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More evidence for the reality of genetic entropy—update


Several years after the publication of “A new look at an old virus: patterns of mutation accumulation in the human H1N1 influenza virus since 1918”1 and the follow-up publication in Journal of Creation,2 some detractors are arguing that the analysis was invalid. Specifically, they are claiming that the human H1N1 influenza virus is still making people sick, and thus the claim that it went ‘extinct’ in 2009 was wrong. This was an intriguing thought. Maybe the human H1N1 virus had still been circulating but was missed by major epidemiological laboratories worldwide? To get at the root of this, I re-did the original analysis and extended it to include all H1N1 viral genomes reported to date.

Figure 1. Number of mutations since 1918 occurring in all H1N1 viruses infecting humans (dark diamonds) and swine (light diamonds) reported in the Influenza Research Database through late 2018. (1) The human H1N1 lineage goes extinct for the first time in 1957. (2) The human H1N1 reappears in 1976 after an accidental release in Moscow. This creates a disjunction in the trendline and allows for easy visual separation of the swine and human versions. Sporadic swine H1N1 infections occur in humans between 1976 and 2009. (3) The human H1N1 virus disappears from reporting in March 2009, the same year the swine H1N1 goes pandemic in humans. We first reported this in 2012. (4) Six years later, all currently circulating H1N1 viruses infecting humans derive from viruses the same distance removed from the 1918 strain as a subset of the main swine version.

Every available H1N1 virus that had infected both human and swine as of 18 October 2018 was retrieved from the Influenza Research Database.3 Some sequences had to be removed due to quality control issues. Specifically, sequences with many Ns (i.e. missing data) tended to also be more diverged. This indicated the existence of poor-quality data. I culled every viral genome with more than five Ns. Also, some sequences were incomplete or missing one or more genomic segments.

There was a group of six consecutively named sequences from patients in New Zealand who were co-infected with the swine and human versions in 2009. These came from a study that claimed to have discovered reassorted viruses (genetically recombined swine and human H1N1) in several patients, even though other studies of a similar nature had failed to detect any reassortment.4 They also claimed the reassorted viruses did not spread to any other person. No other such ‘hybrid’ version can be seen in the massive database of viral genomes, and they left no viral descendants, so they were removed from the analysis.

The final dataset included 10,372 complete genomes that spanned 100 years of sampling.

I created an alignment for each of the eight genomic segments, trimming any sequence before the start codon or after the final stop codon and manually adjusting for indels. These were concatenated and entered into a single FASTA file, one line for each viral genome, totalling 13,133 nucleotides each. Distance was calculated by tabulating the number of differences compared to the 1918 strain (figure 1). The A/Brevig Mission/1/1918 strain is used as a reference for segments 1–3 and 5–8. The A/South Carolina/1/18 strain was used as a reference for segment 4 (see reference 1 for details). Occasional gaps and a few places where the sequence included an ambiguous letter call (e.g. an ‘S’ in a sequence indicated the letter was either a G or a C) were not counted as differences. There were no ambiguous calls in the reference sequence. Due to heavy sampling during specific years and in specific localities, there were many identical and near-identical sequences among the data. A pairwise comparison of all sequences was performed. If any pair differed by 10 or fewer nucleotides, the second member (alphabetically by strain name) of each pair was removed. This created a subset of 6,360 sequences with a minimum distance of 11 mutations. A neighbour-joining phylogenetic tree was created from a FASTA file of this subset in MEGA (version 7),5 then rooted to the 1918 strain (figure 2).

Figure 2. A phylogeny of human and swine H1N1 influenza. The tree is rooted to the 1918 strain. The ‘human’ branch is clockwise to the right of the dotted line. The ‘swine’ branch is counterclockwise to the left. Sporadic infections of humans by the swine version (asterisks) were reported over the years, but it was not until the 2009–2010 ‘swine flu’ pandemic that this version became common in humans. All currently circulating H1N1 viruses infecting humans are derived from the 2009–2010 pandemic viral strain. A thin grey circle was added to help the reader see how the genomic distance from the original 2009 outbreak viral genome increases over time in the long arm leading to the 2018 viral genomes.


As before, a clear break between the ‘human’ and ‘swine’ versions of the H1N1 virus can be seen (figure 1). This was caused by the accidental re-release of the virus in 1976 after being frozen in a sample dating back to approximately 1952.6 One can see occasional ‘swine’ H1N1 infections in humans over the years, and a huge burst after the 2009–2010 swine flu pandemic. In fact, from figure 1 it appears that all modern H1N1 infections in humans trace back to the swine version. It also suggests that the human version went extinct.

