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Journal of Creation 28(1):16–17, April 2014

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More evidence for the reality of genetic entropy


Figure 1. Mutation accumulation in human H1N1. The published Brevig Mission strain from 1918 was used as the baseline (bold line) for comparison with all available human-infecting H1N1 genomes. There are two distinct trend lines in the data. The 2009–2010 outbreak samples and additional samples from 2011–2012 are circled. These and the scattered points are all derived from swine H1N1 versions. The remaining points represent mutation accumulation in the ‘human’ version of H1N1: from 1918 to its initial extinction in 1957, a break of 19 years, its re-introduction in 1976 (of a strain from approximately 1955, after which the mutation count picks up where it left off), and asecond disappearance in 2009.

My colleague John Sanford and I have recently published a paper in a secular journal with what we believe are profound implications.1 Our basic claim is that ‘genetic entropy’ works in the real world, which brings questions about the role of natural selection and the long-term survival of species into the future.

A new look at an old virus

The paper analyzed mutation accumulation in the human H1N1 influenza genome using over 95 years’ worth of genetic sequences (figure 1). This type of data is a rarity in the world of genetics, since most sequence data are from recent organisms with long generation times. The influenza virus, however, has been isolated and sequenced from human tissue samples all the way back to 1918. With a human-to-human transmission on average every three days or so, this makes over 11,000 disease generations and many times more than that number of viral generations. The number of viral generations is possibly comparable to the number of generations since the supposed human-chimpanzee split.

Photo: Wikipedia/Cybercobra influenza-virus
Figure 2. Electron micrograph of H1N1 influenza virus that caused the 2009–2010 ‘swine’ flu outbreak.

We provided data that more than suggests that the various influenza viruses that infect humans cannot survive long term, and we were the first to notice the disappearance of the human version of the H1N1 influenza virus in mid-2009. We closed our arguments by suggesting government agencies are barking up the wrong tree in their quest to detect newly evolving strains. Instead, scientists should be focusing their efforts to understand the appearance of new viruses, because once a virus makes a cross-species jump it burns fast and hot and eventually burns out. It is the new versions that are the greatest threat, not the old, worn-out ones. We discussed the 2009-2010 ‘swine’ flu outbreak, noting that it was far less serious than expected, and that this was probably due to the fact that the virus (figure 2) had picked up thousands of mutations and was much less robust compared to the original H1N1 ancestral virus that entered the swine population about the same time the human version appeared.

Implications of the study

There are additional implications to our work, although most of these were not explicitly stated in the text.

First, this is apparently the first experiment designed to test the Darwinian mutation/selection model in any species over tens of thousands of generations. All other experiments (even Lenski2) used many fewer generations, or assumed common ancestry (e.g. anything written about the evolution of humans and chimpanzees from a common ancestor) without actually testing it.

Figure 3. Relative percentage changes in the four nucleotides in the human H1N1 virus from 1918 to 2009. Years are adjusted for the reintroduction of a strain from approximately 1955 in 1976, giving a total sampling period of 70 years. The break in the data around year 55 does not represent the 1957 extinction but missing data from 1990–1994.

Second, despite pervasive and demonstrable natural selection among these viruses, the 1918 version of the human H1N1 virus went extinct, twice, at the appearance of a competing strain, apparently due to a lack of robustness caused by mutation accumulation. The first time was in 1957 when a competing serotype appeared. After an accidental reintroduction of human H1N1 in 1976, the second extinction occurred when a recombined version of the swine H1N1 appeared in humans, and after more than 10% of the human H1N1 genome had ‘rusted away’.

Third, accumulating mutations are not silent, even those that do not affect the amino acid chain of a protein, because codon usage influences translation efficiency. Circulating levels of the many transfer RNAs are proportional to the frequency of their corresponding codons. Thus, changing from common to rare codons is expected to decrease the speed of translation.3 Unchecked mutation accumulation leads to a breakdown in codon bias, potentially affecting translation efficiency in the host cell.

Lastly, since the various mutations accumulated in a linear fashion, those mutations that escaped the selective filter (that would be most of the mutations) apparently accumulated according to the laws of chemistry. Thus, genetic change is overwhelmingly a product of thermodynamics (figure 3), not selection. Over time there was, approximately, a 1% net increase in A, a 0.5% net increase in U (H1N1 is an RNA virus), a 0.5% net loss of C, and a 1% net loss of G.

