This point was neatly illustrated in a paper published in PNAS a couple of days ago which showed that the genome of single-celled, eukaryote organisms contains ancient 'fossil' endogenous retroviruses (ERVs) that do nothing but need to be replicated every time the organism replicates, wasting resources and risking error. Altogether the team found remnants of over 30,000 such viruses.
The discovery was made by a group of researchers led by Dr. Christopher Bellas and colleagues from the University of Innsbruck, Austria, with colleagues from the University of Groningen, The Netherlands and Max Planck Institute for Medical Research, Heidelberg, Germany.
The team were interested in the new 'Polinton-like viruses' that two of the team had previously found in protista from an Austrian alpine lake. According to my AI software, ChatGPT:
Apart from having to design the virus to overcome the defences it designed to protect us from the viruses it creates to harm up, if you follow me, it then has to continually modify its design to overcome the defences human medical science devises, such as vaccines (which only work because we have those defences in the first place, no matter how inadequate). It is as though Creationism's supposedly omniscient, omnipotent designer doesn't have a clue about the future and can only respond when it happens.
And, like a true amnesiac, it seems to forget entirely what it designed yesterday, and why it designed it, so it ends up in a pointless and wasteful arms race with itself; continually designing solutions today to the solutions it designed yesterday which it now thinks are new problems to be solved.
And now we learn from a study by researchers at Sweden's Karolinska Institutet that infection by one of its earlier designs, the OC43 corona virus which causes the common cold, produces antibodies that give some protection against its SARS-CoV-2 coronavirus!
Figure 2
Intra- and inter-ring interactions. A The primary intra-ring interface between two subunits (green and cyan) within a ring. B Schematic quantifying interactions from a single subunit (α) to illustrate the extensive, cooperative network. Numbers and line widths (not lengths) correspond to quantification of the interactions between α and neighboring subunits as calculated by the PDBePISA server (Supplementary Tables 3 and 4). C Surface representation of two subunits reveals a ball and socket geometry between rings. A single subunit (orange) has two loops (Loop1 and Loop2) that fit into sockets (Socket1 - gray, and Socket2 - white) of a subunit in the ring below it (green). D Surface electrostatics of ring interfaces demonstrate an important role for electrostatics in inter-ring interactions.
Agnello, et. al., (2023), Journal of Biological Chemistry
Creationists would have us believe that there are two forms of life on Earth - that designed by their putative, omnibelevolent, omniscient, omnipotent god and that designed by some magical thing (or is it a process?) called 'sin'. For some mysterious reason, their supposedly omnipotent, omniscient god doesn't have enough power to overcome this 'sin' and is reduced to playing inevitable games with it such as indulging in arms races to defend its creation while 'sin' tries to harm it.
In addition, Creationists believe one of two things:
Their god didn't know when he created the mythical founder couple, Adam & Eve, that this would result in this 'sin' thing being created.
It did know, but created them anyway, presumably not understanding the consequences.
And of course they believe in the literal truth of the Bible where their god is reported as telling Isaiah that in fact he created evil.:
I form the light, and create darkness: I make peace, and create evil: I the Lord do all these things.
Isiah 47:7
And they also believe that their god created everything on Earth for his special creation, them of course, or more generally, all humans
Not for the first time, Creationism requires its dupes to believe two or more mutually exclusive things simultaneously. g a
So, with that in mind, imagine being a Creationist and trying to understand what on Earth your magic god was trying to achieve when it created bacteria, then created the phage viruses to parasitise them, described in the research by a team from the Department of Biochemistry and Molecular Biotechnology, University of Massachusetts Chan Medical School, Worcester MA, USA.
Their research is published open access in the Journal of Biological Chemistry and described in the magazine for the American Society for Biochemistry and Molecular Biology (ASBMB). It describes a phage virus, P74-26, nicknamed the “Rapunzel bacteriophage”, with an extraordinarily long 'tail' which is capable of parasitising even extremophile bacteria that live in hot springs where temperatures can reach 170oC. Neither these bacteria nor the phage virus appear to have any benefit to mankind.
The study was to determine the construction and function of the very long 'tail'.
The discovery was of something that the Creationist idol, Michael J Behe would undoubtedly proclaim as 'irreducibly complex', therefore proof that the locally popular god did it.
To make matters worse for Creationists, the study casually and unintentionally refutes one of the lies that their cult leaders fool them with - that the Theory of Evolution (TOE) is being increasingly rejected by mainstream biologists in favour of their childish, magical and supernatural explanation. The scientists who did the study are in no doubt that the 'tail' is a product of an evolutionary process and that the TOE is a perfect model for explaining and understanding the observed facts.