This is confirmed in figure 2, where we see that every H1N1 reported in humans since early 2009 traces back to the swine version. Indeed, the human version is clearly extinct after nearly a decade of non-reporting.


Genetic entropy is supported by strong theoretical work, powerful numerical simulations, and real-world examples. The H1N1 virus is not immune to the effects of genetic entropy and we see major strains either weakening or disappearing entirely over time. This comes after decades of natural selection failing to remove thousands of incremental errors in the genome.1,2 Also, new viral lines have appeared suddenly, sometimes with significantly more mutations than comparable contemporaneous strains. These can be seen in the data presented here. This might be an example of the ‘mutator strain’ hypothesis of Carter, Lee, and Sanford.7 Or perhaps sudden mutation surges are part of the long-term history of the H1N1 virus, but this would make it even more prone to genetic entropy.

What is in store for the H1N1 virus? Over time, it should continue to accumulate mutations faster than selection can remove them. It should continue to become more and more attenuated and, barring an infusion of fresh genetic elements from a wild strain currently circulating in aquatic waterfowl, it should eventually meet its demise. Only the future can tell.

References and notes

  1. Carter, R.W. and Sanford J.C., A new look at an old virus: patterns of mutation accumulation in the human H1N1 influenza virus since 1918, Theor. Biol. Med. Model 9:42, 2012; tbiomed.com/content/9/1/42. Return to text.
  2. Carter, R.W., More evidence for the reality of genetic entropy, J. Creation 28(1):16–17, 2014. Return to text.
  3. Influenza Research Database, fludb.org. Return to text.
  4. Sonnberg, S., et al., Pandemic seasonal H1N1 reassortants recovered from patient material display a phenotype similar to that of the seasonal parent, J. Virology 90(17):7647–7656, 2016. Return to text.
  5. Tamura, K., Stecher, G., Peterson, D., Filipski, A., and Kumar, S., MEGA6: Molecular evolutionary genetics analysis version 6.0, Molecular Biology and Evolution 30:2725–2729, 2013. Return to text.
  6. Nakajima, K., Desselberger, U., and Palese, P., Recent human influenza A (H1N1) viruses are closely related genetically to strains isolated in 1950, Nature 274:334–339, 1978. See also reference 1. Return to text.
  7. Carter, R.W., Lee, S., and Sanford, J.C., Overview of the independent histories of the human Y-chromosome and the human mitochondrial chromosome; in: Whitmore, J.H. (Ed.), Proceedings of the Eighth International Conference on Creationism, Creation Science Fellowship, Pittsburgh, PA, pp. 200–216, 2018. Return to text.

