A Critique of 'Human Endogenous Retroviruses (HERVs) - Evolutionary “Junk” or God’s Tools?'


A Critique of 'Human Endogenous Retroviruses (HERVs) - Evolutionary “Junk” or God’s Tools?'
The following is a critique of a page from a website called Answers in Genesis, Human Endogenous Retroviruses (HERVs) - Evolutionary "Junk" or God's Tools? by Dr. Georgia Purdom. The text of the page is indented and in green.
  • Human Endogenous Retroiruses (HERVs) - Evolutionary "Junk" or God's Tools?

  • Let’s begin by understanding what a retrovirus is. Most people are familiar with the human immunodeficiency virus (HIV), which causes acquired immunodeficiency syndrome (AIDS). HIV is an exogenous retrovirus, meaning that it originated outside the organism’s body. This type of virus has an interesting life cycle that allows it to incorporate itself into the genetic material of the host it infects. Unlike our genome, which is composed of DNA, the retroviral genome is composed of RNA. Once the retrovirus enters a host cell, its RNA genome is made into DNA (through an enzyme the retrovirus carries) and the DNA is integrated into the host genome—becoming a type of endogenous retrovirus, meaning that it is now a part of the genome in that cell. In the case of HIV, it can remain “quiet” for many years and, for unknown reasons, suddenly begin using the cell as a virus factory to make many copies of infectious HIV. These subsequently infect other cells—specifically, a type of immune system cell, which is destroyed and lowers the ability of the immune system to fight disease.

Well, it's a bit misleading to call the integrated retroviral DNA an "endogenous retrovirus". Provirus is the normal term for it, whereas "endogenous retrovirus" is the name for a proviral-like structure which is to be found in exactly the same place in the DNA of every nuclear cell of an organism. Proviruses result from infection by exogenous retroviruses. Endogenous retroviruses are inherited.

And by the way, it is not for "unknown reasons" that HIV proviruses become activated. Just google "HIV provirus activation".
  • Many families of endogenous retroviruses exist throughout the human genome (forming as much as 8% of the genome), as well as throughout the genomes of most other living organisms. Unlike HIV, these “ancient” retroviruses purportedly integrated themselves into the genome long ago and have since accumulated mutations that have rendered them unable to produce infectious, exogenous viruses. In the past, they may have been a type of transposable element comprised of pieces of the genome that “jump” from one site to another. In humans, this activity is not currently observed with HERVs and no exogenous counterparts of HERVs exist. Until recently, many scientists considered HERVs a type of “junk” DNA and thought they served no function but rather were remnants of past infections.

Each endogenous retrovirus is thought to have entered the genomes of organisms by infecting a germ-line cell, an egg or a sperm cell, of an ancestor. Among the reasons for concluding this is the fact that ERVs are virtually identical in structure to proviruses. The structure is very detailed, containing telltale markers and traces of integration, and the genes required to enter a cell, make a DNA copy of its RNA, integrate it with the host cell's DNA, assemble the new virus components that the cell is forced to make, and exit the cell to infect other cells. The only difference in structure between proviruses and ERVs is that one or more genetic elements of an ERV are broken. ERVs even have the same viral codon bias as proviruses. ERVs may or may not serve some function in the organisms they inhabit. It is misleading of Purdom to suggest it is an either/or situation ("they served no function but rather were remnants of past infections"). It is clear that they are the remnants of past infections, but there is no reason why they should not now serve useful or even vital functions for host organism, and many reasons to expect that they can serve such functions. More on this later, but let's look at a piece of evidence for ERVs being inherited remnants of proviruses, as described by Purdom herself!
  • Scientists, in a recent Genome Research article, claim to have reconstructed an infectious retrovirus that purportedly incorporated itself into the human genome less than 5 million years ago. The virus has been named Phoenix and was constructed through comparison of DNA sequences from the human endogenous retrovirus K family (HERV-K). HERV-K is proposed to be a fairly young (less than 5 million years) family, as it still contains a complete set of genes (albeit with mutations) necessary for a retrovirus to produce infectious viruses. The scientists involved in this recent study compared sequences of HERVs from many parts of the human genome and constructed a retroviral sequence they believe resembles the sequence of the “ancestral” retrovirus of this family. (HERVs throughout the genome have presumably accumulated different mutations, and through comparison a consensus sequence can be determined.) A virus containing the ancestral sequence was produced and found capable of infecting a human cell line.

Now why on earth would Phoenix function as a retovirus if the HERV-K family of ERVs were not the inherited remnants of retroviral proviruses?

  • What Are the Proposed Roles of HERVs?

  • Contrary to being “junk” DNA, HERVs are thought to play at least three major roles. One role is to control the regulation of genes (the expression of proteins from genes). Members of the HERV-K family are typically found in areas near genes. The regulatory role of HERVs has been demonstrated in the liver, placenta, colon, and other locations. It was recently reported that an endogenous retrovirus in sheep was necessary for maintaining pregnancy, as it was important in the formation of the placenta. HERVs also play a role in disease, and have been linked to various cancers and male infertility.

It is misleading to call HERVs just "junk". HERVs are inherited copies of malfunctioning proviruses.