From the ASBMB magazine:
A recent study in the Journal of Biological Chemistry has revealed the secret behind an evolutionary marvel: a bacteriophage with an extremely long tail. This extraordinary tail is part of a bacteriophage that lives in inhospitable hot springs and preys on some of the toughest bacteria on the planet.
Bacteriophages are a group of viruses that infect and replicate in bacteria and are the most common and diverse things on Earth.
The bacteriophage P74-26 has a tail 10 times longer than most other phage tails and is nearly 1 micrometer long, about the width of some spider’s silk.
Angnello, et al.(2023) Journal of Biological Chemistry
Bacteriophages, or phages for short, are everywhere that bacteria are, including the dirt and water around you and in your own body’s microbial ecosystem as well.
Each phage tail is made up of many small building blocks that come together to form a long tube. Our research finds that these building blocks can change shape, or conformation, as they come together. This shape-changing behavior is important in allowing the building blocks to fit together and form the correct structure of the tail tube.
We used a technique called cryo-electron microscopy, which is a huge microscope that allows us to take thousands of images and short movies at a very high magnification. By taking lots of pictures of the phage’s tail tubes and stacking them together, we were able to figure out exactly how the building blocks fit together.
Bacteriophages are gaining ever-growing interest as an alternative to antibiotics for treating bacterial infections. By studying phage assembly, we can better understand how these viruses interact with bacteria, which could lead to the development of more effective phage-based therapies. … I believe that studying unique, interesting things can lead to findings and applications that we can’t even yet imagine.
Emily Agnello, first author
Department of Biochemistry and Molecular Biotechnology
University of Massachusetts Chan Medical School
Worcester, MA, USA.
Unlike many of the viruses that infect humans and animals that contain only one compartment, phages consist of a tail attached to a spiky, prismlike protein shell that contains their DNA.
Phage tails, like hairstyles, vary in length and style; some are long and bouncy while others are short and stiff. While most phages have short, microscopic tails, the “Rapunzel bacteriophage” P74-26 has a tail 10 times longer than most and is nearly 1 micrometer long, about the width of some spider’s silk. The “Rapunzel” moniker is derived from the fairy tale in which a girl with extremely long hair was locked in a tower by an evil witch.
Brian Kelch, an associate professor of biochemistry and molecular biotechnology at UMass Chan who supervised the work, described P74-26 as having a “monster of a tail.”
transmission electron micrograph of multiple bacteriophages attached to a bacterial cell wall; the magnification is approximately 200,000.
Professor Graham Beards, (Wikimedia Commons)
Compared with most phages, P74-26 uses half the number of building blocks to form stacking rings that make up the tail.
Phage tails are important for puncturing bacteria, which are coated in a dense, viscous substance. P74-26’s long tail allows it to invade and infect the toughest bacteria. Not only does P74-26 have an extremely long tail, but it is also the most stable phage, allowing it to exist in and infect bacteria that live in hot springs that can reach over 170° F. Researchers have been studying P74-26 to find out why and how it can exist in such extreme environments.
To work with a phage that thrives in such high temperatures, Agnello had to adjust the conditions of her experiments to coax the phage tail to assemble itself in a test tube. Kelch said Agnello created a system with which she could induce rapid tail self-assembly.
I like to think about these phage building blocks as kind of like Legos. The Lego has studs on one side and the holes or sockets on the other. Imagine a Lego where the sockets start off closed. But as you start to build with the Legos, the sockets begin to open up to allow the studs on other Legos to build a larger assembly. This movement is an important way that these phage building blocks self-regulate their assembly.
We think what has happened is that some ancient virus fused its building blocks into one protein. Imagine two small Lego bricks are fused into one large brick with no seams. This long tail is built with larger, sturdier building blocks. We think that could be stabilizing the tail at high temperatures.
Brian A. Kelch, corresponding author
Department of Biochemistry and Molecular Biotechnology
University of Massachusetts Chan Medical School
Worcester, MA, USA
The researchers used high-power imaging techniques as well as computer simulations and found that the building blocks of the tail lean on each other to stabilize themselves.
They found P74-26 uses a “ball and socket” mechanism to sturdy itself. In addition, the tail is formed from vertically stacking rings of molecules that make a hollow canal.
Kelch pointed out that, compared with most phages, P74-26 uses half the number of building blocks to form stacking rings that make up the tail.
