Rosa Rubicondior: Creationism Refuted - Complex Specified Information in 'Spanish Flu' Virus Makes ID Creationists Sick

Thursday, 24 July 2025

Creationism Refuted - Complex Specified Information in 'Spanish Flu' Virus Makes ID Creationists Sick

Swiss Genome of the 1918 Influenza Virus Reconstructed | UZH

A major stumbling block that non-biologist Christian fundamentalist theologian William A. Dembski has blundered into is that his so-called ‘proof of intelligent design’ (i.e., the Christian god) also, by the same reasoning, constitutes evidence for malevolent design — something found in virtually every genome of every parasite and pathogen. This presents CDesign proponentsists with a fatal paradox: either their ‘proof of intelligent design’ also proves the existence of an evil designer, or ‘complex specified information’ is not the definitive evidence for design they like to claim it is.

A classic example — and another blow to creationist reasoning—has just been described in a study by researchers from the Swiss universities of Basel and Zurich. They have recovered and analysed the genome of the virus responsible for the 1918–1920 ‘Spanish flu’ pandemic, which killed more people than were killed in the First World War. In fact, the term ‘Spanish flu’ is a misnomer; the virus is now believed to have originated in a U.S. military base in Kansas and was brought to Europe by American soldiers.

The Swiss team discovered that from the outset, the virus appears to have been pre-adapted for infectivity and immune evasion. They identified three key mutations that remained unchanged as the virus evolved over the course of the pandemic. Two of these mutations made the virus resistant to an antiviral component of the human immune system, while the third enabled it to bind more effectively to receptors on the surface of human cells, allowing it to enter and infect them more readily. These mutations were so effective that victims frequently died within hours of the onset of symptoms.

What is known of the evolutionary origin of the 'Spanish flu' virus and the course of the pandemic? The “Spanish flu” pandemic of 1918–1920 was caused by an unusually virulent strain of influenza A virus, subtype H1N1, and is considered the deadliest influenza pandemic in recorded history, killing an estimated 50 million people worldwide, possibly more. Here’s what is known about its evolutionary origin and the course of the pandemic:

Evolutionary Origin

Avian Origins
Genetic and phylogenetic studies suggest the 1918 H1N1 virus was of avian origin, or at least closely related to avian influenza viruses. Its internal genes (those not involved in host recognition) are particularly similar to those of wild waterfowl, long recognised as natural reservoirs of influenza A.
Zoonotic Jump
The virus likely jumped to humans from birds, possibly via intermediate hosts, such as pigs, which can serve as “mixing vessels” for avian and human influenza viruses. However, the exact pathway of zoonosis remains unclear. The virus already possessed key mutations enabling human infection by the time it began to spread widely.
Pre-adaptation and Human Adaptation
The 2025 study (described in this blog post) from the Universities of Basel and Zurich (Schünemann et al.) shows that early strains already carried mutations aiding in:

Resistance to human immune responses (e.g., interferon pathways).
Effective binding to human cell receptors (specifically α2,6-linked sialic acids). These suggest the virus may have already been highly adapted to humans when the pandemic began, potentially indicating a period of cryptic circulation in humans before the outbreak was recognised.

Course of the Pandemic

Three Waves (1918–1920)
The pandemic came in three main waves, each more deadly than the last:

Spring 1918: The first wave was relatively mild, with typical flu-like symptoms and lower mortality.
Autumn 1918: The second wave was the deadliest. It spread rapidly and globally, causing severe pneumonia and high mortality, especially in healthy young adults.
Winter 1918–1919 and beyond: A third wave occurred in early 1919, with intermediate severity, followed by smaller flare-ups into 1920.

High Mortality in Young Adults
Unusually, the pandemic had a W-shaped mortality curve, with high death rates among:

Infants
Elderly adults
Young adults (20–40 years) — possibly due to a cytokine storm, where a strong immune reaction became fatal.

