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).
Credit: Borzo Gharibi, Science Advances (2026).
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.
From Viral Invaders to Useful Genes^ Evolution’s Borrowed Machinery. Retroviruses reproduce by inserting a DNA copy of their genetic material into a host cell’s genome. If an insertion enters the germ line — the lineage of cells that produces eggs or sperm — it can become hereditary - a rare example of a trait acquired after birth becoming hereditary. Over generations, mutations usually disable the virus, leaving an endogenous retrovirus: an inherited viral sequence embedded in the host’s DNA.More detail was provided by a Francis Crick Institute news item:
Occasionally, part of that viral inheritance acquires a useful role. This is exaptation: the recruitment of an existing feature for a different function. Both viral protein-coding genes and viral regulatory switches have been co-opted in this way.
How Can Something Acquired by Chance Become Essential?
- Syncytins: Viral Fusion Proteins Put to Work in the Placenta
Retroviral envelope proteins help a virus enter a cell by enabling membranes to fuse. In several mammalian lineages, genes encoding these proteins have been recruited to help placental cells fuse into a multinucleate layer called a syncytiotrophoblast.
These domesticated proteins are called syncytins. Humans and mice use different, independently acquired retroviral genes for this purpose. Experiments in mice have shown that disrupting syncytin genes can cause serious defects in placental development; loss of syncytin-A causes embryonic death. The repeated recruitment of different viral genes illustrates how evolution can arrive at similar solutions using independently acquired material.
Sources: Independent acquisition of human and mouse syncytins; review of syncytin evolution and function.
- Opossums: Another Independent Recruitment
Marsupials also form placentas, although these are generally shorter-lived than those of placental mammals. In certain South American opossums, researchers identified syncytin-Opo1, another independently acquired retroviral envelope gene.
The gene is expressed at the placental interface between mother and embryo, and its protein promotes cell fusion in laboratory experiments. Its conservation across related opossum species provides further evidence that natural selection has preserved a useful function. This is another instance of evolution recruiting viral machinery into reproduction.
Source: Retroviral envelope gene captures and syncytin exaptation for placentation in marsupials.
- MER41: Viral DNA Recruited into Immune Defence
A viral contribution need not encode a protein. Retroviruses also carry regulatory DNA that controls gene activity. Once embedded in a host genome, some of these sequences can acquire control over nearby host genes.
Members of the MER41 family of retroviral remnants help regulate responses to interferons, signalling proteins involved in immune defence. One such sequence acts as a regulatory element for AIM2, a gene involved in detecting DNA inside cells and triggering an inflammatory response. Deleting this element disrupted interferon-induced AIM2 expression in the cells studied.
This is particularly relevant to the HERVH–calbindin research: evolution can produce a new functional arrangement by attaching an existing gene to a borrowed switch. Novelty lies in the regulation, without requiring an entirely new protein.
Source: Regulatory evolution of innate immunity through co-option of endogenous retroviruses.
- Suppressyn: An Ancient Viral Protein That Can Block Infection
Suppressyn is a human protein derived from an ancient retroviral envelope gene. It binds to a cell-surface receptor called ASCT2, which certain retroviruses also use to enter cells.
Experiments in cultured human cells showed that suppressyn can interfere with infection by viruses using this receptor. An inherited remnant of one viral invasion can therefore provide protection against another. This is evidence of a specific protective effect in laboratory experiments, rather than evidence that suppressyn gives people general immunity to retroviruses.
Source: National Institutes of Health: Ancient viral DNA may help humans fight infections.
An ancestral organism need not have depended on the same mechanisms as its descendants. After a useful sequence is acquired, further evolutionary changes can build on it, modify its role or reduce reliance on older mechanisms. A contribution that began as an optional advantage can consequently become an indispensable part of a later system.
Removing that component today may cause the system to fail, but this does not mean the ancestral system could never have functioned without it. Present-day indispensability is not evidence that all the parts had to appear together.
These examples also make the meaning of new genetic “information” concrete: an organism can acquire a protein-coding sequence, gain a regulatory switch or evolve a new relationship between existing components. Horizontal acquisition supplies material; exaptation gives it a new role; inheritance and natural selection can preserve the result. None of these processes requires foresight.
