Lessons from the pandemic: A new look at an new virus: patterns of mutation accumulation in SARS-CoV-2 since 2019

In 2005 a landmark paper was published, Characterization of the Reconstructed 1918 Spanish Influenza Pandemic Virus, with authors including virologists Terrence Tumpey and Jeffery K. Taubenberger. It was notable in that it was the result of dogged sleuthing which at last provided enough long sought viral genome to sequence the 1918 influenza.

Genomic RNA of the 1918 virus was recovered from archived formalin-fixed lung autopsy materials and from frozen, unfixed lung tissues from an Alaskan influenza victim who was buried in permafrost in November of 1918. The complete coding sequences of all eight viral RNA segments have now been determined, and analysis of these sequences has provided insights into the nature and origin of this pathogen.

Without samples from that one permafrost frozen victim, and a few pathology slides, we would have nothing at all. In contrast, the GISAID Covid database has a staggering eleven million genome sequence submissions. Nothing in history comes remotely close to this genetic scrutiny of evolution in real time. While the Sanford Carter influenza paper promoting Genetic Entropy was incoherent and rife with error, the pandemic has made a further mockery of those ideas. As covid has come up in a few threads recently, I thought it may be time to dedicate a topic to have the forum explore the implications of lessons learned to GE and ID. To prime this:

One - extinction is not due to Genetic Entropy.

Carter Sanford on H1N1: A new look at an old virus: patterns of mutation accumulation in the human H1N1 influenza virus since 1918

These extinctions appear to be due to a continuous accumulation of mutations.

Clades do not just fade away and go extinct due to Genetic Entropy; they are squeezed out by successive mutant strains which are more adapted to circumvent rising host immunity. The essence of GE is that downstream generations will suffer the relentless accumulation of slightly deleterious mutations resulting in fitness decline and ultimate extinction. SARS-CoV-2 has progressed as a clear counter-example, in that existing strains have been successively out-competed by their more fit descendents. This was true of H1N1 influenza as well, but given influenza’s multi stranded mix and match propensity to frequent recombination, GE proponents pitched the appeal that fitness was refreshed from contributions from natural reservoirs. SARS-CoV-2 recombination has been between circulating strains.

Generally, the virus has trended from high infectivity to unprecedented infectivity, so in that respect the gain in fitness has been both relative and absolute. Eventually, caseloads and severity will drop off, and we may be seeing some of that, but that will be due to the build in herd resistance and the viral response to host adaptation, and not any accumulation of mutation.


It’s 24th of May 2022, roughly 2 years have passed since the Covid pandemic first broke. SARS-Cov2 still exists and has not gone extinct to genetic entropy. It won’t.

I think we should start commemorating the continuing circulation and evolution of SARS-Cov2 -not that we like the fact that it exists and isn’t going away - but it’s ongoing falsification of Genetic Entropy.

What do you say, should we meet here again once a month? Every 3 or 6 months?

I’m sure GE proponents would have various kinds of misleading things to say about why GE “is in the process of occurring it just hasn’t happened yet, just wait and keep believing it will”. But you have to wonder how long they can keep that going before it starts to become an embarassment to them. I suppose since they refuse to give a timeline to extinction, they can always just keep pretending in 5, 10, and even 50 years from now that it’s continued existence still isn’t an embarassment to GE and we just have to have faith.

It’s simple. Ask them when. If they can’t tell, it’s not a falsifiable theory.


When have they refused or written about SARS-CoV-2?

I made a post awhile back about possible recombination with previously circulating coronaviruses. Has that been ruled out?

Coronaviruses have to be constantly replicating in order to exist. Coronoviruses don’t just hang out for decades outside of the host waiting to infect a new person as they walk by. Therefore, recombination isn’t a solution for the genetic entropy claim. Any recombination event will be between two strains of coronavirus that have suffered the same amount of genetic entropy, according to the genetic entropy model.

