Is Covid-19 evolving?

No, but it is changing rapidly



Many people have asked us if the mutations we are seeing in the SARS-CoV-2 virus is proof that it is evolving. This is a fair question and answering it allows us to explain the difference between mutation and evolution while putting the entire Covid-19 pandemic squarely into a creation context. We have dealt with similar matters in the past, but this new disease causes a new group of people to ask the same questions. Yet, it wasn’t true for swine flu, it wasn’t true for the peppered moth, it wasn’t true for Darwin’s finches, and it isn’t true for SARS-CoV-2. Why is it that the evolutionists continue to beat an old, outdated drum?

How much change do we expect to see?

In Michael Behe’s book The Edge of Evolution, he explains how much ‘evolution’ we can expect to see in any species. Given a specific genome size, a known mutation rate, and a certain population size, one can estimate the probability of any mutation happening during some window of time. One example he uses is the malaria parasite Plasmodium falciparum and how long it took to develop resistance to anti-malarial drugs. Many drugs did not last long before they were no longer useful. In each case, only one mutation was required to overcome the medicine. In the case of chloroquine, however, at least two mutations are needed. It can be estimated that only one in 1020 (100 quintillion) P. falciparum will have the necessary mutations and there would be about 1021 of these parasites in one billion infected people. Thus, resistance to chloroquine has appeared, but only rarely. This is within our expectations. The math tells us that such changes are possible.

Yet, for any specific change, there is always a waiting time problem.1 In a human-like population, any ‘evolutionary’ change that requires multiple mutations is not going to happen in any reasonable amount of time.2 However, for things like viruses, which have very high population sizes and very high mutation rates, if a specific change is possible, it should also be expected to occur. The waiting time in such cases can be quite low.

In other words, if a simple mutation will make a virus more infectious to humans, we should be looking for it. It will happen.

Is mutation the same thing as evolution?

The answer to this question is simple: NO!

DNA is a sensitive molecule. Water, oxygen, and radiation are constantly breaking it down. DNA can get overly twisted and literally snap in half. DNA copying enzymes constantly make mistakes. The cell uses all sorts of sophisticated DNA repair systems to continually scan and fix the errors that constantly pop up in this very sensitive of molecules. Yet, these systems are imperfect. Mutations are mistakes. Despite all the effort at fixing them, mutations still slip through the net. Being that the entire universe is under a ‘Curse’, mutations are expected to occur.3

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.

Not only that, but some mutations are much more likely than others. When we see how mutations accumulate over time, we see a specific directionality. In other words, change over time is predictable, which is not supposed to be true in evolution. The human H1N1 virus clearly shows how this works (figure 1). Given four letters in the viral RNA genome (A, C, G, and U), after 70 years in circulation, the number of As and Us consistently went up and the number of Gs and Cs went down.4

In one sense, these changes follow the laws of chemistry. For example, one of the most common chemical changes in DNA and RNA happens when water attacks a cytosine (C). This causes the loss of an amine (–NH2), which changes cytosine to uracil (figure 2). There are also RNA editing enzymes (e.g. APOBEC) that do this on purpose, perhaps to hasten the demise of a virus.5

Figure 2: Spontaneous deamination of cytosine (left) by water, converting it to uracil (right).

Mutations happen. This is a given fact. Species change. This is also a given fact. Yet, none of this explains the origin of life, the complexity of life, etc. In other words, ‘change over time’ is fully part of the creation model. While it is true that ‘change’ is necessary for evolution, simple change is not enough. They need enough change over enough time to explain the common ancestry of all life. Yet, there is no mechanism to produce the vast amount of new information required by evolution, including incredibly complex biochemical pathways, etc. This is why we are comfortable talking about ‘change’ in a creation context. Mutation is not the same thing as evolution.