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Readers’ comments

Joel E.
So if the human version went extinct (due to genetic entropy?) in 1957, why would it pick up where it left off and go on another rampage for a further few decades before crashing again? I guess I just don't understand what real effect genetic entropy has in this case. Am I missing something?
Robert Carter
The reason it picked up where it off as far as mutation count goes was that it was effectively in a state of suspended animation for a couple of decades. But it did not go on another "rampage" and that is key. It quietly circulated, causing few deaths and milder symptoms that several other circulating flu strains, then disappeared in the year that a more aggressive cousin swept through. It was as if the newly-introduced swine H1N1 immunized so many people that the human H1N1 had no more targets. It was unable to complete and died off.
Joseph B.
Great work, solid points! I think Genetic Entropy is a strong supporter for Creation and a great problem for Evolution. The more research that supports it (and disproves any counter arguments that may arise), the stronger a case we have for Creation being true and Evolution being flawed.
Hope to see much more of this, keep it up!
Terry D P.
Dict. entropy: lack of order or predictability; gradual decline into disorder. How could evolution (a gradual increase in genetic order) occur, of a single cell into male and female pair of humans? when all the scientific evidence (viz. death) points to a “rapid breakdown in genetic order”.
Robert H.
Perhaps Robert Carter can apply his research to a consideration of covid 19. For H1N1 there is a wealth of historical data spanning just over a century, with analysis by many laboratories over many years. But for covid 19 there is only a few months of study. So any inferences drawn will necessarily be speculative. However, it may be instructive to suggest what could be the future of covid 19 if it follows a similar pattern to H1N1. That would also be a case of applying a Creationist approach - genetic entropy - to a real life science problem, and making a prediction which can be tested by future observation. The critics, wrongly, accuse us of not being able to make predictions, although there are many examples of science predictions correctly made using creationist assumptions.
Robert Carter
I have done exactly that, and it has involved many days of intense study. You are right that not enough time has elapsed to get a good handle on the long-term trajectory of the virus. But the mutation rate (on average, with a large standard deviation) is similar to H1N1 (and Ebola, another virus I put to the test), and the types of mutations that are accumulating are similar to the ones that occurred in the the human H1N1 from 1918 to 2010. I hesitate, however, to make a prediction. I think it will attenuate over time, and I think this will be over the course of a couple of years, but this does not mean that a mutation that makes it more infectious or more deadly cannot arise even as the genome, in general, is wasting away.
Thomas R.
After some more thought, I am now wondering if the “life expectancy” of COVID19 can be estimated. Specifically, the recurrence timeline of the dangerous waves. And also whether the longevity of such viruses is related to the world population size. It seems like the larger the population, the greater the longevity of the virus would be.
Robert Carter
These are difficult questions to answer. But the size of the population has little to do with the expected viral lifetime. With exponential growth, it does not take much longer for a virus to reach one billion than it does one million people.
Samuel S.
Ok so I have studied genetics and understand how evolution fails but why does it seem like we fail in geology I under stand that dating of the rocks is not necessarily accurate but when it comes to explanations of how geological strata formed is seems crazy that so many miles or rocks were laid down in one event and I also under stand that there are not enough rocks for uniformatism but how can they be formed by just one flood along with so many major mountain ranges i also know that slow mountian formation also doesn't work because all of them formed in the same geological eara ...and finally how can so much erosion happen. All at once in just one flood ...it seems like uniformatism and the bible fail on this one
Robert Carter
This is a little off topic as far as this article is concerned. It is also a huge subject. See our Geology Questions and Answers page.
Thomas R.
The wisdom of the Lord is beyond comprehension. Very nice. Thanks for the hard work, and for the endorsement of creation through scientific endeavors. It seems that genetic entropy is what kills people, but it also saves them in cases like this. Now, I wonder how H1N1 compares to COVID19 in this trajectory.
Robert Carter
I have spent many hours studying the genome of Covid-19 and have several thousand sequences in my database already. It is taking a similar path as H1N1 (both the mutation rate and the types of mutations occurring), but the virus has not been with us long enough for many mutations to accumulate, so we cannot say much yet. I did a similar study on Ebola, but with only 45 years of mutation accumulation, and with discontinuous genetics, it was also not possible to draw anything but general conclusions.
Dan M.
So you could say, Adam and Eves sin, was the primary extinction-level event, (dying you will surly die Gen 2:17) along with another that occurred later called the flood? That of course is what they, (Evo's) will not acknowledge even though the narrative fits the observations so well in all the fields of science. But the truth is in the eye of the beholder in this day and age. The evidence abounds that the genome was once pure in the beginning. So what is destroying it? The Evo's have no answer because the evidence flies in the face of the hypothesis of evolution and that is anathema, punishable by dismissal. This world is dying just like God said it would if they ate that fruit. Not because the fruit poisoned them, but because disobedience, (sin) did. Come, Lord, and restore this corrupt and dying world.
Abe M.
This totally flew over my head, naturally. Since discovering Creation.com in 2017, the subject of mutations written about here seems to me to be the 'silver bullet' (yes, I know from your other articles, there's no such thing) against 'evil'ution. Since 2017, I've been engaging Atheist's on this subject using your material, and they have no refutation for this, including the so-called high-intellectuals on the subject. I've found the more I study your articles about the same subjects, comparing them side by side, I am able to reach the understanding about the topics you write about, particularly mutations, genetics and genetic information. Keep doing what you're doing, and keep emphasizing the bottom line -- our need to recognize we have no atonement for our sins without the Savior of the world, Jesus Christ.

Thank you,

Martyn M.
"The H1N1 virus is not immune to the effects of genetic entropy and we see major strains either weakening or disappearing entirely over time." Why I wonder have not all viruses, good and bad disappeared?
Robert Carter
That is an excellent question. As far as the major zoonotic viruses that affect humans are concerned, the genetic evidence tells us that they are only a few hundred to a few thousand years old. In other words, they jumped to humans from another species within recent history, and there is no telling how many others that once affected us are already extinct. Viruses are in a delicate balance. Just one interruption of the infection cycle (near extinction of the host, herd immunity from spreading too fast, etc.) can wipe them out. But I suspect most viruses had, initially, a good and beneficial function in one species or another. These might be deliberately maintained by the host species and so would be expected to persist for a very long time.

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