If you do think recombination cures genetic entropy, then sexually reproducing species should not suffer genetic entropy because every generation is the product of recombination.


I don’t really follow creationism that closely (I usually get news about it indirectly through websites such as this) so I’d definitely be interested to hear if they have advanced any predictions for when this RNA virus should go extinct to GE. Are you aware of any such writings?

Why would it need to? Suppose it has recombined with other circulating coronaviruses(that also haven’t gone extinct yet for some reason), does that somehow mean GE isn’t happening and SARS-Cov2 won’t go extinct?

Timely question. I may have to update my earlier statement. I missed this recent preprint which has been picked up in the popular media which suggests that omicron had incorporated sequences from other viral or human genome Omicron variant of SARS-CoV-2 harbors a unique insertion mutation of putative viral or human genomic origin

Whereas the substitution and deletion mutations have appeared in previous SARS-CoV-2 lineages, the insertion mutation (ins214EPE) has not been previously observed in any SARS-CoV-2 lineage other than Omicron. The nucleotide sequence encoding for ins214EPE could have been acquired by template switching involving the genomes of other viruses that infect the same host cells as SARS-CoV-2 or the human transcriptome of host cells infected with SARS-CoV-2 from host genome.

So if the ins214EPE sequence is indeed acquired, it would be interesting to ascertain the source. In any event, there is no support for the concept of a circulating strain being reinvigorated by recombination with unattenuated reservoir genome. Once spillover occurs, viruses are assisted by adaptations which optimize for fitness in people rather than fitness in their prior wild hosts. There may be more concern with the progression of reservoir → people → pets and agribusiness → people, because the spillback round trip would drive more variation with potential threat. That is the opposite of GE, where Sanford Carter actually advocate accelerating variation as a means to fight epidemics.

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I don’t follow it that closely either. But that’s why I responded. Your wording insinuated that there has been a dialogue of some kind, which I was doubtful had occured or it would already have been discussed. But since you asked, I went looking. This seems to be the only blog post related to this virus and entropy. Is Covid-19 evolving? - creation.com There isn’t a specific prediction, except - not soon.

I don’t know why anyone thinks Sanford and Carter think it should be soon. If they did, they’re not reading them carefully at all…

From that blog post:

Figure 1 . 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. From Carter (2014). Similar changes will be occurring in SARS-CoV-2 genome, but over a long time period.

As each viral strain in circulation picks up more and more mutations, it should become less and less robust. This is the essence of genetic entropy and we saw it happen within the human H1N1 virus. Yet, the process took decades in H1N1 and SARS-CoV-2 has only been around for a short time. Will genetic entropy degrade the virus? Yes. Will it happen this year? No. And, while it is degrading, it might also pick up a mutation that makes it spread faster or one that makes it more deadly.

Huh? Please cite that.

I didn’t think it was; just my understanding was that it would slow entropy.

The insertion would also need to be degraded by VSDMs, so that slows entropy.

Interestingly I posted about molnupiravir in the forum before because I was interested in mutational meltdown as a pharmaceutical option, how well it worked, and how that related to GE generally. I thought about posting about it again later when I noticed how many scare articles there were in popular media about it introducing new variants. That made me think we really don’t know how evolution/mutation works. We should know whether new variants are a concern or not a concern. These definitely are polar opposite views of what mutation can do. (Btw, I don’t care about the distinction Carter makes with the word evolution. To me, it’s all evolution whether up or down or backward or forward or neutral. :joy: It’s just understood or misunderstood evolution.)

Five years from now, we’ll know much more about viral evolution from SARS-CoV-2. Let’s revisit GE then after we see what happens. :slightly_smiling_face:

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That is execrable. It includes almost every deceptive creationist trope. Shouldn’t real theories make real empirical predictions?

I think that they should be making predictions. That’s what real scientists do.

How is that relevant to anything, in your mind?