Most importantly, the existence of useful viral remnants does not mean that every endogenous retroviral sequence is useful. Many are degraded or have no demonstrated host function. Exaptation describes particular cases supported by evidence, not a purpose assigned to every fragment of DNA.
Brief Glossary
- Endogenous retrovirus (ERV)
- A retroviral sequence integrated into the germ line and inherited as part of the host genome.
- Horizontal genetic transfer
- The acquisition of genetic material from another biological source, rather than through ordinary parent-to-offspring inheritance.
- Exaptation
- The co-option of an existing feature for a different function.
- Regulatory element
- A DNA sequence that helps control when, where or how strongly a gene is expressed.
- Convergent evolution
- The independent evolution of similar features or functions in different lineages.
An ancient advantage, hijacked by cancer
Researchers show that an anti-ageing mechanism hijacked by cancer cells to evade normal biological limits, also plays an important role in helping the embryo develop, having evolved from remnants of viral DNA.
Three years ago, George Kassiotis and his team made an unexpected discovery: a specific way of producing a protein called calbindin was found to help cancer cells survive by stopping them ageing. This left George, who runs the Crick’s Retroviral Immunology Laboratory, confused. Why would a mechanism that boosts cancer growth exist in the first place?
Calbindin removes calcium from the cell, which can become toxic in high amounts. It’s normally found in the brain and the kidney where calcium levels need to be tightly controlled. But George’s team identified that a certain form of calbindin was present in lung cancer cells, being switched on by a remnant of viral DNA now embedded in our genome.
This remnant is called a ‘human endogenous retrovirus’ or ‘HERV’, a hangover from a virus inserting its genetic material into our genome during an infection. No longer infectious, these stretches of DNA are generally only retained over evolution if our cells have found another use for them. We thought this must be the case for the type of HERV (called HERVH) which switches on calbindin.
George Kassiotis, senior author.
Retroviral Immunology Laboratory
The Francis Crick Institute
London, UK.
Embryonic efficiency
The HERV-calbindin switch had already been seen in cells that make up the early embryo, suggesting it might play a role in this critical period of development.
In research published in Science Advances, Judith Pape, then postdoctoral researcher in George’s team, teamed up with Kathy Niakan’s team, who pioneered genetic editing in human embryos, previously at the Crick and now at the University of Cambridge. Their expertise allowed the researchers to investigate the impact of removing calbindin or the HERVH driving it specifically in human embryonic stem cells.
We managed to genetically edit the cells to remove the ancient HERVH switch so they couldn’t produce calbindin. The cells were unhealthy, either failing to grow or becoming fixed as a certain type of cell prematurely. Expertise from our colleagues in the Crick’s Stem Cells and Organoids team helped us to keep these unhealthy cells alive long enough to study them further, which was no mean feat.
Judith Pape, first author.
Retroviral Immunology Laboratory
The Francis Crick Institute
London, UK.
Human blastocysts developing from embryos with (left) and without (right) HERVH-calbindin.Credit: Afshan McCarthy, Science Advances (2026).
Judith and George next went on to work with the Cell and Tissue Mechanobiology lab at the Crick to demonstrate an essential role for HERVH-driven calbindin in blastoids, models which mimic an embryonic stage called the blastocyst.
Blastoids without calbindin weren’t able to form properly. This suggests that HERVH-calbindin might help the blastocyst’s ability to develop and then implant in the uterus.
Judith Pape.
A fortuitus development from the Quantitative Stem Cell Biology lab at the Crick gave Judith another avenue to explore: the role of HERV-calbindin in the structures that support the embryo. “Researchers in this lab, who work on how embryonic stem cells become different tissues of the body, had just developed ‘post-gastrulation amnioids’, models which mimic the developing amniotic sac, which supports and cushions the embryo,” she says. “So, we genetically removed HERVH-calbindin from amnioids, and those without it couldn’t develop properly. Some failed to form a sac-like structure entirely.”