It is also misleading (there seems to be a theme here!) to say that HERVs play certain roles in organisms. Some components of some ERVs play useful and even vital roles, but the last thing you want is a fully functional ERV like Phoenix! Still, some components are implicated in late onset diseases. Most do nothing. To accuse God of unnecessarily embedding vital, useful, useless and deadly bits of DNA in false proviral structures just to fool geneticists is a bit cheeky, perhaps even blasphemous, and in 'explaining' everything, it 'explains' nothing.

  • Another role is—allegedly—in evolution. One article stated, “Genomic rearrangements caused by scattered homologous proviral sequences gave rise to countless genetic variations on which the evolutionary powers of selection and adaptation could work.” This means that retroviruses jumping in and out of the genome caused changes that were selected for, supposedly resulting in microbes becoming microbiologists. This type of evolution requires a gain of information that is not accomplished by retroviruses jumping around in the genome. In fact, mobility of transposable elements seems to be highly controlled by the host to provide stability to the host genome.

Evolution works by selecting from variations. It doesn't matter what the source of variation is. Broken retroviral genes and promoters are a rich source of variation, retroviral integration being an error-prone process. If a new variation enhances reproductive fitness, it will naturally tend to become more frequently represented in the population, generation upon generation. Whether this "gains information" or not is not particularly relevant. Adaptive evolution is only interested in reproductive fitness. Once a provirus fails to replicate itself by getting the host cell to do it for it, it is finished - unless it happens to be in a germ cell. From that point on, its only route to replication is via the normal reproduction of the organism. It is in the same evolutionary boat as the rest of the genome, and will more likely persist if a bit of it happens to do something useful. The case mentioned above, of a part of an ERV playing an essential role in the attachment of the placenta in sheep, involves the env(envelope) gene of the ERV, whose job, as a retroviral gene, is normally to attach the retrovirus to the target cell. Different ERVs, with different env genes have been found in primates and different ones again in rodents, all doing the same job, a job which is, tellingly, very close to the job a retroviral env gene does. So anyway, what happens to the common design => common designer argument?

  • The location of integration sites of transposable elements are used to determine evolutionary relationships: “A specific retroviral integration site shared by two species is indicative of a common ancestor because the likelihood of independent integrations at exactly the same locus (insertional homoplasy) is negligible.” Their presupposition of common ancestry is supporting their interpretation of the evidence for common ancestry. Could it also be indicative of a common designer? It is possible that certain sites are predisposed to the insertion of retroviruses. Since chimp and human genomes are similar, identical sites in the genomes may have seen incorporation of these retroviruses in the past.

Whether or not ERVs are a result of God or any other sort of intelligent designer inserting false proviruses in our genomes, they are inherited. For hundreds of thousands of such elements to correspond in, say, chimps and humans, the most straightforward explanation is that they were inherited from common ancestors. There is no prior assumption of common ancestry necessary. It is the obvious conclusion to be drawn from the evidence. And does Purdom think that it was a mad designer at work, or does she think common ERVs are similar integrations to similar targeted sites? The straws Purdom is grasping for contradict one another. Doublethink? And here, Purdom's attempts to mislead turn into serious, deliberate deception. Research shows that retroviruses do not target specific sites. This, with the variability of an error-prone insertion process makes just a handful of coincidental integrations way beyond the bounds of sane credibility, let alone hundreds of thousands of coincidences.

  • How do Biblical Creationists View the Roles of HERVs?

  • Obviously, there is no problem understanding that HERVs have roles in regulating genes (a God-designed function) and causing disease (due to mutations in HERVs as a result of the Fall). It has been suggested that HERVs and other transposable elements played a role in rapid genetic changes that occurred post-Flood to allow humans and animals to adapt to different environments, as suggested by the AGEing (altruistic genetic elements) mechanism. One article states, “Whether these repeated sequences [referring to transposable elements] are now ‘junk DNA’ is a complex issue.” Biblical creationists do not think that HERVs are “junk” DNA, but much work needs to be done to gain a greater understanding of the role of HERVs in the past and present. The difference is our starting point—the Word of God versus the word of man.

I have a problem understanding how direct manipulation by God accounts for essential, useful, useless and deadly DNA embedded in a structure that unnecessarily and falsely resembles a retroviral provirus integration. The starting point should be the physical evidence, not the word of man, whether or not the word of man is making claims about being the Word of God.

The Answers in Genesis Statement of faith goes,

  • By definition, no apparent, perceived or claimed evidence in any field, including history and chronology, can be valid if it contradicts the scriptural record. Of primary importance is the fact that evidence is always subject to interpretation by fallible people who do not possess all information.

The above Statement of Faith was typed by a fallible person who was not in possession of all the information. Still, it serves as a warning of the sort of mental trap that people can fall into when they follow the word of man (in this case the word of man making claims about scripture being the Word of God) rather than applying their reasoning powers to the available evidence. It also serves as a warning that trying to reason with such people is usually a complete andutter waste of time.


Taking Purdom's unsupported speculation about endogenous proviruses having to be designed in in common locations, then creating exogenous retroviruses, which then become re-endogenized, how can we tell which of these are designed-in proviruses, and which are endogenized ERVs? And the question remains, why are the endogenized ERVs in corresponding loci?

Additionally, fellow creationist Todd Wood has criticised similar arguments from other creationists, Lee and Soper, asking them to explain why, if endogenous proviruses were designed into two unrelated species, do they share common disabling mutations? 


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