No, we did not, as the H1N1 subtype (not a virus, not a strain) is still killing people today. They are playing immoral word games–people can and do die because they don’t understand this.

In the former case, its fitness is increasing. That’s evolution.

There’s nothing in the model to suggest that recombination helps anything.

No one’s shown any entropy to be slowed. You’re just making that up.

Your equivocation between them with the slash indicates that you don’t.


Progress! So why do you treat Carter as some sort of expert when you can see through his rhetorical sleight-of-hand?


We will not require such patience; there is plenty enough information now to discredit GE.

In an article Fitness and ‘Reductive Evolution’”, @PDPrice and Robert Carter reference the Carter Sanford influenza paper and write:

While there has been no peer-reviewed, scientific attempt to attack the validity of this paper to date (and in fact it has been cited several times by other scientists in the field), some online skeptics wish to throw stones at the paper and debate its accuracy.

According to Pubmed, this paper has been cited a total of eight times, one by another Sanford paper. That it is about as low in influence as you get. Contrast that with the paper, first published in January of 2020. Hold onto that date.

Wan et al; Receptor Recognition by the Novel Coronavirus from Wuhan: an Analysis Based on Decade-Long Structural Studies of SARS Coronavirus

which sits currently at 1,993 citations listed by Pubmed. So why the difference?

It may be that more than 99% of scientists readily discern that the Carter Sanford paper has no merit or heuristic value. In contrast the Wan paper pointed the way to understanding and progress, and unlike the vague carnival fortune telling of Carter Sanford, actually contained a highly specific prediction. Based on actual study of the prior SARS and MERS outbreaks, and affinity of the viral spike for human ACE2 receptors, Wan writes [ Bold mine ]

several other critical residues in 2019-nCoV RBM (particularly Asn501) are compatible with, but not ideal for, binding human ACE2, suggesting that 2019-nCoV has acquired some capacity for human-to-human transmission.

Asn501 in 2019-nCoV RBD provides more support to hot spot 353 than Ser487 but less than Thr487. This analysis suggests that 2019-nCoV recognizes human ACE2 less efficiently than human SARS-CoV (year 2002) but more efficiently than human SARS-CoV (year 2003).

Because ACE2-binding affinity has been shown to be one of the most important determinants of SARS-CoV infectivity, 2019-nCoV has evolved the capability to infect humans and some capability to transmit among humans.

Alarmingly, our data predict that a single N501T mutation (corresponding to the S487T mutation in SARS-CoV) may significantly enhance the binding affinity between 2019-nCoV RBD and human ACE2. Thus, 2019-nCoV evolution in patients should be closely monitored for the emergence of novel mutations at the 501 position.

Half a year later in early fall, the first cases of B.1.1.7 alpha variant were coming to light in the UK. By winter B.1.361 beta emerged in South Africa and P.1 gamma in Brazil. What all these variants held in common was the definitive mutation N501Y, a substitution which was to challenge the world. Out of ten thousand codons, Wan’s team identified a critical one to watch. If that is not recognized as a fulfilled prediction based on an evolutionary understanding of the molecular biology of virus and host, we are done talking. It would have been perfect, but for the preferred amino acid turning out to be tyrosine instead of threonine.

Seconded, because a successful prediction is evidence for the general principle offered as an explanation, in this case evolutionary positive selection of variation given a novel host.

GE proponents predict that eventually covid will lose virulence, except when it doesn’t. Thanks for nothing. They may as well predict that the stock market will go up and down. The standard evolutionary arms race understanding of epidemiology also predicts that as herd immunity develops and the pool of susceptible population shrinks, the pandemic will abate. GE has nothing to say about adaptation of the virus to the host. Nor does GE address adaptation to the virus by the host population, which GE relegates to a passive sideshow as the virus supposedly withers on its own accord. Another lesson from the pandemic: GE makes no useful or differentiating predictions.


It’s a basic fact. Any recombination event between two strains of a virus will necessarily involve two strains that have both been accumulating mutations. If accumulating mutations means the viruses are becoming less fit then the recombination event will not fix it.

