AI depiction of the ancient retroviral DNA that is essential for embryo development but can help lung cancer cells survive too
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Post-gastrulation amnioids - models with mimic the development of the amniotic sac forming as expected (top panel). Amnioids without a key calcium-buffering gene and its accompanying switch don't form as expected (bottom two panels).
Some 13 million years before anyone could have written a creation myth, a retrovirus inserted its genetic material into the genome of an ancestral ape. Today, part of that viral legacy helps regulate early human development. This presents creationists with several difficulties at once: a history vastly older than their biblical chronology permits, genetic material acquired from a virus, and an evolutionary innovation produced by putting an existing sequence to a new use. There is also an uncomfortable sting in the tail for advocates of a benevolent intelligent designer: cancer cells can exploit the same biological machinery.
The research, reported in Science Advances, concerns a remnant of an ancient retrovirus known as HERVH. This sequence acts as a switch controlling a form of calbindin, a protein involved in buffering calcium inside cells. Removing the switch or calbindin disrupted the growth and developmental behaviour of human embryonic stem cells and the organisation of models of early embryonic structures.
The evolutionary distinction matters. The original acquisition of viral DNA represents horizontal genetic transfer: genetic material crossed from a virus into its host, rather than arriving through ordinary inheritance from a parent. Once incorporated into the germ line, however, that material could pass vertically through successive generations. Its recruitment to regulate a host gene is an example of exaptation — the co-option of an existing feature for a different function. The virus did not need to invent calbindin, nor did evolution need to create an entirely new protein from scratch. A new regulatory relationship could arise by combining material with different evolutionary histories.
This is precisely the sort of process obscured by the creationist slogan that new genetic “information” requires an intelligent author. Biologically useful novelty can involve changes in when, where and how an existing gene is expressed. Imported DNA can supply a regulatory element; subsequent evolution can preserve and modify its contribution. Calling the result “information” does not erase the natural processes that produced it, still less establish that someone intended the outcome.
The chronology is equally inconvenient. Comparative primate evidence places this insertion roughly 13 million years ago, after the lineage leading to humans and the African great apes had separated from the orangutan lineage. Orangutans are themselves great apes; the relevant event occurred within the broader great-ape family tree. Either way, this is inherited molecular history extending far beyond the few thousand years allowed by a literal young-Earth reading of Genesis.
Yet a mechanism useful during development need not remain beneficial in every context. Earlier research showed that lung squamous cell carcinoma can activate this viral switch, helping cancer cells avoid senescence — a state in which cells stop dividing. The cancer biology is complex, but the central evolutionary point is clear: machinery that supports normal development can also become available for malignant cells to exploit.
That is consistent with an evolutionary cost-benefit trade-off. Natural selection can preserve a developmental advantage despite a vulnerability elsewhere in life; it has no foresight with which to guarantee lifelong protection from every possible consequence. But if intelligent-design advocates insist that useful genetic arrangements demonstrate deliberate engineering, they must apply that reasoning consistently. A designer credited with the developmental benefit cannot simply be excused responsibility for the exploitable weakness. On their own premises, the result raises questions about competence, benevolence, or even malevolent design. Evolution requires no such theological contortions: an ancient infection, inherited variation and the opportunistic reuse of existing material are sufficient ingredients for the story.
AI-generated conceptual illustration of BC200’s transfer from human DNA into a poxvirus, with background neurons representing its association with neuronal regulation.
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AI-generated conceptual illustration of BC200’s transfer from human DNA into a poxvirus, with background neurons representing its association with neuronal regulation.
Creationists who insist that functional genetic information requires an intelligent designer have another evolutionary history to explain. A genetic element associated with neuronal regulation in primates began as a “jumping gene”, acquired a cellular function, and nevertheless retained its ability to generate copies elsewhere in the genome. Copies even escaped into a human virus. Far from resembling a collection of sealed, immutable designs, genomes reveal a history of copying, repurposing and exchange.
The element is BC200, the subject of a paper in Science by Pu Gao and colleagues, published on 24 September 2026. Its ancestor was a transposable element recruited into a cellular role approximately 40 million years ago. BC200 produces a non-coding RNA: its product is an RNA molecule, rather than a protein. Abundant in neurons, it is thought to help regulate protein production, although its precise physiological role remains incompletely understood.
This is an example of evolutionary exaptation: existing biological material acquires a new use. A sequence whose ancestral significance lay in its capacity to propagate could become useful to its host. No foresight is required. Variants arise without anticipating future needs, and natural selection can preserve those that improve reproductive success. The new function need not have been the reason the original sequence existed.
The unusual feature here is that recruitment did not end BC200’s mobility. Genes derived from transposable elements typically lose that ancestral capacity; BC200 retained it. The researchers identified two independent transfers into molluscum contagiosum virus during the history of modern humans. Whether the acquired sequence benefits the virus remains an open question.
There are two distinct difficulties here for creationism. For young-Earth creationists, the roughly 40-million-year history already places these events far outside their biblical chronology. For intelligent-design advocates, the difficulty is mechanistic: biological function can emerge through the modification and recruitment of material that already exists. Calling the resulting function “designed” adds no explanation of the evidence.
Nor does transfer into a virus mean that a human became a virus, or that every transferred sequence must be adaptive. It demonstrates something more precise: genetic material can cross the boundary between a host genome and a viral genome. BC200’s history combines inherited ancestry, evolutionary repurposing and continuing mobility — exactly the sort of untidy, contingent history that evolutionary biology allows researchers to investigate.
One of the recurring mistakes in creationist arguments is to assume that a complex biological system must always have performed its present function. If its components now work together, the argument goes, they must have been created together for that purpose. Evolution, however, can recruit existing machinery for new roles. Two papers in *Science* now provide evidence that this process may help explain the origin of an important form of microbial immunity—with the intriguing possibility that bacteria acquired the precursors of their antiviral weapons from viruses themselves.
To appreciate the discovery, it helps to understand what CRISPR immunity actually is. Although CRISPR is familiar as a tool for editing genes, its natural role is defence. Many bacteria and archaea possess CRISPR–Cas systems that retain molecular records of past invaders. Short pieces of foreign DNA are incorporated into the cell’s genome, between repeated sequences. These stored fragments provide templates for small RNA molecules, which guide CRISPR-associated—or Cas—proteins to matching genetic material during subsequent infections. Depending on the system, the resulting response can destroy invading DNA or RNA. This is adaptive immunity: protection directed against particular threats, with a genetic memory that can pass to descendants.
