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.
The paper in Cell Host & Microbe was accompanied by a news item from UCSF by Levi Gadye:
A Single Molecular Change May Help Viruses Jump from Bat to Human
Most pandemics start when a pathogen spreads from animals to humans. It’s a leading explanation, in fact, for the COVID-19 pandemic: the SARS-CoV-2 virus, which causes COVID-19, is a cousin to coronaviruses that live in bats.
Now, researchers at the UCSF Quantitative Biosciences Institute, Icahn School of Medicine at Mount Sinai, Institut Pasteur, and Fred Hutchinson Cancer Center report that a single change in an amino acid — a building block of proteins — alters how coronaviruses interact with bat and human immune systems, shifting the body's response to infection.
The discovery helps explain how benign animal viruses can adapt to humans and cause severe disease. The study appeared in Cell Host & Microbe on May 13.
Researchers looked at SARS-CoV-2 and a related coronavirus called RaTG13, which only infects bats, and compared how each virus interacted with proteins in bat and human lung cells. The experiments relied on the first laboratory-grown lung cell line from the greater horseshoe bat.
A viral protein called Orf9b emerged as a key factor. The SARS-CoV-2 and RaTG13 versions of Orf9b are 93% identical but behave very differently. In human cells, the SARS-CoV-2 version disabled an immune alarm system, allowing the virus to multiply. In bat cells, the RaTG13 version activated a protein that helped suppress the virus.
The team found that changing just one of Orf9B’s 100 amino acids reversed its ability to evade the immune system.
The difference between a virus that stays in bats and one that spills over into humans and causes catastrophic disease can come down to remarkably small genetic changes. By mapping these interactions at the protein level — across two viruses and two species — we can read the molecular signatures that predict spillover risk. It’s the kind of early warning system the world needs.
Dr. Nevan J. Krogan, senior author.
Quantitative Biosciences Institute (QBI)
University of California, San Francisco
San Francisco, CA, USA.
Authors: UCSF authors are Jyoti Batra, PhD; Yuan Zhou, MS; Rithika Adavikolanu; Durga Anand; Sooraj Verma; Martin Gordon, MS; Shivali Malpotra, MS; Jack M. Moen, PhD; Ajda Rojc, MS; Atoshi Banerjee, PhD; Sourobh Maji, PhD; Monita Muralidharan, PhD; Helene Foussard, PhD; Irene P. Chen, PhD; CJ San Felipe, PhD; Lorena Zuliani-Alvarez, PhD; Promisree Choudhury, PhD; Kirsten Obernier, PhD; Rahul Suryawanshi, PhD; Taha Y. Taha, PhD, PharmD; Kliment A. Verba, PhD; James S. Fraser, PhD; Robert M. Stroud, PhD, MA; Melanie Ott, MD, PhD; Ben Polacco, PhD; Danielle L. Swaney, PhD; Ignacia Echeverria, PhD; and Manon Eckhardt, PhD. For all authors see the paper.
Publication:
And so we are left with the problem creationists prefer not to notice. If a molecular mechanism that enables a bacterium to swim, a parasite to evade a drug, a coronavirus to suppress an immune response, or an influenza virus to exploit dying cells is evidence of intelligent design, then the designer is not merely designing flowers, butterflies and sunsets. It is also designing the means by which pathogens infect, spread, persist and cause suffering.
The alternative, of course, is the scientific one: no designer is involved. These are not acts of malice or benevolence, but the result of natural selection acting on variation in organisms and viruses whose only 'aim', in a metaphorical sense, is replication. A mutation that benefits a virus is beneficial, irrespective of whether it is harmful to us. Evolution has no obligation to make humans comfortable, healthy or safe; it merely preserves whatever works in the circumstances in which it arises.
That is why creationist special pleading is so transparent. When a structure or process appears impressive, they claim it as design. When the same reasoning points to a designer of disease, parasitism, immune evasion and suffering, they change the subject and invoke 'The Fall', 'Sin', or some other theological escape clause. The evidence has not changed; only the apologetics have.
This papers and the next are yet more examples of why biology makes sense in the light of evolution and becomes morally grotesque when forced into the mould of intelligent design. Natural processes explain why viruses adapt, why pathogens exploit opportunities, and why small molecular changes can have large consequences. Creationism, by contrast, is left trying to praise the ingenuity of a designer while pretending not to notice the evil that ingenuity is being used for.
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.