Rosa Rubicondior: Refuting Creationism - Co-Evolution of Humans and Influenza Viruses

AI-generated image (ChatGPT4o)

H3N2 virus is a respiratory viral infection of the influenza A virus.

Large-scale immunity profiling grants insights into flu virus evolution | For the press | eLife

In a striking confirmation of evolutionary theory—and a clear rebuttal of several fundamental creationist claims—scientists have demonstrated a close correlation between population-level immunity and the evolution of influenza viruses to evade that immunity. The findings, reported in eLife, align perfectly with predictions made by evolutionary biology: as the immune landscape of a population shifts, so too does the genetic makeup of viruses in an ongoing evolutionary arms race.

Disappointingly for creationists hoping for signs that biomedical science is abandoning evolution in favour of supernatural explanations, there is no such evidence. Nowhere in the study is there a hint that scientists are retreating from evolutionary principles or embracing a non-falsifiable belief system involving mysterious, unexplained entities. On the contrary, the researchers are clear and unequivocal: their results reinforce the view that viral evolution is a dynamic, adaptive process shaped by natural selection in response to host immunity.

Even more troubling for proponents of Intelligent Design (ID) is the unavoidable implication that the viral mutations observed in this study constitute what William A. Dembski calls "complex specified information"—which he argues can only arise through the intervention of an intelligent designer. If one follows that line of reasoning, the logical (if deeply uncomfortable) conclusion is that this designer is actively modifying viruses to undermine the very immune systems it supposedly created to protect us. Such behaviour can hardly be described as intelligent and is incompatible with the benevolent deity so often associated with the Intelligent Design movement.

About the H3N2 Influenza Virus. H3N2 is a subtype of the Influenza A virus, one of the primary viruses responsible for seasonal flu epidemics in humans. It first emerged in 1968 during the "Hong Kong flu" pandemic, which caused an estimated 1–4 million deaths worldwide.

Key Facts:

Type: Influenza A virus
Subtype designation: H3 (haemagglutinin) and N2 (neuraminidase) surface proteins
Natural hosts: Wild birds (reservoir); pigs and humans act as intermediate hosts
Transmission: Airborne droplets, direct contact, contaminated surfaces

Why It Evolves Rapidly:

H3N2 undergoes:

Antigenic drift – gradual mutation in viral genes, especially in HA and NA proteins, allowing it to escape immune detection.
Antigenic shift – occasional reassortment with other influenza viruses, potentially leading to novel strains.

Public Health Challenges:

Known for rapid evolution, making vaccine updates frequently necessary.
Tends to cause more severe illness in the elderly and young children.
Vaccination remains the best defence, although effectiveness varies by season due to its fast mutation rate.

The team’s findings are explained in an eLife press release:

Large-scale immunity profiling grants insights into flu virus evolution
A new study has shown that person-to-person variation in antibody immunity plays a key role in shaping which influenza (flu) strains dominate in a population.
The work, published today as a Reviewed Preprint in eLife, uses a high-throughput sequencing-based assay to quantify antibody immunity against circulating H3N2 flu strains in both children and adults. The editors describe this as an important study that advances our understanding of population-level immunity, and say that the strength of evidence is compelling. The work will be of interest to immunologists, virologists, vaccine developers and researchers working on mathematical modelling of infectious diseases.

Flu viruses accumulate mutations that help them evade antibodies generated by the immune system after prior infections or vaccinations. This process means that people can be reinfected with the flu multiple times in their lives, and vaccines must be regularly updated to remain effective. The human immune response to flu is shaped by a variety of factors, including the strains an individual has previously encountered.

Differences in infection and vaccination histories within a group of people mean that population immunity to a specific variant of the flu is highly varied. Understanding how this variety in antibodies across a population affects the evolutionary success of new flu strains has remained challenging, in part because conventional methods to quantify antibody levels are too slow and can only assess a handful of samples at a time.

Dr. Caroline Kikawa, co-lead author
Division of Basic Sciences and Computational Biology Program
Fred Hutch Cancer Center
University of Washington, Seattle, WA, USA.

To address this challenge, [Caroline] Kikawa, [Andrea N.] Loes and colleagues developed a high-throughput neutralisation assay to measure how well individual serum samples – the component of blood that contains antibodies – can block infection by a panel of different flu viruses. High-throughput refers to the assay’s ability to process large amounts of data simultaneously.

The team produced viruses expressing 78 distinct hemagglutinin (HA) proteins from 2023-circulating flu viruses and recent vaccine strains, and tagged each one with a unique genetic ‘barcode’. HA proteins are a part of the virus recognised by antibodies, and can rapidly change to evade the immune response. The team mixed these viruses with sera and used a technique called Illumina sequencing to quantify how well each virus was neutralised.