The researchers now plan to use genetic manipulation to alter the length of the phage tail and see how that changes its behavior.
Phages occupy almost every corner of the globe and are important to a variety of industries like healthcare, environmental conservation and food safety. In fact, long-tailed phages like P74-26 have been used in preliminary clinical trials to treat certain bacterial infections.
More technical detail is given in the teams open access paper in the Journal of Biological Chemistry:
Abstract
Tail tube assembly is an essential step in the lifecycle of long-tailed bacteriophages. Limited structural and biophysical information has impeded an understanding of assembly and stability of their long, flexible tail tubes. The hyperthermophilic phage P74-26 is particularly intriguing as it has the longest tail of any known virus (nearly 1 μm) and is the most thermostable known phage. Here, we use structures of the P74-26 tail tube along with an in vitro system for studying tube assembly kinetics to propose the first molecular model for the tail tube assembly of long-tailed phages. Our high resolution cryo-EM structure provides insight into how the P74-26 phage assembles through flexible loops that fit into neighboring rings through tight “ball-and-socket”-like interactions. Guided by this structure, and in combination with mutational, light scattering, and molecular dynamics simulations data, we propose a model for the assembly of conserved tube-like structures across phage and other entities possessing Tail Tube-like proteins. We propose that formation of a full ring promotes the adoption of a tube elongation-competent conformation among the flexible loops and their corresponding sockets, which is further stabilized by an adjacent ring. Tail assembly is controlled by the cooperative interaction of dynamic intra- and inter-ring contacts. Given the structural conservation among tail tube proteins and tail-like structures, our model can explain the mechanism of high-fidelity assembly of long, stable tubes.
Agnello, Emily; Pajak, Joshua; Liu, Xingchen; Kelch, Brian A.
Conformational dynamics control assembly of an extremely long bacteriophage tail tube
Journal of Biological Chemistry; (2023). DOI: 10.1016/j.jbc.2023.103021
So, from a Creationist point of view, a massively complex solution to the problem of how to get through the defences of a bacterium that was designed to protect it from viruses in order to kill bacteria that, because they inhabit such extreme conditions, are or complete indifference to humans, being neither harmful nor harmless.
Creationists also argue that bacteria and viruses were created by 'sin' in some unexplained magical process, so this 'sin' thing is designing parasites to attack the parasites it creates!
It takes some special mental gymnastics to believe these organisms and the relationships between them are the result of an intelligent design process and not the result of a mindless, utilitarian natural process in which neither magic nor magicians was involved.
An open access paper published a couple of weeks ago in the journal Genes should have set alarm bells ringing in Creationists circles, assuming anyone in Creationist circles reads peer-reviewed science and risks having their cherished superstitions spoilt with facts.
The paper was a report on the findings of a team of researchers from the University of Illinois at Urbana-Champaign, Illinois, USA into why, during a summer 2022 outbreak of the highly infectious viral disease of white-tailed deer, Odocoileus virginianus, some deer remained unaffected while scores of others died within days of infection.
The disease, epizootic haemorrhagic disease (EHD), is caused by a double-stranded RNA virus, spread by a midge. There are outbreaks of this disease every 3-5 years.
The team sequenced the entire genome of the white-tailed deer for the first time and found variations in one particular gene associated with apparent immunity to EHD.
So, why should this concern Creationists?
Bearing in mind that Creationists insist their supposed intelligent [sic] designer is omniscient and so knows exactly what its designs will do when it designs them, if we buy into this evidence-free superstition, we have to believe:
Creationist's intelligent [sic] designer designed the virus that causes EHD to kill white-tailed deer, and designed the midge to act as the vector for the disease to ensure the virus gets spread to kill new victims.
It then gave some deer a modified gene which protects it from the virus it designed to kill them.
It could have given all white-tailed deer this protective gene, but chose not to.
Therefore the only conclusion is that it wanted most deer to be susceptible to the fatal disease it had designed to make them suffer and die.
As though that evidence of malevolence wasn't enough, what we have here is a simple example of how a mutant alle can give carriers of that mutation a significant advantage over carriers of the non-advantageous alle. It would take an exceptional degree of denialism to conclude that killing carriers of the non-protective allele while allowing carriers of the protective mutation to survive is not going to lead to an increase in the copies of that protective allele in the population gene pool over time.
In other words, what we have here is a perfect example of evolution by mutation and natural selection - the very same process that created the viral parasite in the first place. Evolution being defined by biological science as change in allele frequency in a population over time, not the childish Creationist parody of one species magically turning into another, unrelated species, in a single event.