Global Spread via Troop Movements
The First World War played a key role in the rapid global dissemination of the virus, particularly through:

Military camps
Trenches and battlefield conditions
Demobilisation and civilian repatriation

Misnomer: ‘Spanish Flu’
The name arose because Spain, being neutral in WWI, did not censor press reports about the outbreak, unlike the belligerent nations. This gave the false impression that Spain was the origin, though evidence now suggests it began in rural Kansas, USA, and spread via U.S. troops to Europe.
Legacy and Descendants
The 1918 H1N1 virus is the progenitor of all later seasonal H1N1 strains. It re-emerged in various forms:

As a human seasonal flu virus until 1957
In 2009 as part of the swine-origin H1N1 pandemic virus (a reassortment involving 1918-lineage genes)

Summary

The 1918 H1N1 virus likely originated in birds, may have circulated in pigs, and underwent crucial mutations that allowed it to infect and kill humans efficiently. The pandemic’s unparalleled spread and lethality were exacerbated by WWI conditions and global troop movements. Evolutionary analyses now show that the virus was not only naturally evolved but also pre-adapted for efficient human infection, making it a poor fit for any intelligent design argument — unless one posits a malevolent designer.

The research team, led by Professor Verena Schünemann, a palaeogeneticist at the University of Basel, has just published their findings in the journal BMC Biology and explained them in lay terms in a news release from Universität Zürich (UZH).

Swiss Genome of the 1918 Influenza Virus Reconstructed
Researchers from the universities of Basel and Zurich have used a historical specimen from UZH’s Medical Collection to decode the genome of the virus responsible for the 1918–1920 influenza pandemic in Switzerland. The genetic material of the virus reveals that it had already developed key adaptations to humans at the outset of what became the deadliest influenza pandemic in history.
New viral epidemics pose a major challenge to public health and society. Understanding how viruses evolve and learning from past pandemics are crucial for developing targeted countermeasures. The so-called Spanish flu of 1918–1920 was one of the most devastating pandemics in history, claiming some 20 to 100 million lives worldwide. And yet, until now, little has been known about how that influenza virus mutated and adapted over the course of the pandemic.

More than 100-year-old flu virus sequenced

An international research team led by Verena Schünemann, a paleogeneticist and professor of archaeological science at the University of Basel (formerly at the University of Zurich) has now reconstructed the first Swiss genome of the influenza virus responsible for the pandemic of 1918–1920. For their study, the researchers used a more than 100-year-old virus taken from a formalin-fixed wet specimen sample in the Medical Collection of the Institute of Evolutionary Medicine at UZH. The virus came from an 18-year-old patient from Zurich who had died during the first wave of the pandemic in Switzerland and underwent autopsy in July 1918.

Three key adaptations in Swiss virus genome

This is the first time we’ve had access to an influenza genome from the 1918–1920 pandemic in Switzerland. It opens up new insights into the dynamics of how the virus adapted in Europe at the start of the pandemic.

Professor Verena J Schünemann, senior author.
Institute of Evolutionary Medicine
University of Zurich,
Zurich, Switzerland.

By comparing the Swiss genome with the few influenza virus genomes previously published from Germany and North America, the researchers were able to show that the Swiss strain already carried three key adaptations to humans that would persist in the virus population until the end of the pandemic.

Two of these mutations made the virus more resistant to an antiviral component in the human immune system – an important barrier against the transmissions of avian-like flu viruses from animals to humans. The third mutation concerned a protein in the virus’s membrane that improved its ability to bind to receptors in human cells, making the virus more resilient and more infectious.

New genome-sequencing method

Unlike adenoviruses, which cause common colds and are made up of stable DNA, influenza viruses carry their genetic information in the form of RNA, which degrades much faster.

Ancient RNA is only preserved over long periods under very specific conditions. That’s why we developed a new method to improve our ability to recover ancient RNA fragments from such specimens.

Christian Urban, co-corresponding author.
Institute of Evolutionary Medicine
University of Zurich
Zurich, Switzerland.