CRISPR stands for “clustered regularly interspaced short palindromic repeats”, a description of the DNA arrangement in which those memories are stored. The best-known gene-editing protein, Cas9, belongs to class 2, whose targeting machinery centres on one large protein. Class-1 systems instead use assemblies of several proteins to recognise their targets. It is the evolutionary origin of this latter machinery that the new research addresses.
The studies, published on 17 September 2026 investigate a compact system called VIPR, short for viral interference programmable repeat. Found in viruses and bacteria, it combines a small protein with a guide RNA. The researchers propose that an ancestral VIPR-like system involved in competition between viruses was recruited into bacterial defence, eventually contributing to the evolution of class-1 CRISPR. This would be evolutionary co-option: machinery favoured in one context becoming useful in another.
One of the problems with claiming that biological complexity proves intelligent design is that the argument cannot stop conveniently at butterflies, flowers and the human eye. If complex biological machinery requires a designer, then the same reasoning must apply to parasites and pathogens. A virus’s ability to infect us cannot become an unfortunate accident merely because crediting the supposed designer would now be embarrassing. Nor can the animal that carries it from host to host be excluded from the reckoning.
A newly identified tick-borne virus in China provides another uncomfortable example. Described in a correspondence in The New England Journal of Medicine, Asian longhorned tick nairovirus, or ALTNV, is associated with fever, fatigue, gastrointestinal symptoms and, in some patients, reduced platelet counts. Its vector is the already familiar Asian longhorned tick, Haemaphysalis longicornis; experiments demonstrated transmission to mice. “New” here means newly recognised by science, not shown to have come into existence recently.
The clinical findings deserve care. All 56 patients reported with ALTNV alone recovered without lasting effects. However, seven of 38 patients infected with both ALTNV and Dabie bandavirus died. These deaths do not establish that ALTNV alone is lethal, or determine its contribution to the fatalities. They do place the discovery within a system of tick-borne infections capable of causing serious illness and death.
Now apply the creationist rule that functional complexity and genetic information require an intelligent author. On that premise, the designer must take responsibility for the infectious agent and its means of delivery. Here is a blood-feeding animal whose activities provide a route for viruses to enter other animals, including humans. If every relevant adaptation was knowingly intended by an all-knowing creator, then the resulting suffering cannot be dismissed as an unforeseen side-effect. The alleged designer knew what its creations would do.
That is the force of the malevolent-designer argument. It does not require us to believe that a supernatural intelligence actually makes viruses. It asks why features that serve pathogens should count as evidence of loving craftsmanship when equivalent features serving their victims are routinely presented as precisely that. If the designer receives credit for our defences, it must also answer for the threats those defences sometimes fail to overcome. Deliberately creating the means of making people ill is hardly an obvious expression of benevolence.
Created in Northumbria in the eighth century, this copy of the Epistles of St Paul is among the oldest books held in the Trinity College Cambridge Library.
Credit: the Master and Fellows of Trinity College Cambridge
DNA of the ancient virus was extracted from millennium old sheepskin Bible parchment, now in the collections of the University of Cambridge.
Credit: the Master and Fellows of Trinity College Cambridge.
Sometimes history leaves two very different records on the same page. One was deliberately written in ink by medieval scribes, copying stories that religious authorities declared to be sacred truth. The other was written unintentionally in molecules: fragments of viral DNA preserved in the animal skin on which those stories were written.
Unlike the supernatural claims in the text, this second record does not depend on faith, revelation or ecclesiastical authority. It can be extracted, sequenced and compared with DNA recovered from other archaeological specimens and from viruses circulating today. Ironically, manuscripts intended to preserve the Christian message have also preserved independently verifiable evidence of evolution.
As reported in Science Advances, an international research team led by scientists at University College Dublin has now recovered DNA from sheeppox virus (Capripoxvirus sheeppox) in medieval parchment manuscripts, including the approximately 1,000-year-old York Gospels, the earlier Corpus Glossary and other codices from Britain and continental Europe. Because parchment was manufactured from the skins of sheep, goats and cattle, each sheet can retain a molecular record of the animal from which it came—including traces of pathogens infecting it when it died. In several manuscripts, viral DNA occurred on several pages, suggesting that the skins of infected animals had been used in their manufacture.
Certain bacteriophages found in the human gut have mutation hotspots scattered throughout their genomes that help them modify key defense genes, researchers report.
Credit: Sundharraman Subramanian and Alaina Pabbathi Cryo-EM Core Facility Michigan State University
One of the more persistent creationist falsehoods is the claim that mutations can only damage or destroy genetic information and can therefore provide none of the variation needed for evolution. The claim is usually protected from contrary evidence by leaving “information” conveniently undefined or by dismissing every beneficial mutation as merely a “loss of function”.
However, a new study by Jasper B. Gomez, Jeffrey E. Barrick and Christopher M. Waters of Michigan State University provides an especially clear demonstration of mutation generating heritable variation on which natural selection can act. Their findings were published in Nature Microbiology.
The researchers found that the genomes of the bacteriophages T2 and T4 — viruses that infect bacteria such as Escherichia coli — contain regions of repetitive DNA called contingency loci. These are mutational hotspots in which the DNA-copying machinery is particularly liable to slip while copying a run of repeated bases. It may insert or omit one of the repeats, changing the way the remainder of a gene is read and consequently altering the protein it produces.
Such replication errors occur in these regions thousands of times more frequently than mutations across the rest of the phage genome. Far from producing a population of genetically identical copies, therefore, phage replication continually generates a mixture of variants with different inherited characteristics.
The discovery arose from experiments involving a bacterial antiviral system called TgvAB, normally found in Vibrio cholerae, the bacterium that causes cholera. The researchers transferred the genes for this defence system into laboratory E. coli and exposed the bacteria to T2 phages. Although the defence initially restricted the phages, the viral population began overcoming it within hours.
Dead cells after the self-destruction and fragmentation process. The large green areas are the “eat me” signals which alert immune cells to kick-start clean-up and recycling process, while the small green circles are the “Footprint of Death” F-ApoEVs left behind by the dying cell.
My previous post was about the discovery, reported in Cell Host & Microbe in May 2026, that a single amino-acid change in a coronavirus protein can alter how a bat-related coronavirus interacts with the immune systems of bats and humans. In the case of SARS-CoV-2, the virus that causes COVID-19, such changes help to explain how a virus that may be relatively benign in its natural host can become a serious pathogen when it crosses the species barrier into humans. By creationists' own criteria, this should qualify as intelligent design.
This post concerns another example which, if creationists applied their criteria for intelligent design consistently, would be further evidence of malevolent design. It is the finding, reported in Nature Communications, that influenza A virus can exploit part of the normal process of programmed cell death to help infect neighbouring cells.