Using this approach, the researchers measured neutralisation titers – a measurement of how much serum is needed to neutralise the virus – against the 78 flu variants using 150 serum samples, from children and adults, collected in 2023 in the US. In total, they generated over 11,000 individual titer measurements, creating a detailed snapshot of population immunity at the start of the 2023–2024 flu season.

The results showed wide variation in neutralisation responses between individuals. For example, some of the sera collected from children strongly neutralised nearly all tested strains, while others had a much weaker response. Adults generally showed more consistent immunity, but still displayed considerable variation individually. Overall, the highest rates of neutralisation responses were found in a subset of children, consistent with the idea that neutralising antibody responses are highest to strains encountered during the first decades of life. It could also be that children are more prone to flu and could therefore be more likely to have recent immunological boosting. These findings highlight that immunity to the flu is highly personalised.

To evaluate how this variation affects virus evolution, the researchers compared neutralisation titers with the growth rates of each viral strain during the 2023 flu season. They used a statistical model called multinomial logistic regression to analyse how the frequency of each strain changed over time in the human population, and compared this to the fraction of serum samples that had low neutralisation titers against each strain.

They found that the strains that spread most successfully were those that escaped neutralisation in a larger fraction of the sera. Specifically, strains were more likely to grow in frequency when a high percentage of individuals had titers below a threshold, indicating weaker immunity against that strain. This suggests that large-scale sequencing-based neutralisation assays can help inform our understanding of flu virus evolution.

This relationship held when neutralisation was measured using individual sera, but not when the sera were pooled together. In some virus surveillance systems, pooled serum samples are used to estimate population immunity. However, this finding suggests that pooled measurements may fail to capture the full range of responses seen in individuals.

Our findings show that individual-level immune variation, not just average immunity across the population, is a key factor in determining which flu strains are most successful.

Andrea N. Loes, co-lead author.
Division of Basic Sciences and Computational Biology Program
Fred Hutch Cancer Center
University of Washington, Seattle, WA, USA.

While the study involved a large number of titer measurements, the authors note that the samples were collected from a limited set of locations and age groups. Most child samples came from a hospital in Seattle, while adult samples were drawn from vaccinated cohorts in Philadelphia and Australia. As a result, the dataset may not fully reflect global patterns of immunity.

This is nevertheless one of the largest datasets linking human antibody immunity to the success of flu virus strains in a population. It provides a framework for understanding how diverse immune histories can affect viral evolution. These methods could complement existing surveillance systems and support vaccine composition decisions by providing more detailed insights into population immunity.

Professor Jesse Bloom, senior author.
Division of Basic Sciences and Computational Biology Program
Fred Hutch Cancer Center
University of Washington, Seattle, WA, USA.

eLife Assessment
This important study advances our understanding of population-level immune responses to influenza in both children and adults. The strength of the evidence supporting the conclusions is compelling, with high-throughput profiling assays and mathematical modeling. The work will be of interest to immunologists, virologists, vaccine developers, and those working on mathematical modeling of infectious diseases.

https://doi.org/10.7554/eLife.106811.1.sa4

Abstract
Human influenza viruses rapidly acquire mutations in their hemagglutinin (HA) protein that erode neutralization by antibodies from prior exposures. Here, we use a sequencing-based assay to measure neutralization titers for 78 recent H3N2 HA strains against a large set of children and adult sera, measuring ∼10,000 total titers. There is substantial person-to-person heterogeneity in the titers against different viral strains, both within and across age cohorts. The growth rates of H3N2 strains in the human population in 2023 are highly correlated with the fraction of sera with low titers against each strain. Notably, strain growth rates are less correlated with neutralization titers against pools of human sera, demonstrating the importance of population heterogeneity in shaping viral evolution. Overall, these results suggest that high-throughput neutralization measurements of human sera against many different viral strains can help explain the evolution of human influenza.

Introduction
Infection or vaccination with influenza virus elicits a neutralizing antibody response targeting the viral hemagglutinin (HA) protein^1,2. These antibodies correlate with protection against infection and so provide substantial immunity to strains that they neutralize^1-11. However, the HA of human influenza evolves rapidly, acquiring mutations that erode neutralization by antibodies elicited by prior infections and vaccinations^12–14. New HA variants with reduced neutralization are generally the most evolutionarily successful, and repeatedly replace the current dominant variant(s) in a process known as antigenic drift^13,15–17. As a result, people are reinfected roughly every five years^1,18,19 and vaccines are updated annually to attempt to match the currently dominant influenza strains²⁰.

