A Single Molecular Change May Help Viruses Jump from Bat to Human | UC San Francisco
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: