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Creation 36(4):52–55, October 2014

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Mistakes about mistakes



If two students hand in an assignment containing exactly the same mistakes, their teacher will rightly suspect that one (or both) has been copying the other’s work. This is because the chance of them independently making the same mistakes is very small. Similarly, when an identical mutation is found in the DNA of apes and humans, evolutionists claim that the only reasonable explanation is that the mutation occurred in a common ancestor and was then passed down to its descendants.

There are many parts of our DNA that look like virus DNA, and some evolutionists argue that this shows that these parts of our DNA came from viruses. Our ancestors, they say, were infected by viruses which added DNA to our ancestors’ DNA, and this was then passed down to us. These short stretches of genetic material are often referred to as ERVs (Endogenous RetroViruses; see box) and are said to be ‘junk’ having no useful purpose. Since we sometimes find the same ERVs in the same locations in the DNA of apes and humans, evolutionists claim that ERVs provide strong evidence for evolution. The probability, they say, of the same viruses randomly inserting the same stretches of DNA in the same locations in human and ape DNA is negligible. It is far more likely, they say, that a common ancestor passed on its ERVs to both humans and apes.

As convincing as it sounds, however, closer examination reveals serious flaws in this argument.

Are ERVs really junk?

Given the number of times that evolutionists have had to backtrack on their claim that our bodies are full of junk, one would think they would by now have learnt their lesson. For example, dozens of organs were wrongly labelled ‘vestigial’, said to be non-functional leftovers from our evolutionary past. Organs such as the appendix were said to have been used by our ancestors millions of years ago but, over the course of evolution, had become redundant. However, most if not all of these ‘vestigial organs’ now have known functions.1 Similarly, evolutionists claimed that much of our DNA has no function; but recent research indicates that this is nonsense.2 Significantly, functions of many ERVs have also been discovered, and they are known to interact with the rest of our DNA in a particularly sophisticated manner. For example, they enable the same stretches of DNA to be read and used in different ways. Research indicates they play an active role in at least one-fifth of our DNA.3

Did ERVs come from viruses?

When seeking to explain observations, good scientists must think laterally. We should therefore ask the question, “Did ERVs come from viruses or did these viruses actually come from ERVs?” How can evolutionists ‘know’ that ERVs came from viruses?

Since many ERVs have already been found to be functional, it is reasonable to think that they are there by design. The fact that we find the same ERVs in humans and apes is really no surprise. If humans and apes share the same creator and were made to live in the same world and to eat the same sort of food, it is hardly surprising that they were made with similar DNA (although the differences are much greater than evolutionists expected, which is a major problem for their story4).

As with all alleged evidence for evolution, the argument may appear convincing when first presented. However, when we scratch beneath the surface, a very different picture emerges—and one that is entirely consistent with a belief in biblical creation. As scientists make the effort to study ERVs, more of their functions are becoming known, indicating that they are not junk. Moreover, evidence is mounting that they play crucial roles (for example in embryonic development)5,6 and in controlling the way DNA works. The same ERVs are found in humans and apes because we share a common designer rather than a common ancestor.

More mistakes about mistakes

Sometimes genes appear to have become non-functional due to mutations, and are referred to as ‘pseudogenes’. Since we sometimes find the same mutations in the same ‘pseudogenes’ in humans and apes, it is argued that this must be due to humans and apes sharing a common ancestor. The probability, they say, of the same mutations occurring independently in humans and apes is just too small. Again, however, this argument—which evolutionists thought so conclusive—is losing its teeth.

Firstly, functions of ‘pseudogenes’ are being discovered, indicating that at least some are not ‘pseudogenes’ at all; perhaps few, if any, will turn out to be truly functionless. For example, they have been found to produce proteins, switch genes off when they’re not needed, and control the amounts of proteins that are to be made.7 Following a major research project studying human DNA (the ENCODE8 project), some geneticists have suggested that probably very little (if any) of our DNA is non-functional.9 This undermines both the ERV and the pseudogene arguments.

Secondly, geneticists now realise that mutations often do not occur randomly, and certain parts of DNA are more susceptible to mutation than others. These are known as ‘hotspots’. In some cases, it might be true that the same mutations occurred independently in humans and apes; but this is not surprising if they are at ‘hotspots’.10

It seems that as our knowledge of human DNA increases, the case for evolution gets weaker and weaker. It’s a theory that thrives on ignorance.


‘Shared mistakes’ would only provide evidence for evolution if they really were mistakes and if they had been shown conclusively to have occurred randomly. It is increasingly doubtful that DNA is littered with such mistakes, as has been suggested in the past, and geneticists now realise that it cannot be assumed that a particular mutation has occurred randomly.

Evolutionists very readily accept evidence for evolution without carefully considering alternative explanations for the data. Experience has shown that supposedly unanswerable arguments for evolution quickly fall as more facts become known.


What is a virus?

Viruses are tiny infectious agents that can reproduce only by hijacking the machinery inside the cells of the plant or animal they infect. Lacking a ribosome, for example, they are unable to manufacture proteins unaided. They also have no way of producing the essential energy unit, ATP, required to assemble proteins from amino acids.

What is a retrovirus?

Some viruses are made up from DNA and others from RNA. In the normal working of the cell, RNA for protein manufacture is produced from DNA. Many viruses which contain only RNA reverse this process and first produce a DNA copy of their RNA. These viruses are called ‘retroviruses’ (from the Latin word retro meaning ‘backwards’). The virus then implants this DNA into the infected cell and uses the cell’s machinery to reproduce itself.

What is an endogenous retrovirus (ERV)?

‘Endogenous retroviruses’ are said to be sequences of DNA, derived from retrovirus RNA, that have found their way into germ cells (sperm or eggs) and have thereby been passed down to the descendants of the infected organism. They are ‘endogenous’ because they are said to have become ‘endogenized’, i.e. integrated into the descendants’ genome (from the Greek words endo meaning ‘within’ and genous meaning ‘producing’). The term ‘endogenous retrovirus’, however, is unfortunate because it assumes a particular explanation for their origins. Creationist molecular biologist Ian Macreadie (Associate Professor at RMIT University, Melbourne, Australia) sees retroviruses as genetic material that escaped from cells, rather than the originators of ERVs.1,2

Are all viruses harmful?

Some bacteria and viruses are very beneficial and were likely created by God in the beginning. For example, bacteria are essential for decomposing organic matter, enabling old plant material to be recycled. They also help us digest our food. Viruses can increase plants’ tolerance to heat and drought,3 destroy cancer cells,4 and help keep soil fertile. Just as bees carry pollen from flower to flower, viruses can transfer genes between bacteria, enabling them to perform their many useful functions.5 Harmful versions of these bacteria and viruses are probably degenerate forms of originally benevolent designs that arose after sin entered the world (Genesis 3).

References and notes

  1. Wieland, C. and Batten, D., Creation in the research lab: An interview with leading Australian molecular biologist and microbiologist Ian Macreadie, Creation 21(2):16–17, March 1999; creation.com/macreadie.
  2. See also Borger, P., The design of life: part 3—an introduction to variation-inducing elements, J. Creation 23(1):99–106, April 2009; creation.com/vige-introduction.
  3. Roosink, M.J., Beneficial microbes for agriculture, The Samuel Roberts Noble Foundation, October 2008; noble.org/ag/research/microbes.
  4. Kim, M., Biological view of viruses: creation vs evolution, J. Creation 20(3):12–13, 2006; creation.com/bioviruses.
  5. Bergman, J., Did God make pathogenic viruses? J. Creation 13(1):115–125, April 1999; creation.com/viruses.
Posted on homepage: 14 March 2016

References and notes

  1. creation.com/vestigial-qa. Return to text
  2. Statham, D.R., More nails in the coffin of ‘junk DNA’; creation.com/junk-dna-functions. Return to text
  3. Doyle, S., Large scale function of ‘endogenous retroviruses’, J. Creation 22(3):16, December 2008; creation.com/functions-erv. Return to text
  4. Batten, D., The myth of 1%, Creation 36(1):35–37, January 2014. Return to text
  5. Mallet, F. et al.,The endogenous retroviral locus ERVWE1 is a bona fide gene involved in hominoid placental physiology, PNAS 101(6):1731–1736, 2004; pbil.univ-lyon1.fr/members/duret/publications/PDF/2004-Mallet-PNAS.pdf. Return to text
  6. National Centre for Biotechnology Information, ERVW-1 endogenous retrovirus group W, member 1 [Homo sapiens (human)]; ncbi.nlm.nih.gov. Return to text
  7. Wells, J., The Myth of Junk DNA, pp. 91–92, Discovery Institute Press, Seattle, 2011. Return to text
  8. ENCODE stands for Encyclopedia of DNA Elements. Return to text
  9. Batten, D., Dazzling DNA, Creation 35(1):38, 2013; creation.com/dazzling-dna. Return to text
  10. Truman, R., and Borger, P., Why the shared mutations in the hominidae exon X gulo pseudogene are not evidence for common descent, J. Creation 21(3):118–127, 2007; creation.com/gulo. Return to text

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