Applied consistently, these discoveries would portray creationists' putative designer god as a malevolent entity that designs ways to increase suffering. But, since creationists need to portray this alleged designer as the omnibenevolent god of the Bible, this supposed 'evidence of intelligent design' somehow ceases to be evidence of design at all and becomes evidence of 'Sin' and 'The Fall', as creationists abandon any pretence of science and retreat into Biblical mythology to explain away inconvenient facts.
The discovery, by a team led by PhD candidate Stephanie Rutter in Professor Ivan Poon’s lab at the La Trobe Institute for Molecular Science (LIMS), shows how each step in the process of cell death and renewal is important in helping a dying cell break down and be cleared away by the body’s immune system. The team found that, as cells self-destruct, they change shape, lift away from their surroundings, and leave behind a residue which the researchers dubbed the 'footprint of death'. This contains a previously undescribed type of extracellular vesicle (EV). EVs are small packages used by cells to transport proteins, lipids, DNA and RNA to other cells, acting as an important means of communication between cells.
These new vesicles, known as FOOD-derived apoptotic extracellular vesicles, or F-ApoEVs, normally mark the site of a dead cell and help the immune system identify and clear away the remaining fragments, preventing inflammation and other harmful consequences. But this useful clean-up process can also be turned into a weakness. The researchers found that, when dying cells are infected with influenza A virus, viral proteins and even virus particles can be carried in these F-ApoEVs, providing another route by which infection can spread to neighbouring cells.
Had this process been beneficial to humans, rather than to influenza viruses, creationists would doubtless hail it as a marvel of intelligent design by their god. Yet, because the benefit is to a virus and the result can be disease, suffering and death, the same kind of complexity somehow ceases to count as evidence of design and is quietly reclassified as a mysterious consequence of 'The Fall'.
Creationists get into this bind because they are trying to force the evidence into their preferred mythology. Science has no such problem. The immune system, cell-death pathways and the pathogens that exploit them are all products of evolutionary history, not foresight. They are parts of a continuing arms race in which every useful biological process presents opportunities for parasites, viruses and other pathogens to exploit. An influenza virus that stumbles upon a weakness in a host system does not need to understand it, plan it, or design it; it merely needs to leave more copies of itself than viruses that did not.
Two recent papers should delight admirers of creationism's putative intelligent designer, because both show the sort of biochemical ingenuity they normally rush to claim as evidence of design. One, published in Cell Host & Microbe in May 2026 and reported by UCSF in June, shows how a single molecular change can alter the way a coronavirus interacts with bat and human immune systems, helping to explain how viruses related to SARS-CoV-2, the virus that caused the COVID-19 pandemic, can cross the species barrier. The other, published in October 2025 in Nature Communications, which will be the subject of my next blog post, shows how influenza A virus can exploit the remnants of dying cells to help spread infection to neighbouring healthy cells.
However, that excitement is likely to be tempered somewhat when it dawns on them that, if these systems are the products of intelligent design, their designer can only be regarded as malevolent, since the result is an increase in the sum total of suffering in the world. But this does not seem to trouble ID proponents who cite Michael J. Behe's favourite examples — the Escherichia coli flagellum and anti-malarial drug resistance in Plasmodium falciparum — as evidence of irreducible complexity and hence of intelligent design, while ignoring the awkward fact that these supposed examples of design help microorganisms survive, move, infect, or evade human attempts to control them.
This puts creationists in a familiar bind. On the one hand, they like to claim any useful biological complexity as evidence of their Biblical god. On the other, when the same logic points to a designer of pathogens, parasites, immune evasion, drug resistance and viral spread, they retreat into vague claims about 'Sin', 'The Fall', or some mysterious corruption of nature, thereby absolving their god of responsibility for the very mechanisms they were praising as designed only moments earlier.
The first paper, in Cell Host & Microbe, was by a large team of researchers from the University of California San Francisco (UCSF) Quantitative Biosciences Institute, the Icahn School of Medicine at Mount Sinai, the Institut Pasteur and the Fred Hutchinson Cancer Center. It showed that a single amino-acid change in a viral protein can alter how coronaviruses interact with bat and human immune systems, changing the host's response to infection.
Bats are important viral reservoirs because their immune systems and physiology can allow them to tolerate viruses that might cause serious disease in other mammals. They can therefore harbour viruses for long periods, providing opportunities for viral lineages to persist, diversify and acquire mutations that may matter greatly when those viruses encounter a new host species. The UCSF-led study helps to explain how relatively small genetic differences can make the difference between a virus that remains associated with a bat reservoir and one that is better able to evade human immune defences.
This is precisely the sort of thing creationists should, by their own logic, have to call 'complex specified information'. The change is functional; it affects a specific biological outcome; and it is beneficial from the point of view of the viral lineage. The problem, of course, is that creationists usually smuggle in the assumption that 'beneficial' must mean beneficial to humans. If it benefits a virus, a bacterium, a parasite or a cancer cell, they suddenly decide it does not count.
Comparing SARS-CoV-2 with a related bat coronavirus, RaTG13, the researchers found that a viral protein called ORF9b was a key factor. The SARS-CoV-2 and RaTG13 versions of ORF9b are very similar, but behave very differently. In human cells, the SARS-CoV-2 version helped disable an innate immune alarm system, allowing the virus to multiply more effectively. In bat cells, the RaTG13 version interacted with a restriction factor that helped suppress infection.
The team found that changing just one of ORF9b's roughly 100 amino acids reversed its ability to evade the immune response. In creationist thinking, if the phrase is to mean anything at all, this would be new functional genetic information. Yet the actual explanation requires no magic, no designer and no supernatural intervention: a mutation changed an amino acid; that change altered protein interactions; and the result affected viral fitness in different host-cell environments. In other words, ordinary chemistry and physics, operating through mutation, selection and host-virus interaction, produced exactly the kind of functional change creationists insist cannot happen naturally.
A paper recently published in the journal Advanced Science, by researchers including Assistant Professor Jack Chi-Ho Ip, from Lingnan University, Hong Kong, is deeply problematic for creationists, not only because it describes a process that took place over an immense period of time incompatible with the biblical narrative, but also because it deals with a mechanism for evolution that cannot be waved aside as mere "variation within a kind", or something creationists like to dismiss as "micro-evolution".
Creationists continue to insist that large-scale evolution does not happen, so everything must have been specially created more or less as it is, with only limited variation within the "kind" — a term always left conspicuously undefined, so the goalposts can be moved whenever the evidence becomes inconvenient. This is despite the well-attested mechanisms by which biodiversity arises, including classical Darwinian natural selection acting on inherited variation, and genetic drift, in which chance changes in allele frequencies can lead to a neutral mutation becoming fixed in, or eliminated from, a population gene pool.