Natural selection is not the solution

These viruses are at war with the human immune system. Only the ‘strongest’ survive and any virus that is not as robust as another is going to have a hard time getting past the immune system to infect another person. Even if it does make it to another person, if the virus does not replicate as fast as others, it will be left behind in the viral reproduction race. Thus, there is abundant natural selection happening here. But despite strong selection, mutations tend to build up in predictable ways and at predictable rates. If mutations cannot be checked, the entire system will eventually degrade. There are many ways to measure this. For example, we saw a loss of codon bias and a decline in expected replication efficiency in the human H1N1 virus over time.6

In the case of SARS-CoV-2, we can see similar patterns. If you tabulate all the mutations that have occurred in the viral genome since the pandemic first appeared, C→T mutations dominate (data not shown). The problem is that the virus has only been circulating for about 20 months, so the total number of mutations per virus is still quite low (about 25 single letter changes and an occasional small insertion or deletion). Yet, the number of viruses that have existed over this timeframe is truly vast. Essentially, every possible simple mutation has already occurred. Most mutations are lost due to random chance,7 but if any simple change could make the virus more infectious, it will tend to dominate among the viruses in circulation. Hence, the rise of the Delta variant (aka B.1.617.2).

New strains of Covid-19 are not proof of evolution

Through simple single-letter mutational changes, the Delta variant lineage has picked up 13 amino acid differences, four of them in the spike protein (figure 3).8 The “Delta plus” variant has an additional amino acid change in the spike protein. Delta is much more infectious than the original virus, people infected by it shed more viral particles, and younger people are being infected at a much higher rate. Due to enhanced infectivity, it is not surprising that Delta has become the dominant strain in many countries of the world. To date, the main vaccines are still protective against Delta, although not as effectively as they are against the original strain, and there is a very real possibility that some additional mutation could trigger a true breakthrough virus that does not interact with the antibodies that vaccinated and formerly infected people carry.9

Figure 3: Amino acid mutations of SARS-CoV-2 Delta variant plotted on a genome map of SARS-CoV-2 with a focus on Spike.

Changes like this are expected. This does not mean the virus is ‘evolving’. In fact, over time viral infectivity should wane. 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.

Many people are alarmed by the rise of new variants of SARS-CoV-2. Many others feel that this clinches evolution. They look at these adaptive changes and conclude that long-term evolution must be a done deal. They are not right. All of this fits the creation model. There is no ‘evolution’ to see here.

Published: 24 August 2021

References and notes

  1. Batten, D., The waiting time problem, Creation 43(3):15, 2021. Return to text.
  2. Sanford, J., Brewer, W., Smith, F., and Baumgardner, J., The waiting time problem in a model hominin population, Theoretical Biology and Medical Modelling 12:18, 2015; tbiomed.biomedcentral.com/articles/10.1186/s12976-015-0016-z. Return to text.
  3. Thus, if mutations are part of the creation model they cannot be seen as proof of evolution. See Carter, R., How to think (not what to think), Creation.com, 1 Nov 2016. Return to text.
  4. Carter, R.W., More evidence for the reality of genetic entropy, J. Creation 28(1):16–17, 2014. Return to text.
  5. Rice, A.M. et al. Evidence for strong mutation bias toward, and selection against, U content in SARS-CoV-2: implications for vaccine design. Mol Biol Evol 38(1):67–83, 2021. Return to text.
  6. 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. Biol. Med. Model. 9:42, 2012; tbiomed.com/content/9/1/42. Return to text.
  7. See Rupe, C.L. and Sanford, J.C., Using numerical simulation to better understand fixation rates, and establishment of a new principle: Haldane’s Ratchet; in: Horsetmeyer, M. (Ed.), Proceedings of the Seventh International Conference on Creationism, Creation Science Fellowship, Pittsburgh, PA, 2013; digitalcommons.cedarville.edu/icc_proceedings/vol7/iss1/32. Return to text.
  8. Stanford University Coronavirus Antiviral & Resistance Database, covdb.stanford.edu/page/mutation-viewer/#sec_delta, accessed 19 July 2021. Return to text.
  9. Katella, K., 5 things to know about the Delta variant, 15 July 2021; yalemedicine.org/news/5-things-to-know-delta-variant-covid. Return to text.

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