Creationists need to explain why the patently obvious isn't true and why malevolent intent is a better explanation for these deer being killed by a virus, and Creationism's putative designer's apparent malevolent intent in creating the disease in the first place.
The research team's work was explained in a University of Illinois news release. As you read this, bear in mind that what the article is describing is what Creationists believe was created deliberately by their allegedly omniscient, omni-benevolent deity:
URBANA, Ill. – It was the height of summer 2022 when the calls started coming in. Scores of dead deer suddenly littered rural properties and park preserves, alarming the public and inconveniencing landowners. According to officials at the Urbana Park District, it was Epizootic Hemorrhagic Disease (EHD), a midge-borne viral illness that pops up in white-tailed deer populations around the state every few years. And when susceptible deer are infected, they die within days.
Now, University of Illinois scientists have found gene variants in deer associated with the animals’ susceptibility to EHD.
This is the first time this gene has been sequenced completely in white-tailed deer. This is important because without the sequences, there's no starting point to do any kind of research.
The team sequenced the gene for Toll-Like Receptor 3 (TLR3), a protein that spans membranes of intracellular organelles in immune cells and helps recognize double-stranded RNA (dsRNA) viruses. When a dsRNA virus, such as the one that causes EHD, enters the cell, TLR3 activates the host’s first immune defenses, triggering inflammation and priming the rest of the immune system.
When the team sequenced TLR3 from EHD-infected and uninfected deer, they found dozens of variable sites in the DNA known as single-nucleotide polymorphisms (SNPs). Two of the SNPs were significantly more common in uninfected deer.
Because we found mutations in TLR3 more frequently in EHD-negative animals, we think deer with these mutations are less susceptible to EHD.
Yasuko Ishida, co-author
Department of Animal Sciences
University of Illinois, Urbana-Champaign, USA.
That conclusion is rooted in the probability that many white-tailed deer in Illinois are exposed to EHD in their lifetimes, but only some will die from the disease.
In many areas, outbreaks occur every 3-5 years, when environmental conditions favor the life cycle of midges that carry the virus. The midges spend their larval stages in mud under ponds and puddles where deer drink during drought conditions. As those water sources dry up, usually during late summer, the midges’ muddy habitat is exposed and the adult flies emerge to bite and infect deer. The cycle can be interrupted locally by a soaking rain or a cold snap, which is why outbreaks don’t happen every year.
The researchers emphasize that EHD is not transmissible to humans or pets through midge bites or consumption of infected deer meat.
Although there’s not much wildlife managers can do to disrupt the cycle and prevent outbreaks in natural habitats, the team says it’s still helpful to understand the genetic underpinnings of the disease. Theoretically, deer in captive herds could be sampled to characterize the level of vulnerability to EHD, and wild herds could be sampled during the hunting and EHD-outbreak seasons, informing managers and the public of future risk.
The value of this research is that it helps inform the public about EHD. It helps them to understand not only what the disease will look like, but potentially the severity of an outbreak in a particular area. Sometimes there's value in knowing what to expect.
It’s very complicated to respond to an outbreak of EHD because there are often large numbers of deer found dead near water. People don’t know what to do when that happens, but we encourage the public to report potential EHD outbreaks to their local IDNR wildlife biologist for the surveillance and future study of the disease.
Jacob Wessels, first author
Now a conservation police officer with the Illinois Department of Natural Resources
Considering the disease’s episodic nature, it’s not likely to present as a severe outbreak again in Urbana parks anytime soon. But it is an increasing threat to the state’s northern regions, including Chicagoland. Another recent study by Mateus-Pinilla, Roca, and others shows the disease has been slowly but steadily moving northward in Illinois. The researchers don’t know whether that’s due to climate change or greater reporting, but it’s clear EHD isn’t restricted to rural parts of Illinois.
The article, “The Impact of Variation in the Toll-like Receptor 3 Gene on Epizootic Hemorrhagic Disease in Illinois Wild White-tailed Deer (Odocoileus virginianus),” is published in Genes [DOI: 10.3390/genes14020426].