The human antibody response to influenza is shaped in part by past exposures to related strains, a phenomenon known as imprinting^21-23. While an individual’s exposure history is partially dependent on their birth year^19,24,25, HA’s rapid evolution along with variation in which strains infect even individuals with similar birth years create heterogeneous exposure histories both between and within birth cohorts^2,22,26-28. These heterogeneous exposure histories lead to substantial differences in how the neutralizing antibodies of different people target HA, and hence how their neutralizing antibody immunity is affected by viral mutations^26,29,30.

Determining how population heterogeneity in human neutralizing antibody specificities shapes influenza virus evolution has been challenging because conventional methods (e.g., hemagglutination inhibition³¹ and neutralization assays³²) are low throughput. It is therefore experimentally daunting to use these methods to measure neutralizing titers for large numbers of human sera against the full diversity of influenza virus strains that circulate in a single season. In part because of these limitations, a common approach is to use sera from singly infected ferrets to estimate antigenic distances between different viral strains^13,33. However, growing evidence indicates sera from singly infected ferrets are an imperfect proxy for human populations with complex and heterogeneous exposure histories^{23,26,27,30,34-37}. Therefore, the reports from the bi-annual influenza vaccine-strain selection meetings have increasingly referenced titer measurements for human sera, made using either individual sera or serum pools^38-42.

Here, we use a new sequencing-based assay⁴³ to measure the neutralization titers of 78 recent H3N2 viral strains by a large set of children and adult sera. These measurements quantify the heterogeneity of neutralizing antibody immunity to influenza across different members of the population. We find that the evolutionary success of different H3N2 strains is highly correlated with the fraction of sera that have low titers against each strain, suggesting that large-scale sequencing-based neutralization assays can help inform understanding of influenza virus evolution.

These findings present a serious challenge to creationist narratives, particularly those rooted in Intelligent Design. Rather than showcasing a static biological world crafted by a perfect designer, the research illustrates an ongoing, natural evolutionary struggle between host and pathogen — one that plays out precisely as evolutionary theory predicts. The virus evolves in direct response to the selective pressure exerted by host immunity, and this adaptation is measurable, observable, and repeatable.

For creationists, especially those who argue that evolution cannot produce new information, this is an inconvenient truth. The influenza virus demonstrably accumulates genetic changes that enable it to escape immune detection — clear evidence of the generation of new, functional information without any need for supernatural intervention. Attempts to dismiss this as "microevolution" or trivial variation fall flat when these changes have such profound consequences for public health and viral fitness.

More uncomfortably still for proponents of Intelligent Design, if one insists that such changes involve “complex specified information” and therefore must be the result of an intelligent agent, one must reckon with the implications. Either viruses evolve naturally, or an intelligent designer is deliberately re-engineering pathogens to be more effective at causing illness and evading the immune defences it supposedly created. Neither option supports the theological or scientific claims made by creationists. This research doesn't just support evolution — it makes creationism appear both scientifically untenable and ethically incoherent.

Advertisement

The Malevolent Designer: Why Nature's God is Not Good

This book presents the reader with multiple examples of why, even if we accept Creationism's putative intelligent designer, any such entity can only be regarded as malevolent, designing ever-more ingenious ways to make life difficult for living things, including humans, for no other reason than the sheer pleasure of doing so. This putative creator has also given other creatures much better things like immune systems, eyesight and ability to regenerate limbs that it could have given to all its creation, including humans, but chose not to. This book will leave creationists with the dilemma of explaining why evolution by natural selection is the only plausible explanation for so many nasty little parasites that doesn't leave their creator looking like an ingenious, sadistic, misanthropic, malevolence finding ever more ways to increase pain and suffering in the world, and not the omnibenevolent, maximally good god that Creationists of all Abrahamic religions believe created everything. As with a previous book by this author, "The Unintelligent Designer: Refuting the Intelligent Design Hoax", this book comprehensively refutes any notion of intelligent design by anything resembling a loving, intelligent and maximally good god. Such evil could not exist in a universe created by such a god. Evil exists, therefore a maximally good, all-knowing, all-loving god does not.

Illustrated by Catherine Webber-Hounslow.

Available in Hardcover, Paperback, Audio book or eBook for Kindle

The Unintelligent Designer: Refuting The Intelligent Design Hoax

ID is not a problem for science; rather science is a problem for ID. This book shows why. It exposes the fallacy of Intelligent Design by showing that, when examined in detail, biological systems are anything but intelligently designed. They show no signs of a plan and are quite ludicrously complex for whatever can be described as a purpose. The Intelligent Design movement relies on almost total ignorance of biological science and seemingly limitless credulity in its target marks. Its only real appeal appears to be to those who find science too difficult or too much trouble to learn yet want their opinions to be regarded as at least as important as those of scientists and experts in their fields.

Available in Hardcover, Paperback, Audio Book or eBook for Kindle

Advertisement

Amazon