There is also the founder effect, where a non-representative sample of a population becomes isolated from the parent population, usually by a physical or ecological barrier. The new population therefore begins with a different allele-frequency profile from the population from which it came. Then there is hybridisation, where hybrid offspring can, in some circumstances, become reproductively isolated from both parent species, forming a new genetically distinct population or species.
And lastly, we have horizontal gene transfer, where an organism acquires genetic material from another biological lineage in its environment. This is especially familiar in bacteria, but it also occurs in animals, often through viruses. Retroviruses are particularly important in this respect because they insert a DNA copy of their genome into that of their host. Over time, the viral sequence may be disabled by mutation, or the host may evolve a defence against it. Either way, the remnant of the virus can become part of the host genome, where it is free to mutate over time. Occasionally, such inherited viral DNA is exapted for a new function, creating useful new genetic information without the slightest need for supernatural assistance. One well-known example is syncytin, derived from ancient retroviral genes, now involved in the formation and function of the mammalian placenta.
Now researchers at Hong Kong's Lingnan University and their collaborators have shown that a viral-derived gene in apple snails is probably involved in their ability to lay eggs out of water — a key adaptation in the evolution of aerial egg-laying and one reason some apple snails have become such successful invasive pests. The gene, associated with the perivitelline fluid surrounding the developing embryo, was probably acquired by the ancestor of the Ampullariidae during the Jurassic. It would be interesting to see a creationist explain how acquiring a gene from an entirely unrelated viral lineage can be described as "variation within a kind". It would also be interesting to see them explain why an intelligent designer would need to borrow viral genetic material to equip a snail to lay eggs above the waterline.
A recent paper in the Cell Press journal Cell Reports Medicine by researchers at the Fred Hutch Cancer Center in Seattle reports the development of monoclonal antibodies against Epstein-Barr virus (EBV), a pathogen carried by an estimated 95% of the global human population. The mere existence of such a virus, together with the fact that human scientists have now produced what looks like a promising way of blocking it, should be acutely embarrassing to any creationist prepared to follow the evidence where it leads.
For devotees of creationism’s putative intelligent designer, EBV is an awkward example of its supposed handiwork. It is superbly adapted for what it does: infecting human cells, evading immune defences, and contributing to a range of diseases, including several cancers. If one were looking for something that appears exquisitely “designed” to do harm, EBV would be a strong candidate.
It is especially effective at finding and entering its target cells. The viral glycoprotein gp350 helps it bind to receptors on human cells, while gp42 helps it fuse with and enter them. In other words, it possesses precisely the sort of functional complexity that Intelligent Design advocates such as William Dembski and Michael Behe habitually point to as evidence of design. By their own argument, a system so finely tuned to perform a specific task should count as “specified complexity” or even “irreducible complexity”. The problem, of course, is that the task in question is the infection of human beings by a cancer-associated virus.
Creationists who lean on these arguments are therefore trapped by them. If complexity and functional integration are proof of a designer, then they must also account for the obvious implication: a designer responsible for EBV would have to be, at best, indifferent to human suffering and, at worst, positively malevolent. To escape that conclusion, they usually have to abandon Intelligent Design’s own logic and retreat instead to the theological fallback of “The Fall” and “sin” from the Abrahamic creation myths. In doing so, they quietly concede that their alleged scientific proof of design proves far more than they want it to.
This paper adds a further layer of discomfort. Human scientists have begun to do what any competent and benevolent designer should have done in the first place: devise antibodies capable of blocking the virus from infecting human cells. The study reports monoclonal antibodies against gp350 and gp42, with one anti-gp42 antibody preventing infection in mice with human immune systems. So the obvious question for intellectually honest creationists is this: if human science can engineer a way to interfere with such a pathogen, why was an all-powerful designer unable, or unwilling, to equip us with protection from the outset?
Predictably, most will not confront that question. They will retreat into the familiar refuge of mystery: “we cannot know the mind of God”. But that is precisely where religion and science part company. Science does not declare a problem solved by calling it unknowable. It treats mysteries as challenges to be investigated, understood and, where possible, overcome. That is exactly what these researchers have done with EBV.
Ushikuvirus: A newly discovered giant virus may offer clues to the evolutionary relationships
Researchers discover a new virus called the "ushikuvirus" that provide evidence for the viral eukaryogenesis hypothesis and reveal virus-host interactions, shaping the evolution of eukaryotic cells.
One of the remaining questions in evolutionary biology is how the complex (eukaryotic) cell acquired its defining feature: a membrane-bound nucleus in which the DNA is stored.
Prokaryotic cells — bacteria and archaea — possess a single circular DNA molecule located in the cytoplasm. By contrast, all eukaryotic cells contain their genetic material within a membrane-bound nucleus. Now scientists at the Graduate School of Science, Tokyo University of Science (TUS), Japan, led by Professor Masaharu Takemura, have provided further evidence that the eukaryotic nucleus may have originated from a giant DNA virus, similar to those that infect certain species of amoeba. Their findings suggest that the origin of the nucleus may be closely linked to the evolutionary history of this class of virus as it adapted to different hosts.
Professor Takemura and Dr Philip Bell, from the Department of Biological Sciences at Macquarie University, Sydney, independently proposed the viral eukaryogenesis theory (a term coined by Dr Bell) in 2001, suggesting that large DNA viruses — such as poxviruses — might represent plausible ancestors. Since then, beginning in 2003, the discovery of several giant DNA viruses has provided more compelling candidates. When these viruses infect a host cell, they establish so-called ‘virus factories’ within the cytoplasm. In some cases these structures are enclosed within membranes that resemble the nuclear envelope.
The hypothesis proposes that, rather than destroying its host, such a virus formed a long-term association with it. Over evolutionary time, it may have incorporated host genes and transitioned from parasite to symbiotic genetic compartment — eventually becoming the nucleus.
For advocates of “irreducible complexity”, the nucleus is often presented as an all-or-nothing structure: a fully formed membrane, nuclear pores, transport machinery, chromatin organisation and regulatory systems supposedly appearing together or not at all. Yet the viral eukaryogenesis model shows how this argument collapses once intermediate stages are recognised. Giant DNA viruses already construct membrane-bound replication compartments inside host cells; they encode components involved in DNA replication, transcription and even elements of translation.
These viral “factories” function as semi-autonomous genetic centres within the cytoplasm — in effect, simplified proto-nuclei. If such a structure entered into a stable symbiotic relationship with a host cell, incremental gene exchange and co-evolution could gradually integrate and refine the system. Each step would confer immediate functional advantages — protection of DNA, separation of transcription from translation, improved regulation — without requiring the simultaneous appearance of a fully modern nucleus. What is claimed to be irreducible instead looks like a product of stepwise evolutionary integration.