More detail is provided in the team's open access paper in Genes:
Abstract
Epizootic hemorrhagic disease (EHD) leads to high mortality in white-tailed deer (Odocoileus virginianus) and is caused by a double-stranded RNA (dsRNA) virus. Toll-like receptor 3 (TLR3) plays a role in host immune detection and response to dsRNA viruses. We, therefore, examined the role of genetic variation within the TLR3 gene in EHD among 84 Illinois wild white-tailed deer (26 EHD-positive deer and 58 EHD-negative controls). The entire coding region of the TLR3 gene was sequenced: 2715 base pairs encoding 904 amino acids. We identified 85 haplotypes with 77 single nucleotide polymorphisms (SNPs), of which 45 were synonymous mutations and 32 were non-synonymous. Two non-synonymous SNPs differed significantly in frequency between EHD-positive and EHD-negative deer. In the EHD-positive deer, phenylalanine was relatively less likely to be encoded at codon positions 59 and 116, whereas leucine and serine (respectively) were detected less frequently in EHD-negative deer. Both amino acid substitutions were predicted to impact protein structure or function. Understanding associations between TLR3 polymorphisms and EHD provides insights into the role of host genetics in outbreaks of EHD in deer, which may allow wildlife agencies to better understand the severity of outbreaks.
Wessels JE, Ishida Y, Rivera NA, Stirewalt SL, Brown WM, Novakofski JE, Roca AL, Mateus-Pinilla NE.
The Impact of Variation in the Toll-like Receptor 3 Gene on Epizootic Hemorrhagic Disease in Illinois Wild White-Tailed Deer (Odocoileus virginianus). Genes. 2023; 14(2):426. https://doi.org/10.3390/genes14020426
These examples of how the childish Creationist notion of intelligent [sic] design simply makes no sense at all, are almost daily occurrences in biological science, as are the examples of evolution in progress that we see in this example of natural selection favouring immunity to a viral parasite. The basic problem with Creationism and Creationists is that facts and deductive logic are irrelevant, otherwise there wouldn’t be Creationism and Creationists.
The psychology needed to maintain a superstition despite the overwhelming evidence against it must amount to a mental disorder that can only be accounted for by intensive mental abuse in childhood that gives rise to a mind-numbing acute anxiety disorder, or psychotic theophobia. Creationism and the wilful ignorance and science denial that it requires are not normal psychological states.
To inflict this mental disorder on the vulnerable minds of children, reinforced by threats of eternal torture, is a form of coercive child abuse. As someone once said, there are good people who do good things and bad people who do bad thing, but with religion, good people can do bad things believing them to be good. Inflicting Creationism on children is a case in point.
The World Health Organization (WHO) recently confirmed an outbreak of Marburg disease - in Kie Ntem Province of the West African country of Equatorial Guinea. Marburg disease is a haemorrhagic fever which is frequently fatal in humans. So far, 9 victims have died and a further 16 people are suspected of being infected. 200 contacts of these victims have so far been traced and put into quarantine by the WHO.
Marburg is a filovirus like the related ebola, and has a fatality ratio of 88%. It is highly infectious and easily transmitted. At the moment there is insufficient data to compare its infectivity with that of ebola.
The big concern is that this virus could break out of its endemic stronghold in West Africa and, like the SARS-CoV-2 Virus, become a major pandemic in a world in which health services are already overstretched, still dealing with the COVID-19 pandemic, which is far from over.
Embarrassingly for intelligent [sic] design Creationists, it is central to their cult think that all life is the work of their supposed designer deity, which, being omniscient, only ever designs organisms like viruses in the full knowledge of what they will do; de facto it designs them to do exactly what they do. In other words, if Marburg does become a major pandemic, that is exactly what it intended when it designed it.
The following article by Professor C Raina MacIntyre, NHMRC Principal Research Fellow, Head, Biosecurity Program, Kirby Institute, UNSW Sydney, explains what Marburg is, and discusses whether we should be worried. The article is reprinted from The Conversation under a Creative Commons license and reformatted for stylistic consistency. The original can be read here:
As is entirely predictable from the Theory of Evolution, the SARS-CoV-2 virus that has caused the ongoing COVID-19 pandemic, has mutated to produce an even more infectious version - a subvariant of the Omicron variant, given the variant name XBB.1.5 and nicknames 'kraken', under the suggested new protocol of naming significant variants after Greek mythological creatures instead of letters of the Greek alphabet..
This appears to have originated in the USA where a large number of people have resisted getting vaccinated due to the politically-motivated antivaxx campaign by the far right supporters of failed president, Donald Trump,. Trump declared the pandemic to be a hoax and COVID-19 to be a mild illness, early on in the pandemic, when he was out of his depth and panicking over how to cope with the emergency. Having acted out of spite and motivated by racism and a desire to expunge his achievements, Trump had stupidly dismantled the contingencies for just such a pandemic put in place by his hated African-American predecessor, Barak Obama.
