Search This Blog

Who is Your Creator? - ERVs!

A blog page called, "Who Is Your Creator?: Endogenous Retroviruses (ERVS)" is a fine example of creationist misinformation, diversion, spin, cherry-picking, insinuation and quote-mining. My comments in red, the original text in black.

Nowhere does the page address the evidence that ERVs are derived from retroviruses, nor does it explain the case for common descent from ERVs, b
ut the page asks a number of questions, which makes it useful for the FAQ.

But first, let's clear up a number of blunders and misrepresentations in its opening section.

A Case for Common Descent or Another Evolutionary Blunder?

A snide, cheap little shot like this is not a very promising start. What "other" supposed evolutionary blunder is the writer referring to? He/she doesn't say. What is the point of this remark, other than to display their extreme prejudice?

(Because research in regard to endogenous retroviruses has been heavily focused on human endogenous retroviruses (HERVs), many of the cited references include research pertaining exclusively to them.)

Research on ERVs has mostly produced inaccurate, inconsistent, and biased conclusions due to the presupposition that ERVs were originally dangerous viruses that somehow got embedded in germ cell (ones that can be inherited).

Here we have the standard creationist lie that scientific conclusions are based on "presuppositions" rather than the evidence. The aim is to mislead the reader into supposing that there is no evidence. Here is why virologists and geneticists have in fact come to the conclusion that ERVs are derived from retroviruses. There is no support offered for the assertion that the conclusions are "inaccurate, inconsistent, and biased". Just as with the insinuation that there are unspecified "evolutionary blunders", we may apply Hitchens' Razor to these empty accusations: 
"What can be asserted without evidence can be dismissed without evidence."

In addition, most of the research has been spent on attempting to link them directly to disease as well attempting to prove that ERVs miraculously ‘evolved’ into essential genetic material.

Research has implicated ERVs in various diseases and has also identified positive, even essential functions for certain components of certain ERVs. (Never a positive function for a complete ERV.) So much for the creationists' "global multi-generational conspiracy" conspiracy theory, which has scientists supposedly suppressing evidence.

Overview of the ERV Controversy

There is no controversy among researchers into retroviruses and ERVs.

Evolutionists claim that a virulent strain of ancient viruses called retroviruses plagued vertebrates (and most non-vertebrates) as they evolved throughout time.

Numerous retroviruses. Some ancient, and some contemporary. Again, it is no "claim", but a truth that is clear from the evidence.

After their initial outward communicable infection (exogenous), evolutionists also claim that these viruses were able to insert their DNA into their host’s germ cells, which are all sperm and egg related cells. Any viral DNA that integrates into the DNA of a host’s germ cell would be automatically passed down (inherited) to all offspring and that type of transmission and is called endogenous.

This is rather confused. Exogenous retroviruses are viruses with RNA genomes that can enter host cells. The host cells they normally enter are the somatic cells of the body. Here, they create DNA versions of their genomes and integrate the DNA with the host chromosomal DNA. The integrated DNA is called a "provirus". The host cell then dutifully "reads" this retroviral DNA, which causes it to create new exogenous retroviruses which can exit the cell to invade new host cells. If a retrovirus happens to integrate its DNA genome into the DNA of a gamete, that DNA may be passed down to offspring, but it's not automatic. The type of transmission is called "vertical" (as opposed to "horizontal" transfer resulting from direct infection). It is that which is vertically transmitted that is called "endogenous".

ERVs are considered ‘proviral,’ which means they a latent form of an original virus that can no longer replicate and infect.

No. As explained above, a provirus is a retroviral genome sequence found, normally, in the DNA of a somatic host cell, acquired by horizontal transfer (direct infection). The whole point is to be able to replicate and reinfect. ERVs cannot normally replicate and reinfect, but in rare cases, some can.

Because all ERVs lack and have different genetic material than that of exogenous retroviruses, evolutionists commonly refer to ERVs as “retrovirus-like elements” or “remnant sequences.”