Now Professor Takemura’s team report the discovery of a new giant DNA virus infecting amoebae — the ushikuvirus, named after Lake Ushiku where it was isolated — lending further support to the viral eukaryogenesis theory. Their discovery is reported in Journal of Virology.
paper just published in Emerging Infectious Diseases by a team led by Nischay Mishra, of the Columbia University Mailman School of Public Health, shows that Pteropine orthoreovirus (PRV) — a bat-borne orthoreovirus — has crossed the species barrier into humans in Bangladesh, causing a Nipah-like illness that is difficult to distinguish clinically from Nipah virus infection. The disease presents primarily as an acute respiratory infection, sometimes accompanied by encephalitis.
It has long been known that bats possess a markedly more effective antiviral immune system than humans. This fact alone presents a problem for creationists who insist that humans — and, conveniently, themselves — are the special creation of an omnibenevolent deity. There is no coherent reason why such a deity would equip bats with a superior immune system while leaving humans comparatively vulnerable, unless the intention were for humans to suffer more infectious disease than is strictly necessary.
However, the bat immune system appears to have a significant evolutionary trade-off. Rather than eliminating viruses entirely, it often suppresses their pathological effects while allowing persistent infection. As a result, bats function as biological incubators in which viruses can circulate, diversify, and evolve. Inevitably, some of these variants acquire the ability to cross species barriers and infect humans. This remains the most parsimonious explanation for the emergence of SARS-CoV-2, the virus responsible for COVID-19 — the pandemic of 2020–2022 that killed tens of millions of people and inflicted severe damage on the global economy.
Creationists argue that complex, specified genetic information must be supplied by their putative intelligent designer and then, by a glaring act of circular reasoning, claim that the mere existence of such information constitutes evidence for that designer. This line of argument has no more merit than insisting that tins of baked beans can only be made by magic pixies, and therefore that the existence of tins of baked beans proves the existence of magic pixies. It is a form of reasoning that functions only for those who lack even a basic grasp of logic.
An additional difficulty for creationists is that PRV could only become infectious to humans if it possessed the precise genetic features required for that capability. Within the internal logic of intelligent design apologetics, the zoonotic PRV must therefore count as the product of deliberate design — and hence as evidence for a malevolent intelligent designer. The usual response is to abandon any pretence that intelligent design is science rather than religion in disguise, and to retreat into Christian fundamentalism, invoking “the Fall” and claiming that some other supernatural entity was empowered to interfere with creation and design its own suite of pathogens and parasites. This claim borders on blasphemy even within Christian theology, which traditionally reserves the creation of living things exclusively to their deity.
You might expect an intelligently designed system, created by an omnibenevolent designer, to work just as effectively for everybody and not badly for some and only just adequately for others. And yet, as so often with creationism, the facts are not at all what the theory predicts. In science this would be called falsification, but for creationists it is just another inconvenient fact to be ignored or blamed on ‘the Fall’ — or even on the victim.
According to a paper just published in Cell Press Blue, the reason some people suffer more from a cold caused by a rhinovirus is not so much because of differences in the virus, but because their bodies react differently. Some take control and prevent the spread of viruses to adjacent cells of the mucous membrane lining the nasal passages, whereas other people’s bodies fail to prevent the virus spreading.
The paper is by a team at Yale School of Medicine, New Haven, CT, USA, led by Associate Professor Dr Ellen F. Foxman, PhD.
By growing organoids in vitro and infecting them with rhinoviruses, the team were able to show that whether the infection spreads depends on how quickly the infected cells are able to mount an interferon response. A good response limits the infection to just a few cells and the cold does not develop beyond a ‘sniffle’. Where the response is weak, the infection spreads and, in cases where the victim has an underlying respiratory condition such as asthma or COPD, the cold can develop into a serious illness.
Why the interferon response differs between individuals is not known with any certainty, but it could be due to a number of factors, including genetics. However, it is known that in patients with pre-existing respiratory conditions, the interferon response is inhibited.
That, of course, begs the question for ID creationists: why a system supposedly designed to protect us gets downgraded when it is most needed, and, if the difference is due to underlying genetics, why some people got better genes in this respect than others. Under the ID creationist paradigm, genes that produce any given output are deemed to hold ‘complex specified genetic information’ and, as such, are evidence for intelligent design.
Leaving aside the question of why any omnibenevolent designer would design viruses to make us sick and then design an immune response to prevent them doing so, we are left with the question of why this immune system does not always work very well and why some people have a worse version than others. If an omnibenevolent designer can design an effective immune system, why did it not give it to everyone? Does it actually want those people to suffer more from the viruses it supposedly designed?
The evolutionary explanation is, of course, straightforward, with none of the theological conundrums that plague creationism. Evolution does not seek out perfection and has no interest in equity. In the environment of an evolutionary arms race with viruses, the results are inevitably suboptimal and unevenly distributed throughout the population unless there is particularly strong selection pressure to drive the ‘best’ solution to fixation. It is also in the survival interests of viruses to tone down their victim’s responses, thereby reducing that selection pressure. The resulting trade-off and compromise is what we see today in the different responses to the same virus.
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In this illustration, a phage — a type of virus that infects bacteria — rests on the surface of a host cell. Researchers at UW–Madison designed an experiment for the International Space Station to study how phage-bacteria interactions affect the health of the gut microbiome.
In a striking demonstration of the theory of evolution in practice — and something that will have creationists once again insisting on redefining evolution as a theory about one creature turning into an entirely unrelated taxon — an experiment aboard the International Space Station has shown how subtle changes in the environment can dramatically alter an evolutionary trajectory. It also illustrates another major embarrassment for Intelligent Design creationists: evolutionary arms races. Arms races are, of course, utterly incompatible with the idea of an intelligent designer, since running to stand still in a race with yourself is a neat definition of insanity.
Unlike the creationist parody of evolution — carefully engineered to be unprovable because it does not describe what actually happens and what no biologist has ever claimed — the real scientific definition of evolution is simply a change in the frequency of different alleles in a population over time. A definition that creationists know to be irrefutable, hence their persistent attempts to redefine it so that they have something to attack.
The experiment, which had a parallel control on Earth, was designed to observe how bacteriophage viruses that parasitise bacteria and their hosts co-evolved in the microgravity environment of space.
