In 2012, intelligent design proponents Robert W. Carter and John C. Sanford published a paper demonstrating the detrimental effects of mutational accumulation in the influenza virus. Though more than a decade old, this work caught my attention, among other reasons, for its possible relevance to our current experiences with COVID-19.

The paper demonstrates how mutational accumulation degrades genetic code over time — a concept championed by the ID community. The authors present a comprehensive historical analysis of mutational changes within the influenza virus H1N1, examining over 4,100 fully sequenced H1N1 genomes. Their results document multiple extinction events, including the previously known extinction of the human H1N1 lineage in 1957 and an apparent second extinction of the human H1N1 lineage in 2009. They state that the seeming extinctions appear to be due to continuous genetic erosion from the accumulation of mutations in the lineages. 

Fresh Look at a Familiar Virus

From the article, “A new look at an old virus,” in Theoretical Biology and Medical Modelling:

It is therefore reasonable to ask if the striking reduction in H1N1 mortality might be due, in part, to natural attenuation resulting from deleterious mutation accumulation. Herd immunity is undoubtedly an important factor in reduced H1N1 mortality since 1918, but this may not be sufficient to explain the continuous decline in H1N1-related mortality over multiple human generations or the eventual extinction of the viral strain. Likewise, improved medical treatments, such as antibiotic treatment for flu-related pneumonia, were certainly a significant factor reducing H1N1 mortality, but these do not appear to fully explain the nature of the pattern of mortality decline seen for H1N1. For example, the exponential decline in mortality began before the invention of antibiotic treatment.

The Generative Power of Mutations 

ID proponents — including Carter, Michael Behe, Douglas Axe, Winston Ewert, and Stephen Meyer — have been critical of the generative power of mutations to produce information. That includes the information required by viruses to mutate into more virulent forms. Instead, these theorists have championed the idea that mutations overall tend to be harmful, degrading information-rich codes. This paper shows the degenerative effects of mutations even in the H1N1 virus, which has access to large population sizes and to the causal efficacy of natural selection. The authors show that mutations break code apart rather than build novel code. Let’s take a closer look.

The H1N1 influenza virus has circulated in the human population for 95 years. In the notorious outbreak of 1917–1918, it infected a staggering 40 percent of the human population. The H1N1 virus caused a death rate of 2 percent and continued to circulate until 1957, seemingly going extinct, only to reappear in 1977. Carter and Sanford pondered whether natural attenuation, resulting from the accumulation of mutations, could be the reason for the virus’s loss of virulence and its apparent extinction. The authors also discuss the relevance of their work for medicine and public policy. For example, given the prevailing belief that mutations produce genetic novelty, there was much anticipation, up to the 2009 outbreak of “swine flu” (a combination of H1N2 and H1N1), of a resurgence of a highly evolved deadly variant of H1N1.

RNA viruses have a known susceptibility to mutational degeneration, and scientists have even speculated that increasing a virus’s mutation rate may be a way to control viral epidemics. The H1N1 RNA virus’s genome has eight RNA segments, which code for 11 different proteins. For this virus, there is a reconstructed version of the 1918 genome and thousands of fully sequenced influenza viruses. Because of this existing data and knowledge, Carter and Sanford could test their attenuation model by examining mutation accumulation rates in the influenza lineage over time. They also looked to see if codon specificity moved towards a particular host preference — human, swine, and bird (duck).

A Relatively Constant Rate

After plotting the relative mutation count (y-axis) over time (x-axis) for the 2009–2010 “swine flu” outbreak, the authors discovered that mutations were accumulating at a relatively constant rate. The rate of linear accumulation also extended back to the original introduction (meaning the rate of mutation didn’t change and mutations kept accumulating), with one exception. There is a sharp discontinuity between the apparent extinction of the virus in 1957 and its reappearance in 1977. The researchers hypothesized that a frozen strain of the virus may have been reintroduced to the population, and that strain had fewer mutations than the major circulating strain that went extinct. This strain circulated until 2009, at which point it also appears to have gone extinct. 

Carter and Sanford argue that the swine flu of 2009 did not arise from the 1977 reintroduced strain. That is because it carried the full mutational load of the strain that went extinct in 1957. This observation led them to think that it was unlikely to be a significant threat, in contrast to if it had had a more intact genome. Importantly their analysis shows that this virus arose not due to adaptive mutations within H1N1 — as expected if evolution has generative power to design new living systems — but from horizontal transmission of new genetic material from other bird influenza strains. They present strong evidence that the H1N1 genome has been systematically degrading since 1918.

This [referring to systemic degradation] is evidenced by continuous, systematic, and rapid changes in the H1N1 genome throughout its history. For example, there was an especially rapid and monotonic accumulation of mutations during a single pandemic (Figure 1). Similarly, there was a continuous and rapid accumulation of mutations over the entire history of the virus (Figures 2 and 3), including a similar steady increase in nonsynonymous amino acid substitutions (Figure 3). While mutations accumulated in the human H1N1s, there was a parallel accumulation of mutations in the porcine H1N1 lineage (Figure 4).

The authors conclude that while some beneficial mutations occur, many more deleterious mutations are also occurring at the same time. Carter and Sanford also observed a clear erosion of codon bias over time without a net movement towards any single host preference (human, swine, and bird). They write:

It appears that the H1N1 strains currently in circulation are significantly attenuated and cannot reasonably be expected to back-mutate into a non-attenuated strain. The greatest influenza threat, therefore, is the introduction of a non-attenuated strain from some natural reservoir. This suggests that a better understanding of the origin of such non-attenuated strains should be a priority. Our findings suggest that new strategies that accelerate natural genetic attenuation of RNA viruses may prove useful for managing future pandemics and, perhaps in the long run, may preclude the genesis of new influenza strains.

Great Contemporary Significance

As we can see, design-based thinking sheds light on topics of great contemporary significance, such as how viruses spread through populations. For me, having lived through the COVID-19 pandemic, this paper was a refreshing read. It provides hope that as COVID-19 continues to degrade, the human population can expect less of a threat from this nasty virus. As, however, the introduction of a non-attenuated strain from a reservoir would cause the pandemic to continue, there are some caveats to this prediction.