This new method can now be used to reconstruct further genomes of ancient RNA viruses and enables researchers to verify the authenticity of the recovered RNA fragments.

Invaluable archives

For their study, the researchers worked hand in hand with UZH’s Medical Collection and the Berlin Museum of Medical History of the Charité University Hospital.

Medical collections are an invaluable archive for reconstructing ancient RNA virus genomes. However, the potential of these specimens remains underused.

Frank Rühli, co-author.
Institute of Evolutionary Medicine
University of Zurich
Zurich, Switzerland.

The researchers believe the results of their study will prove particularly important when it comes to tackling future pandemics.

A better understanding of the dynamics of how viruses adapt to humans during a pandemic over a long period of time enables us to develop models for future pandemics.

Professor Verena J. Schünemann.

Thanks to our interdisciplinary approach that combines historico-epidemiological and genetic transmission patterns, we can establish an evidence-based foundation for calculations.

Kaspar Staub, co-author
Institute of Evolutionary Medicine
University of Zurich
Zurich, Switzerland.

This will require further reconstructions of virus genomes as well as in-depth analyses that include longer intervals.

Publication:

Christian Urban et at.
An ancient influenza genome from Switzerland allows deeper insights into host adaptation during the 1918 flu pandemic in Europe.
BMC Biology. 1 July 2025. DOI: https://doi.org/10.1186/s12915-025-02282-z

Abstract

Background

From 1918 to 1920, the largest influenza A virus (IAV) pandemic known to date spread globally causing between 20 to 100 million deaths. Historical records have captured critical aspects of the disease dynamics, such as the occurrence and severity of the pandemic waves. Yet, other important pieces of information such as the mutations that allowed the virus to adapt to its new host can only be obtained from IAV genomes. The analysis of specimens collected during the pandemic and still preserved in historical pathology collections can significantly contribute to a better understanding of its course. However, efficient RNA processing protocols are required to work with such specimens.

Results

Here, we describe an alternative protocol for efficient ancient RNA sequencing and evaluate its performance on historical samples, including a published positive control. The phenol/chloroform-free protocol efficiently recovers ancient viral RNA, especially small fragments, and maintains information about RNA fragment directionality through incorporating fragments by a ligation-based approach. One of the assessed historical samples allowed for the recovery of the first 1918 IAV genome from Switzerland. This genome, derived from a patient deceased during the beginning of the first pandemic wave in Switzerland, already harbours mutations linked to human adaptation.

Conclusion

We introduce an alternative, efficient workflow for ancient RNA recovery from formalin-fixed wet specimens. We also present the first precisely dated and complete influenza genome from Europe, highlighting the early occurrence of mutations associated with adaptation to humans during the first European wave of the 1918 pandemic.

Background

A better understanding of historical pandemics can provide relevant information for the prevention of future pandemics [1]. For example, reconstructing the evolution of pandemic pathogens can unveil their animal reservoir, if they are zoonotic, and the mutations associated with host switches [2–5].

The 1918–1920 influenza pandemic was the most devastating of the twentieth century, resulting in an estimated 20 to 100 million deaths, including a disproportionate number of young people [6, 7]. While it is probably the best-researched pandemic [8, 9], there are still important unanswered questions. For example, the evolution of its causative agent, the influenza A virus (IAV), is often assumed to have played a significant role in its multi-wave nature [10–12], but the relative paucity of 1918 IAV genomes has largely prevented substantiating or dismissing this notion. This is in part because valuable information contained in historical epidemiological data and human wet specimens from medical-historical collections has largely remained locked in archives. Furthermore, truly interdisciplinary studies, for example between biologists and historical epidemiologists, are still rare [13].