The results have just been published in PLOS Biology. They show that both the T7 phage virus and the E. coli bacteria developed marked genomic differences compared with the Earth-bound populations. The space-station phages gradually accumulated specific mutations that enhanced infectivity or improved their ability to bind receptors on bacterial cells. Meanwhile, the space-station E. coli accumulated mutations that improved resistance to phages and enhanced survival in near-weightless conditions. In other words, what was observed was a genuine evolutionary arms race — and because the environments differed between the space-station populations and the Earth-bound populations, the divergence can be attributed directly to differences in gravity.
The results highlighted another intriguing angle: the mutations that phages and bacteria acquire in space don’t just reveal fundamental evolutionary dynamics, they can also have practical applications for human health on Earth. After 25 days aboard the ISS, both organisms returned with novel mutations not commonly seen under terrestrial gravity, including changes to bacterial surface proteins and corresponding phage adaptations to bind those altered surfaces.
Researchers then engineered phages carrying these space-derived mutations and tested them against bacterial pathogens responsible for urinary tract infections — many of which are now resistant to antibiotics — finding the space-influenced phages were notably effective at killing these otherwise resistant strains. This suggests that the unique selection pressures of microgravity may reveal evolutionary pathways that could be harnessed to design improved therapies for antibiotic-resistant infections back on Earth.
Palaeontologists at the Federal University of São Paulo, Brazil have analysed the DNA recovered from two ancient humans and discovered that they were both carriers of the Human Papillomavirus HPV16, a virus implicated in several cancers. They have presented their evidence, ahead of peer-reviewed publication in the pre-print server, bioRxiv.
The interesting thing from the point of view of virology is that this discovery shed considerable light on when HPV entered the human virome and commenced co-evolving with us, with one theory being that we acquired them from Neanderthals. From the point of view of creationists however, the news could scarcely be worse.
The first sample, obtained from the famous 'Ötzi the Iceman', the 5,300 year-old mummified body recovered from a glacier on the Italian-Austrian border, is probably not too much of a problem for creationists as it just about falls within the timeline of the Bible mythology, apart from the little problem of it being from before they believe the was a general reset of Earth's biosphere in a genocidal flood which would have destroyed the glacier and everything in it, so Ötzi should not have been there.
But, the second is a massive problem, since it was recovered from a leg of a man, Ust'-Ishim man, recovered from western Siberia and dated to 45,000 years BP - way before creationists believe Earth existed, and tens of thousands of years before the mythical 'Fall', when creationists believe viruses didn't exist. This specimen provided the oldest complete human genome so far recovered and the DNA contains the unmistakable genome of HPV16. Creationist mythology just keeps getting further and further from reality as exposed by science using real-world evidence.
Traditionally, creationists claim Earth is 6,000 - 10,000 years old and was created perfect in every way, with no deaths or diseases, so no viruses, parasites or pathogens, bodies that always functioned perfectly and genomes that never failed to replicate perfectly. Then, along came 'sin' which, by some mysterious process, was able to thwart the omnipotent creator god's perfect plan and create viruses and other pathogens and make perfect physiology begin to malfunction and genomes to fail to replicate perfectly, causing variations and genetic weaknesses, etc.
Why a reputedly omnipotent creator failed to anticipate the effects of 'sin' and make its creation robust enough to resist them is never explained, although, apparently, it provided immune systems in preparation for something that, although omniscient, and even claimed to have created 'evil' (Isiah 45:7), it then failed to anticipate. But, as though those myths aren't too ridiculous for any adult with even a basic education to believe, creationists have to continually think of ways to ignore the evidence and continue holding plainly absurd beliefs, under the child-like delusion that their ability to do so is a sign of strength.
The paper itself sets out to address a long-standing question in human virology: how long oncogenic human papillomaviruses have been associated with our species, and whether their origins lie in relatively recent cultural changes or deep evolutionary history.
An international research team led by the University of Vienna and the University of Tartu (Estonia) — in collaboration with the University of Cambridge and University College London — has shown that ancient genomes of human betaherpesvirus 6A and 6B (HHV-6A/B) entered the human genome and then co-evolved with humans over the last 2,000 years. Their study, published in Science Advances a few days ago, confirms that these viruses have been evolving with, and within, humans since at least the Iron Age.
A common creationist claim, rooted in ignorance of what genetic information actually is, is that new genetic information cannot be created. Claims that new genetic information cannot arise because it would violate the laws of thermodynamics rely on a fundamental category error. The second law applies to closed systems, whereas every biological system on Earth is emphatically open, continuously exchanging energy and matter with its environment. Local decreases in entropy are not only permitted but expected in open systems supplied with external energy — which, on Earth, is overwhelmingly provided by the Sun. Crystals grow, snowflakes form, embryos develop, and genomes increase in length and complexity without violating any physical law.
Moreover, information is not a conserved physical quantity like energy. Shannon information theory concerns the statistical properties of signals in communication channels; it says nothing about biological meaning, function, or heredity. Treating genetic information as though it were interchangeable with thermodynamic entropy is simply a misuse of terminology. When genomes gain duplicated genes, viral insertions, or transferred sequences, no atoms are created, no laws are broken, and no special pleading is required — just chemistry operating under well-understood physical principles.
The creationist claim is flatly contradicted by straightforward observations of several well-understood mechanisms by which new genetic information can enter a species’ genome. These include gene duplication or whole-genome duplication, horizontal gene transfer from one species to another (particularly common in parasite–host relationships), and — as demonstrated by the research discussed here — the insertion of viral DNA into the genome. This last process gives rise to endogenous viral elements that are ubiquitous in biology and which precisely match evolutionary trees established independently from multiple other lines of evidence.
Endogenous viral insertions are especially devastating for the creationist concept of immutable “created kinds”. Viral DNA does not insert itself independently at exactly the same genomic locations in unrelated lineages by chance. When identical viral sequences are found embedded at the same chromosomal positions in different populations — and when their accumulated mutations form nested hierarchical patterns — they provide a precise historical record of shared ancestry.
The HHV-6A/B insertions documented in this study behave exactly as evolutionary theory predicts: they enter the genome at a particular point in time, are inherited by descendants, accumulate mutations at measurable rates, and track human population history. There is no coherent creationist explanation for why a designer would place broken, mutating viral sequences into genomes in patterns that perfectly mirror evolutionary trees derived independently from anatomy, archaeology, and population genetics.
If humans were created as a distinct “kind”, there is no reason for their genomes to contain time-stamped viral relics tracing population divergence over millennia. But if humans evolved — and if viruses have co-evolved with us — this is precisely the pattern we expect to find. The data fit evolution effortlessly, while creationism is left inventing ad hoc excuses to deny what the genome itself records.