How would recombination slow genetic entropy?


How would recombination slow what doesn’t exist?

It’s weird since GE proponents would say that GE is happening in all organisms and viruses, including in those previously circulating coronaviruses (or are they somehow immune?). If so, then how would recombination with viruses that are also experiencing GE help prevent GE?

And if it does, isn’t that also an admission that genetic recombination is able to prevent genetic entropy, while proponents commonly argue that GE is inevitable (without the intervention of some nebulous “intelligence”).


In his H1N1 paper Carter Sanford write:

Our findings suggest that new strategies that accelerate natural genetic attenuation of RNA viruses may prove useful for managing future pandemics

Sanford later collaborated with Smith, both horticulturalists, and computer scientist Brewer, to develop this idea, missed by virologists everywhere, in the follow up Information Loss: Potential for Accelerating Natural Genetic Attenuation of RNA viruses, which states:

while lethal mutagenesis holds promise for treating individuals, a much more significant application may be on the epidemiological level.

So to address Valerie’s post:

There has been intense investigation of mutagenic pharmaceuticals. Even for individual treatment of covid, drugs such as favipiravir, ribavirin, and molnupiravir have presented contested results and guidance remains tentative. On the risk side, there are obvious concerns with administering a mutagenic drug to people who are not yet seriously ill to the point of hospitalization. But even if inducing viral error catastrophe worked with an individual patient, the idea of accelerating viral attenuation among circulating strains is another matter entirely.

Carter, Sanford, and Brewer are so narrowly fixated on virulence as a proxy for fitness decline that they just blank out the vital roles of transmission and herd immunity. How are you supposed to transmit attenuated viral strains? Take patients treated with mutagenics and, like germ warfare of days of old, catapult them into the general population? Gift away their hospital blankets? Droves of gimped up viruses are produced naturally all the time. They fail to register because they are outcompeted by circulating strains that have their act together in respect to infectivity. It is self-evident that without transmission, there can be no degree of virulence; and without community transmission, genetic attenuation goes nowhere.

Hype in popsci articles? Difinitely. But we should not be cavalier either; oops is a bad word in medicine and public health. From another paper in Brewer’s references, Theory of Lethal Mutagenesis for Viruses:

Beneficial mutations invariably exist. … First, some genuine beneficial mutations may increase the intrinsic replicatory ability of the virus … Second, mutations can confer partial or complete resistance to the mutagen.

Beneficial mutations may be exceptional, but highly selected. This opinion piece in Forbes is specifically concerned that molnupiravir could turn patients into supercharged variant factories. Due diligence must be at least considered. Brewer ignores and excludes positive mutations such as actually appeared in covid. Their flippancy has the makings of the opening act of a zombie origin movie. From the Brewer paper:

we shape the mutation distribution such that there is a very substantial fraction of all mutations that have a large effect on fitness (10% of the deleterious mutations reduce fitness by 10% or more). We model beneficial mutations to have a similar distribution as deleterious mutations, but with a much narrower range (maximal fitness effect = 0.01). This upper limit excludes major virulence factor mutations, which are outside the scope of these experiments (we wish to study overall fitness, not singular host/pathogen compatibility factors).

So essentially, they loaded the dice. And excuse me, how are host/pathogen compatibility factors not the core overall fitness determinant?

The third problem faced is that circulating viral strains which have been exposed to a given treatment tend to develop resistance. This can render treatment of an individual ineffective, and if transmitted can establish a resistant strain, which has already been found to occur for monoclonal antibody treatment of covid. Brewer takes no account of such beneficial mutations, but in their own references we find:

Sanjuan - Selection for Robustness in Mutagenized RNA Viruses, from the abstract:

The faster replicator outgrew its robust counterpart in standard competition assays, but the outcome was reversed in the presence of chemical mutagens. These results show that selection can directly favor mutational robustness and reveal a novel viral resistance mechanism against treatment by lethal mutagenesis.