Inhibited from doing so by his narcissistic personality disorder, Trump was then unable to admit he got it wrong and his cronies in the Repugnican Party and the evangelical white Christian sects set about campaigning against any measures to mitigate the effects of the pandemic, including establishing the QAnon cult to promulgate disinformation.
The upshot is a high degree of vaccine scepticism in the USA with a significant majority being vaccinated - a recipe for producing lots of new variants in the unvaccinated population which will then find a niche in the vaccinated population, if they can evade the antibodies.
But is this variant anything to be overly concerned about?
In the following article, reprinted from The Conversation under a Creative Commons licence, Dr. Grace C Roberts, a research fellow in virology at the University of Leeds, assesses the risks from this new variant for the world in general and the UK in particular. The article has been reformatted for stylistic consistency. The original can be read here.
The ‘kraken’ COVID variant XBB.1.5 is rising quickly in the US – here’s what it could mean for the UK
The heavily mutated omicron variant of SARS-CoV-2, the virus that causes COVID-19, was first detected in late 2021.
Due to the many mutations in the spike protein (a protein on the surface of SARS-CoV-2 that allows the virus to attach to our cells) omicron was able to quickly become the dominant SARS-CoV-2 variant. These mutations allowed it to bind to respiratory cells more tightly than previous variants, rendering it more infectious.
Owing to the dominance of omicron, thanks to these mutations, the past several months have seen the emergence of many subvariants of omicron (scientists have identified more than 650 to date).
The latest variant to worry health professionals and virologists alike is XBB.1.5, nicknamed “kraken” by a group of scientists that has been naming new variants after mythological creatures to make the virus’ evolution more accessible to the public. Here’s what we know about it.
XBB.1.5 is a derivative of the XBB variant of omicron. XBB was never designated as a variant of concern by the World Health Organization because data shows that, while XBB’s mutations enable it to evade our immune systems better than previous omicron subvariants, it doesn’t appear to be causing an increase in infection rates.
In addition to the mutations that XBB.1 has, XBB.1.5 also carries a mutation called S486P in the spike protein region. Preliminary laboratory studies, yet to be peer-reviewed, have shown that, similar to XBB.1, XBB.1.5 is less sensitive to antibodies acquired from vaccination than previous variants XBB and BQ1.1. So it’s very good at evading our immune response.
The same preprint showed that XBB.1.5 was able to bind to ACE2 (the receptor the virus uses to infect our cells) more strongly than these earlier variants. This is the characteristic that made the original omicron variant so infectious and so dominant.
Having first been detected in October 2022 in the US, XBB.1.5 has spread rapidly in the country and is now responsible for around 28% of all new infections. Elsewhere, XBB.1.5 has been detected in at least 23 countries, including the UK. But according to the most recent data, it accounts for only 4% of COVID infections in England.
Given what we’re seeing in the US, it’s likely that XBB.1.5 will become the dominant strain in the UK and Europe in time. But as there are always differences in populations (for example, vaccination rates and social behaviour) it’s hard to predict exactly how things will play out.
XBB.1.5 is rife in the US, but not in the UK and Europe at this stage.
Though some of XBB.1.5’s characteristics are concerning, the real-world infection data is not showing an overall increase in infections or deaths globally or in the US (where XBB.1.5. is rife) at present.
It’s too early to tell whether infections from XBB.1.5 are more severe than previous variants, however experts agree that there is no evidence at this stage that it poses any higher risk than variants that have come before it.
Experts also agree that vaccination will continue to protect against serious disease and death from XBB.1.5.
With a new variant, there’s always the risk it will affect clinically vulnerable people more severely. Older people and those with conditions that affect their immune systems mount weaker responses to COVID vaccines, so are less protected than the “healthy” population. This means variants that spread more easily or can better evade our immune system may be more likely to infect these people if they’re exposed.
So, while COVID continues to circulate, it’s best to take extra precautions when meeting vulnerable people such as wearing a mask, washing your hands thoroughly, ventilating the space that you are in (or even meeting outdoors), and not meeting them at all if you are ill.
Published by The Conversation. Open access. (CC BY 4.0)
It almost goes without saying that for a Creationists to claim intelligent [sic] design at work with these new variants is a tacit admission that their beloved creator god is malevolently designing ways to ensure its virus continues to make people sick and die and to disrupt economies indiscriminately across the world. That Creationists prefer us to have this view of their god rather than accept the science of evolution by mutation and natural selection betrays a hidden political agenda behind Creationism that requites people to distrust science and be misinformed about it.