Because IAV isolation only became possible in the 1930s, genomic information on 1918 IAV started accumulating when historical biological material such as permafrost remains and formalin-fixed paraffin-embedded (FFPE) pathology samples were first investigated in the 1990s–2000s [14–19]. These PCR-based efforts culminated with the sequencing of a first complete genome in 2005 [20]. Since then, the use of high-throughput sequencing methods seems to have facilitated the use of fixed biological material, which has been used to generate an additional five high coverage 1918 IAV genomes [12, 21, 22]. However, such studies remain rare as many researchers consider the detection of viral RNA fragments from such specimens to represent a significant challenge.

Indeed, unprotected phosphodiester bonds in RNA are estimated to be 200 times less stable than in DNA [23]. Combined with the action of ubiquitously present RNAs, this can lead to rapid degradation of unprotected RNA [24]. Formalin fixation stops the action of RNAs and generally halts post-mortem decay processes, but it also has many negative effects on RNA quality. The formalin solution can cause deamination [25], crosslinking between proteins and nucleic acids [26, 27], as well as fragmentation [28]. The preparation of samples as FFPE blocks, which adds steps of tissue dehydration and paraffin-embedding, still results in measurable degradation of nucleic acids in a matter of years [29]. Recent studies have already demonstrated the successful extraction of unexpectedly long viral RNA fragments from century-old formalin-fixed wet specimen samples, hinting at a potential long-term RNA preservation mechanism by the viral capsid [12, 30]. Diversifying and improving extraction and library preparation methods will likely be essential to unlock information from the many thousands of specimens in medical collections [31].

Here, we present a new user-friendly ancient RNA (aRNA) workflow, which yielded reliable results from formalin-fixed wet specimen samples linked to the 1918 influenza pandemic. We were able to reconstruct a new well-covered (63.9 × average coverage) genome from Zurich, Switzerland, a country from which genomic information on this pandemic was so far missing. This genome, dating to the early first wave in Switzerland in the summer of 1918, already showed many genomic signs of adaptation to the human host.

Time-scaled phylogeny of HA sequences from 1918 and 1919 pandemic IAV. Sequences from the USA are in grey, published European sequences in green, and the new ZH1502 sequence in red. Support values are given only for branches with > 80% posterior probability. The same model specification as for Fig. 3 by Patrono and colleagues (2022) was used [12]

Christian Urban et at.
An ancient influenza genome from Switzerland allows deeper insights into host adaptation during the 1918 flu pandemic in Europe.
BMC Biology. 1 July 2025. DOI: https://doi.org/10.1186/s12915-025-02282-z

Copyright: © 2025 The authors.
Published by Springer Nature Ltd. Open access.
Reprinted under a Creative Commons Attribution 4.0 International license (CC BY 4.0)

One might think that the 1918 flu pandemic, which killed upwards of 50 million people in the prime of their lives, would give Intelligent Design proponents pause—but somehow, it never seems to. Here we have a virus so exquisitely engineered that it could infect, spread, and kill with breathtaking efficiency. It was resistant to human immune responses, perfectly suited to binding human cell receptors, and so effective that victims could die within hours. If this is “design,” then it’s not the kind you’d expect from a loving deity—it’s more in line with something out of a horror film.

Creationists, however, are oddly selective in their admiration for biological design. They’ll gush over the bacterial flagellum or the human eye, but when it comes to viruses that wipe out millions, suddenly the designer is on holiday—or it’s all the fault of “the Fall.” How convenient. But if they insist that complexity and efficiency equal design, then they must also admit that their designer is disturbingly fond of inventing new ways to make people suffer. Either that, or their favourite apologetic—“complex specified information”—isn’t proof of design at all, but simply a product of evolutionary processes that care nothing for morality or human wellbeing.

In the end, the 1918 flu virus makes one thing clear: if this is the handiwork of a designer, then we’re dealing with someone closer to a Bond villain than a benevolent creator. More likely, though, it’s just what evolution does—churns out whatever works, without the slightest regard for whether it’s beautiful, brutal, or both. A concept creationists might finally grasp, if only they could stop squinting at genomes and pretending not to see what’s staring them in the face.

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