It has been said that all models are wrong, but some are useful. Brewer’s model is both wrong and worse than useless. This paper was published in a creationist symposium, and is not intended as a serious contribution to epidemiology, but is a world building prop to Genetic Entropy.


How on Earth do they get that? Are they proposing that viruses are designed for virulence?

That would certainly raise problems of theodicy, as a malicious creation is implied. Carter and @PDPrice discuss the origin of viruses in the aforementioned CNI article Fitness and ‘Reductive Evolution’.

But what about pathogenic viruses? These are the product of the Fall. Once sin and death came into the world—once corruption was the rule—it may have been only a simple step for an originally-designed beneficial virus to change.

So who needs biology when you have your systematic theology? Beneficial viruses changed to pathogenic? The word they are looking for is evolved.

the influenza virus does not usually cause disease in their host species. However, when it jumps to pigs and people, it burns like wildfire because we do not have the natural regulatory mechanisms that aquatic waterfowl apparently do.

Influenza is not regulated in waterfowl, ducks have adapted over their long association. The defense and immune system attempt to clear the virus. Even though disease is generally asymptomatic, there is no benefit to the host, and infected birds may exhibit lower weight. Species jumps generally progress mutations to optimize for differences in cell receptors, codon bias, and transmission between hosts. The virus circulating in new species almost never remains genetically the same as the prior.

flu strains sometimes arise that are very, very bad for birds. But this might be akin to cancer: a loss of control of cellular reproduction leads to tumor growth.

Highly pathogenic avian influenza is not about loss of control of cellular reproduction; that is indefensibly misleading. HPAI is about variation and mutation.

In the same way, many pathogenic viruses may have arisen through loss of control. They do not need to “evolve”. The system for which they were designed just needs to break.

What an idiodic statement. Price and Carter do not care enough to even speculate what any given pathogenic virus may have originally been designed for, or what system might have broken. It is just wild fantasy to support their theology of a perfect creation and fall. Pathogenic viruses evolve constantly, sometimes in the direction of less virulence, other times more. That much is data, not interpretation.

So even though GE considers virulence to reflect possession of undegraded genetic information resulting in the unrestrained ability to infect and replicate, they simultaneous hold that the same pathogenic viruses were benevolent when created. There is no evidence or even proposed functionality for that benevolence, and no specific suggestions as to how viruses can go from benign to virulent without evolving. As regards viruses, GE is internally incoherent before actual data is even considered.


Yup. It is mind-boggling that they chose a virus to make their incoherent case.

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That is not even coherent,

If virulence is a consequence of the virus changing it seems odd indeed to use decreases in virulence as a measure of “entropy”.

The idea that it is purely the result of the hosts changing makes it worse - surely genetic entropy should produce increasing virulence as the host becomes less able to cope with the virus.

The silly thing is that they never had to tie decreasing virulence to genetic entropy. They chose to do that. Even though it doesn’t really make sense.


Hmm yeah I can see that doesn’t make any logical sense considering that they think viruses were originally beneficial and had some sort of important biological function/purpose.

They think Genetic Entropy degrades fitness (by which they really mean functionality or “integrity of information in the genome”).
They think virulence is a proxy for fitness - that is it must be a proxy for functionality or “integrity of information in the genome”.
They think viruses were originally not virulent at all. They did not cause disease.
They think Genetic Entropy happened due to the fall, and that GE made viruses become massively virulent (massively functional - have extremely high “integrity of information in the genome”).


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The tolerance for cognitive dissonance is amazing. Within a breath of writing about how pathogenic viruses originally held beneficial functions, we read this in Price Carter:

in humans the influenza virus is a parasitic machine with one and only one function: making replicas of themselves using the hijacked equipment of their host’s cells.

What cognitive dissonance?

It all makes sense to creationists, because it fits their way of thinking.