Researchers from Switzerland and Japan, led by Professor Yohei Yamauchi of Eidgenössische Technische Hochschule Zürich (ETH Zürich), have developed a microscopy technique that enables real-time, high-resolution observation of how a virus gains entry to a cell. Their findings are described in the Proceedings of the National Academy of Sciences of the USA (PNAS).
The process, in which a virus exploits the pathways cells normally use to take in larger molecules such as hormones, cholesterol, or iron, involves the active cooperation of the cell as it reaches out to engulf the viral particle. This mechanism is triggered by receptors on the cell surface, to which viruses bind while ‘surfing’ along the membrane, seeking regions rich in receptors to form a stable attachment.
In other words, creationists often portray this as an “irreducibly complex” system, supposedly dependent on all components being present from the outset, requiring what they call “complex specified information” in both virus and cell to produce the receptors and binding proteins. Discovery Institute fellows Michael J. Behe and William A. Dembski present this as evidence of intelligent design.
Their argument depends on a statistical sleight of hand: they treat the entire process as though it originated in a single event involving one cell and one virus, then calculate improbabilities for each step and multiply them together, producing a vanishingly small likelihood of the whole mechanism arising spontaneously. This ignores the fact that evolution operates in populations — often large ones — across long periods, where components accumulate gradually over generations, dramatically increasing the probability of multiple features emerging together in the same lineage.
It also overlooks the billions of years during which viruses and cells have co-evolved. As multicellular organisms evolved ever more sophisticated ways of receiving and responding to external signals and substances, viruses simultaneously improved their ability to exploit those mechanisms.
But to the scientifically illiterate target audience of the ID-creationism industry, evolution is imagined as a single event rather than a continuous process, leaving them oblivious to the misuse of probability and the underlying mathematical errors.
Creationists trying to use this argument for intelligent design usually respond to biologists pointing out the obvious fact that they just presented their putative god as some sort of celestial malevolence, by retreating into Bible literalism and religious fundamentalism and invoking mythical 'Fall', so betraying the claims of the Discovery Institute and its fellows that ID is real science, not bible-literalist creationism dressed in a lab coat, as a lie.
How influenza viruses enter our cellsFor the first time, researchers have observed live and in high resolution how influenza viruses infect living cells. This was possible thanks to a new microscopy technique, which could now help to develop antiviral therapies in a more targeted manner.
In brief
For the first time, a new high-resolution microscopy technique has allowed researchers to watch live as influenza viruses infect cells.
The international team led by ETH Zurich found that the cells actively promote virus uptake.
This technique could now help to develop antiviral therapies in a more targeted manner.
Fever, aching limbs and a runny nose – as winter returns, so too does the flu. The disease is triggered by influenza viruses, which enter our body through droplets and then infect cells.
Researchers from Switzerland and Japan have now investigated this virus in minute detail. Using a microscopy technique that they developed themselves, the scientists can zoom in on the surface of human cells in a Petri dish. For the first time, this has allowed them to observe live and in high resolution how influenza viruses enter a living cell.
Led by Yohei Yamauchi, Professor of Molecular Medicine at ETH Zurich, the researchers were surprised by one thing in particular: the cells are not passive, simply allowing themselves to be invaded by the influenza virus. Rather, they actively attempt to capture it.
“The infection of our body cells is like a dance between virus and cell.
Professor Yohei Yamauchi, corresponding author.
Molecular Medicine Laboratory
Institute of Pharmaceutical Sciences
Department of Chemistry and Applied Biosciences
Eidgenössische Technische Hochschule Zürich
Zürich, Switzerland.
Viruses surf on the cell surface
Of course, our cells gain no advantage from a viral infection or from actively participating in the process. The dynamic interplay takes place because the viruses commandeer an everyday cellular uptake mechanism that is essential for the cells. Specifically, this mechanism serves to channel vital substances, such as hormones, cholesterol or iron, into the cells.
Like these substances, influenza viruses must also attach to molecules on the cell surface. The dynamics are like surfing on the surface of the cell: the virus scans the surface, attaching to a molecule here or there, until it has found an ideal entry point – one where there are many such receptor molecules located close to one another, enabling efficient uptake into the cell.
Once the cell’s receptors detect that a virus has attached itself to the membrane, a depression or pocket forms at the location in question. This depression is shaped and stabilised by a special structural protein known as clathrin. As the pocket grows, it encloses the virus, leading to the formation of a vesicle. The cell transports this vesicle into its interior, where the vesicle coating dissolves and releases the virus.
Previous studies investigating this key process used other microscopy techniques, including electron microscopy. As these techniques entailed the destruction of the cells, they could only ever provide a snapshot. Another technique that is used – known as fluorescence microscopy – only allows low spatial resolution.
Combined techniques, including for other viruses
The new technique, which combines atomic force microscopy (AFM) and fluorescence microscopy, is known as virus-view dual confocal and AFM (ViViD-AFM). Thanks to this method, it is now possible to follow the detailed dynamics of the virus’s entry into the cell.
Video: Nicole Davidson / ETH Zurich.
Accordingly, the researchers have been able to show that the cell actively promotes virus uptake on various levels. In this way, the cell actively recruits the functionally important clathrin proteins to the point where the virus is located. The cell surface also actively captures the virus by bulging up at the point in question. These wavelike membrane movements become stronger if the virus moves away from the cell surface again.
The new technique therefore provides key insights when it comes to the development of antiviral drugs. For example, it is suitable for testing the efficacy of potential drugs in a cell culture in real time. The study authors emphasise that the technique could also be used to investigate the behaviour of other viruses or even vaccines.
Significance
Influenza A viruses (IAVs) continue to cause epidemics worldwide due to their high mutability. Nevertheless, the initial step of infection, viral uptake into cells, has been challenging to observe directly with conventional microscopy techniques. Here, we developed a hybrid imaging system combining atomic force microscopy and confocal microscopy with enhanced mechanical functionality and minimal invasiveness to directly visualize nanoscale dynamics of IAV and cell membranes during viral uptake into living cells. This system enables the analysis of IAV lateral diffusion resulting from IAV–membrane interactions and characteristic membrane morphological changes induced by IAV during endocytosis. Our approach offers a method to rapidly assess the impact of viral mutations on host cell entry, which is critical for understanding emerging IAV variants.