Natural selection had a minimal effect on mutational direction. Does this mean the direction of ‘evolutionary’ change is predetermined? If so, and if the common ancestor of things like humans and chimpanzees is not ‘on the curve’, they should not have a common ancestor. This would be a very interesting line of study.

Creationists and original research

The reader should note that the editor of the host journal permanently flagged the paper “Highly Accessed” while the provisional paper was still up on their website. Clearly, many in the influenza research community downloaded the paper. So, who says creationists never do original research and who says they never publish in peer-reviewed journals?

References and notes

  1. Carter, R. and Sanford J.C., A new look at an old virus: patterns of mutation accumulation in the human H1N1 influenza virus since 1918, Theor. BiolMed. Model 9:42, 2012 | doi:10.1186/1742-4682-9-42; tbiomed.com/content/9/1/42. Return to text.
  2. Blount, Z.D., Borland, C.Z. and Lenski, R.E., Historical contingency and the evolution of a key innovation in an experimental population of Escherichia coli, PNAS 105(23):7899-7906, 2008 | doi:10.1073/pnas.0803151105. See also Batten, D., Bacteria ‘evolving in the lab’?, ‘A poke in the eye for anti-evolutionists’?, 2008; creation.com/citrate. Return to text.
  3. Xia, X., Maximizing translation efficiency causes codon usage bias, Genetics 144:1309-1320, 1996. Return to text.

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Readers’ comments

Ben C.
Drs. Carter and Sanford, I have wondered for some time now about the degradation of DNA after death. It somehow strikes me as odd that we think we can know the DNA of, say, a specific Neanderthal body, after the guy (or gal) has been dead for a few thousand years at least well enough to do comps to modern man. Does DNA really degrade that slowly post-mortem? As it relates to this study, was it the G and C that was decreasing about the same rate as A and U were increasing? As DNA degerades, do these molecules break down completely so that they aren't read at all or can the results be "muddied" with some degrading and being read as others? Thanks so much for yall's fantastic work!
Robert Carter
DNA does not degrade slowly, but it does follow certain rules. Our chromosomes are up to 250 million nucleotides in length, but the Neanderthal genome (at least the first one sequenced) had broken down into pieces 50 nucleotides or less in length. The only way they could 'sequence' it was to compare the various pieces to the complete human genome and even then they could only recreate about 60% of it. One thing they have to take into account is the fact that the nucleotides on the end of a fragment are more likely to react chemically (and thus throw off the sequencing machines, causing false readings). Thus they could use only the central parts of each fragment.

See creation.com/dinosaur-soft-tissue for more discussion of DNA decay rates.
Johan V.
I have a 'side question' concerning the article. In the article it is stated that:

“… influenza viruses that infect humans cannot survive long term…”

As far as I know, viruses just contain ‘code’ which ‘mechanically’ infects a living cell like the injection of a syringe injecting a toxin. Of course in this case the toxin is a chemical molecule known as DNA which is very efficient as it may ‘reprogram’ a living cell in making more ‘toxins’ being the viruses which are released to intoxicate other cells.

Point is, I concluded that viruses are not living species as they have no metabolic activity nor are they capable of reproduction. So viruses do not ‘survive’ they just degrade like in a corrosion process.

Funny enough, the degradation of organic material may be identified as ‘corrosion’ because the chemical (redox) laws governing the decay of metals may just as well apply to organic materials or for that matter also living tissue (aging). Corrosion is still a (very) strong argument against evolution.

Could it be that many people still refer to viruses as ‘living’ as a remainder from the evolution theory in the seventies where at that time (some) scientists were convinced that viruses represented a lower stage proving the missing link of life somewhere between dead matter en living cells, which of course was wrong and is now also rebuked by evolutionary scientists.
Robert Carter
I also do not believe viruses are alive. I used the term in a more colloquial sense. Had I said something like "That satellite can only survive for about 5 minutes upon atmospheric re-entry" nobody would have misunderstood my meaning, but your point is well taken.
sebastián F.
Hello :)
I am myself an agnostic creationist (believes in creation but is not certain) My belief in God remains. Just wanted to ask.. as I am a bit confused. There are many refutations of the genetic entropy as there are many refutations of those refutations. Probably people just take as evidence what supports their views. So I would say it's uncertain whether we evolved or not. Also this is not my field so i can't determine one point of view as correct. Still, these articles are great, At least they offer an alternate explanation to origins rather than evolution alone. so my question is.. as we all have the same evidence but we interpret it differently and take as logical only what supports out position , does that mean many times its about an emotional issue (for both evolutionists and creationists) rather than actual evidence?
Thank you in advance. God bless.
Robert Carter
Sebastian, these are great questions, and you are not the first to ask them.