An evolutionary echo
By comparing primate genomes, the team confirmed that this particular HERVH was integrated after the split of great apes, including humans, from orangutans, approximately 13 million years ago. Calbindin expression in the pre-implantation embryo occurred at exactly the same time – unlikely to be a coincidence.
I see it as making a trade: a chance viral infection gave us a genetic instruction which was more helpful than an old one. We quickly, in evolutionary terms, swapped them out, and the HERVH-calbindin switch became firmly embedded in our blueprint.
Removing calcium stops cancer cells ageing and allows them to become different types, normal features of embryonic development which have been hijacked.
George Kassiotis.
The trade-off for this evolutionary advantage is that, in a very small proportion of people, cancer cells can make use of the same pathway which kept early embryos healthy.
Future steps: from biomarkers to treatments
The researchers are excited that their results could hold promise for a number of different fields. “In the future, researchers could test if the presence of HERVH-calbindin can act as a biomarker for embryo health in fertility treatments, as embryos with it are more likely to form efficiently,” says Judith. “It would also be interesting to explore the role of HERVH-calbindin during and after implantation into the uterus.”
In terms of cancer treatment, George is clear that it’s early days, but because this form of calbindin is different from calbindin in the kidney and brain, it might hold potential as an anti-cancer target. “It may be possible to block the form of calbindin only found in tumours, stopping cancer from hijacking this anti-ageing pathway,” he reasons. “This allows the primary form of calbindin to continue its critical role of buffering calcium toxicity.”
Publication:
The theory of evolution is fundamental to interpreting these findings. Common ancestry explains the distribution of the viral insertion among related primates; horizontal genetic transfer explains how the sequence entered an ancestral genome; and exaptation explains how viral material acquired a role in host development. The researchers did not encounter a failure of evolutionary theory and have to invoke an intelligent designer. They used the evolutionary framework to connect an ancient infection with a present-day developmental function. Nothing in these findings suggests that this framework is inadequate.
Nor does the importance of the sequence today imply that it must always have been present. Evolution can incorporate a useful addition and subsequently build dependencies around it. What began as a chance insertion can become essential in descendants whose biology has continued to evolve. This is precisely why removing a component from a modern system tells us little, by itself, about whether an ancestral system could have functioned without it. Present-day necessity does not establish an “irreducibly complex” origin.
The cancer connection also makes sense in evolutionary terms. A mechanism that supports early development can persist despite being vulnerable to exploitation by malignant cells. This is consistent with an evolutionary trade-off: natural selection favours reproductive success within existing constraints, without anticipating every consequence later in life. The pathway does not inevitably cause lung cancer, and its effects within tumours are complex, but its usefulness to cancer cells exposes the limitations of an arrangement that is beneficial in another context.
For a supposedly supreme, benevolent intelligent designer, those limitations are much harder to explain. An omniscient designer would foresee the vulnerability; an omnipotent one would not be confined to an evolutionary compromise. If creationists insist that the developmental benefit demonstrates deliberate design, they cannot simply exempt the harmful possibilities from the same reasoning. A designer who knowingly builds in an avoidable route to suffering invites the charge of malevolence; one who fails to foresee or prevent it invites the charge of incompetence. Neither resembles the perfect creator they advertise.
Evolution requires neither intention nor an excuse. An ancient viral invasion supplied material that could be co-opted, inherited and incorporated into a changing developmental system. Cancer can exploit the resulting machinery because natural selection offers no guarantee of perfection. The combination of usefulness, historical contingency and vulnerability is entirely intelligible as the outcome of evolution without foresight.
Advertisement
Amazon
Amazon
Amazon
Amazon
Amazon
Amazon
Amazon
Amazon
Amazon
Amazon
Amazon
Amazon
All titles available in paperback, hardcover, ebook for Kindle and audio format.
Prices correct at time of publication. for current prices.
No comments :
Post a Comment
Obscene, threatening or obnoxious messages, preaching, abuse and spam will be removed, as will anything by known Internet trolls and stalkers, by known sock-puppet accounts and anything not connected with the post,
A claim made without evidence can be dismissed without evidence. Remember: your opinion is not an established fact unless corroborated.