Abstract
Influenza A virus (IAV) entry into host cells begins with interactions between the viral envelope proteins hemagglutinin (HA)/neuraminidase (NA) and sialic acid moieties on the cell plasma membrane. These interactions drive IAV’s lateral diffusion along the cell membrane and trigger membrane morphological changes required for endocytosis. However, directly visualizing these dynamic processes, which are crucial for IAV entry, has been challenging using conventional microscopy techniques. In this study, we enabled live-cell observation of nanoscale morphological dynamics of IAV and the cell membrane by reducing the mechanical invasiveness of atomic force microscopy (AFM). A customised cantilever with less than half the spring constant of conventional cantilevers enabled virus-view AFM imaging that preserved IAV–membrane interactions. By combining virus-view AFM with confocal microscopy, we performed correlative morphological and fluorescence observations of IAV lateral diffusion and endocytosis in living cells. Variations in diffusion coefficients of single virions suggested heterogeneity in sialic acid density on the cell membrane. NA inhibition decreased diffusion coefficients, while reduced sialic acid density increased them. The timing of clathrin accumulation at virion binding sites coincided with a decrease in diffusion coefficients, a relationship that was maintained independent of NA activity or sialic acid density. As clathrin assembly progressed, ~100-nm-high membrane bulges emerged adjacent to the virus, culminating in the complete membrane envelopment of the virus at peak clathrin accumulation. Our virus-view AFM will deepen our understanding of various virus–cell interactions, facilitate the evaluation of drug effects and promote future translational research.
Influenza A virus (IAV) is an enveloped RNA virus with two key surface glycoproteins: hemagglutinin (HA) and neuraminidase (NA). The virus surface contains 300 to 400 HA and 40 to 50 NA molecules (1). IAV envelope proteins comprise at least 18 HA and 11 NA subtypes (2), which enable IAV to infect various host species including humans, birds, pigs, bats, and other animals (3). These envelope proteins play crucial roles in IAV infection of host cells.
They interact with sialic acids on cell surface glycolipids and glycoproteins (4) or with major histocompatibility complex class II (MHC class II) molecules (5–7). HA binds to sialic acids at the terminal ends of glycan chains on the cell surface. The HA–sialic acid interactions are inherently weak, with dissociation constants typically in the millimolar range (0.9 to 68.4 × 10−3 M) (8–10). However, multivalent binding of multiple HAs to sialic acids enables IAV to stably adhere to the cell membrane (11, 12). Meanwhile, NA catalyzes the cleavage of sialic acids (13), inhibiting stable adhesion of IAV to the cell membrane. Through these mechanisms, HA and NA effectively regulate the attachment and detachment of IAV to the cell membrane.
The competitive action between HA and NA allows IAV to diffuse laterally along the cell membrane surface topology (). This lateral diffusion represents a critical dynamic macroscopic phenomenon reflecting virus–membrane interactions. However, conventional microscopy techniques have struggled to detect IAV movement on the 10-nm-thick cell membrane, resulting in limited visualization success (15–18).
HA-NA-sialic acid interactions also trigger endocytosis involving morphological changes of the cell membrane. When diffusing IAV binds to functional receptors such as EGFR (19) and Cav1.2 (20) through sialic acids, it initiates the recruitment and assembly of the endocytic machinery including clathrin, actin, and dynamin. IAV utilizes multiple entry pathways including clathrin-mediated endocytosis (CME), macropinocytosis, and both clathrin-independent and dynamin-independent mechanisms (16, 21–23).
IAV primarily utilizes CME for cellular entry (16, 21). Previous imaging of membrane dynamics using atomic force microscopy (AFM) has revealed that in IAV-free CME, clathrin-coated membrane invaginations (pits) larger than 100 nm in diameter form (24, 25). This is accompanied by the emergence of actin-dependent membrane bulges that develop on one side of the pit and eventually lead to its closure. Although electron microscopy has provided morphological snapshots of pits during IAV internalization (26), the membrane dynamics during IAV internalization via CME have yet to be successfully visualized.
AFM enables mechanical imaging of sample morphology with nanometer-scale resolution (27, 28). Since the development of high-speed AFM in 2001 (29), this technique has contributed significantly to molecular dynamics analysis (30–36). Additionally, the advent of cell-imaging AFM in 2013 has enabled advances in membrane dynamics analysis (37, 38). The integration of cell-imaging AFM combined with confocal microscopy has provided unique capabilities for observing nanoscale membrane morphological changes in living cells (24, 25). Despite these advances, a major challenge persists: the mechanical interference of the cantilever with biological samples. Visualizing the dynamic processes of IAV lateral diffusion and internalization requires an innovative technology capable of simultaneously observing the nanoscale morphology of the 10-nm-thick cell membrane and the 100-nm spherical IAV interacting with cell surface sialic acid-bearing glycolipids and proteins. Given that multivalent IAV–membrane interaction forces are relatively weak, ranging from 10 to 25 pN (39), achieving low-invasive imaging capabilities is critical.
In this study, we address and overcome the challenge of mechanical interference by enhancing the low invasiveness of AFM through the use of a customised soft cantilever. In combination with confocal microscopy, low-invasive AFM enables simultaneous live-cell imaging of both morphology and fluorescence. The redesigned cantilever minimizes disruption of IAV–membrane interactions, allowing accurate observation of viral dynamics. Using this system, we investigated the lateral diffusion of single IAV particles under various conditions, including NA inhibition, reduced cell surface sialic acid density, and different viral subtypes. We also analyzed membrane morphological changes before and during IAV endocytosis. While fluorescently labeled IAV was primarily used, we also demonstrate our AFM’s capability to track unlabeled viruses. This virus-view dual confocal and AFM, called ViViD-AFM, enables correlative morphological and fluorescence imaging of IAV–membrane dynamics, providing nanoscopic insights into HA-NA-sialic acid interactions.
What ID advocates never seem to notice is that, in arguing that such mechanisms must have been deliberately engineered, they are attributing to their designer a system in which viruses are given exquisitely tailored tools for invading the very cells it supposedly created. If one insists that this is intentional design, then one must also accept that the designer crafted the molecular equivalent of lockpicks and battering rams, optimised for breaching living tissue. It is difficult to reconcile this with any notion of benevolence.
Indeed, by rejecting evolution as the explanation for viral entry, ID proponents corner themselves into an uncomfortable theological stance: their designer not only equipped viruses with the machinery to exploit cellular signalling, but also ensured that cells remained vulnerable to such exploitation. The result is an ecosystem in which suffering, disease, and death are not unfortunate consequences of natural processes but deliberate design choices.
This is, of course, why mainstream biology requires no such designer. Co-evolution naturally explains why cells have receptors essential for communication and nutrient uptake, while viruses have, over immense timescales, adapted to hijack those same pathways. No malevolent architect is required—only the simple, iterative logic of variation, selection, and replication.
Yet the ID movement persistently overlooks this simpler, evidence-based account, preferring instead an argument that—if taken seriously—presents their putative creator as either unable to prevent viral parasitism or fully complicit in engineering it. Neither option supports the benevolent, omnipotent designer they hope to defend.