Regarding genetic entropy, there actually have not been many attempts at a refutation. See here for one example of a skillful defense against a less-than-informed opponent (which is typical for this subject).

Regarding people ignoring evidence that does not fit their side, sadly this is part of human nature. However, if you read our materials carefully you will see that we try hard to incorporate the views of others in our analyses. In the case of GE specifically, I feel that it is the other side that has yet to come to grips with our evidence. After all, most of the scientists at CMI were once evolutionists and all of us were trained in the secular system with the best evidence evolutionists had to offer. We came to our conclusions after weighing the evidence for both sides.

Yes, absolutely this is an emotional issue! In fact, the question of origins is deep-seated in the human psyche. See here for starters.
Joe B.
I find that the most important and telling conclusion is that "genetic change is overwhelmingly a product of thermodynamics". That - thermodynamics is the prime enemy of evolution - is a message I have tried to communicate for years, only to be bashed as a fool. It's amazing how we ignore basic empirical scientifically validated phenomenon for the sake of our worldview. Keep up the good work and maybe we can get the truth out to the masses before the Lord returns.
Joe C.
Dr. Carter, how do you think the H1N1 virus has survived in waterfowl (or another host) for thousands of years? I find the ERV-first model promoted by Peer Terborg to be interesting, but H1N1 is not a retrovirus.
Robert Carter
I am not certain. It may be that influenza has a more recent origin (ala Terborg), or it may be that the virus replicates much more slowly in its natural host, thus escaping or at least postponing the ravages of genetic entropy. When we consider that there are ~100 viral particles for every bacterium in our gut and that the viruses play a key role in maintaining the species composition and number of bacteria among the intestinal flora, we must realize that most viruses are beneficial. It is when they jump to a new host, one which cannot control the virus, that they burn hot and fast and eventually burn out.
Robert B.
When I heard of the diffuse causes asserted for Honeybee Colony Collapse Disorder, I was reminded of Dr. Sanford's description of the decline in "genetic fitness" that he predicted will occur in every organism as a result of the inevitable accumulation of mutations over time.

The different problems found to be affecting bees are low levels of pesticides in the environment, bees failing to houseclean adequately to eliminate parasites, and viruses which all seem to contribute to the changes in foraging behavior associated with CCD.

Beekeeper practices of inbreeding bees and cloning colonies may be accelerating the process of decline by minimizing hybrid vigor.

I hope I'm wrong. I miss the bees.

I suspect that worldwide, there is an inventory of bee carcasses from the last 200 years or so in the Natural History Departments of the older universities. While that isn't 11,000 generations worth, it is a lot. Investigating the accumulation of mutations in bees over time might help provide some sought after answers. Perhaps someone will follow in your footsteps.

Kudos to Drs. Carter and Sanford for the groundbreaking work!
Rolando R.
Genetic entropy makes perfect sense. Again, it all comes down again to the fact that any theory that violates thermodynamics laws is doomed from the start. In this case the mechanism of natural selection is not denied, but only that is not capable of detecting the "rust" accumulated over time and weed it out. The obvious question: is the evolution "establishment" addressing this important research area? It seems like it is not, confirming once again the bias of a self-contradicting science that makes all its research assuming its central idea of common descent is true by definition. Is that science?
King T.
Thank you for bringing this news and congratulations with the publication.

I believe that genetic entropy is one of the more powerful arguments against the story of Darwinian evolution. With the publication of this paper it will be so much more effective at making evolution-believers think twice since they'll have something concrete to consult without having to refer to the creationist websites that they despise so much.

Please keep up the good work!

Nick K.
I found this article really interesting, and also the published paper that it relates to. Out of interest, do the authors have any thoughts regarding how the original virus came to be 120 years ago - or any hypothesis regarding what a "natural reservoir for a non-attenuated strains" might be?
Robert Carter
The reservoir and source is most likely within wild waterfowl. All strains of influenza circulate within them, to the point where natural waters frequented by ducks, etc. have high concentrations of influenza virus particles within them. But influenza also rarely causes disease in waterfowl. Thus, we have a 'natural reservoir' and plenty of opportunity for the virus to leave its first state and jump to pigs and humans (especially considering certain places in the world where ducks and pigs are intensively farmed in close proximity to one another).

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