ERVs are to be found in a full spectrum of forms, from being (rarely) complete and replication competent, to fragmented and riddled with mutations. (This is why estimates of numbers vary. It depends on how demanding your inclusion criteria are. As they say in science, whatever you think, it's more complicated than that.)

ERV integration points within chromosomes are typically located at the identical position (loci) of related species. Evolutionists believe that integration sites are random upon insertion into the germline from exogenous retroviral infections and claim that those shared loci could only have occurred by common descent. This case of presupposition is why ERVs have been the poster child for biological evolution.

No. In phylogenetically close species, they are typically located in precisely corresponding locations. (It's nonsense to talk of identical loci when comparing different species. "Corresponding locations" means the same position relative to other genetic markers such as important genes. Although often relative, these relative positions are identical down to base-pair resolution.) "Evolutionists" may believe stuff, but there are very few evolutionists (being defined as people who accept evolution on faith rather than evidence). Researchers have gone and found out that integration sites are not entirely random, but neither are they locus specific. They have found this out by actually surveying retroviral integration sites. Not by "presupposing" stuff. It still means that large numbers of coincidentally corresponding integration sites are beyond credibility. That they can only be in corresponding locations by common descent is a conclusion (not a presupposition) drawn from the fact that common descent explains all the facts, whereas, nothing else does.

And now on to the questions.

Q: Genetic alterations to germ cells are rare and have been mostly found to harm overall genetic fitness, not improve it. What would make retroviruses an exception?

A: Multiple genetic alterations are the norm. Retroviruses are not "exceptions". Most alterations to germ cells are neutral. Harmful changes are the next most numerous. Beneficial ones are the rarest, but those are the ones that are most likely to increase in frequency in a population, generation upon generation by a process called "natural selection".

Q: Having healthy and strong germ cells is mandatory to produce a viable zygote, so why would harmful viral-infected egg/sperm cells be considered more fit (positive selection) versus ones without retroviral DNA?

A: Because they are not infected with harmful viral genetic material. Reverse transcription is highly error-prone, and does not always produce viable proviruses.

Q: Apoptosis is an accepted biological phenomenon, so why wouldn’t most germ cells with viral-infected DNA be eliminated?

A: Most would be. But some would not be. Here's why.

Q: Evolutionists claim that retroviruses were in a dormant cycle (lysogenic) upon insertion and were intact before mutations, deletions, and recombination deleted and disabled them. What prohibited the thousands of retroviruses from changing into an infectious cycle (lytic), thus weakening or killing the embryo (especially in hosts with long gestation periods) and weakening or killing young and adult hosts?

A: Nobody "claims" that retroviruses are always intact upon integration. Reverse transcription is highly error prone.

Q: Why would populations with harmful viral-infected germ lines be under positive selection and become prevalent and “fixed” over non-infected populations? (The supposed ‘evolution’ of ERV elements changing into beneficial genetic material must be assumed to have occurred after fixation.)

A: Mutation may occur upon endogenization. Reverse transcription is highly error-prone. The ERV may be immediately useful, or neutral at first, acquiring beneficial mutation later. There is no need for fixation. Why should there be?

Q: Geneticists have problems with controlling retroviruses (vectors) for gene therapy, so how would ERV elements randomly invade healthy germ and somatic cells without damage, thus be eliminated by ‘purifying selection’?

A: Reverse transcription is a highly error-prone process. It does not always produce viable proviruses. Harmful viable ones are eliminated. Non-viable neutral and beneficial ones are not. It's called "natural selection".

Q: There are at least 98,000 different ERVs sequences and 158,000 ERV-like elements just in the human genome. Why is it that only ERVs have supposedly invaded germ cells hundreds of thousands of times, but no other virus has been discovered to do the same?

A: There are many varieties of retroviruses. No other types of virus have been discovered to integrate with host DNA, because all the ones that do do the same get to be called retroviruses. The other ones don't. The clue is in the name, retrovirus.

Q: How is it that ERVS are Considered Copies of Disease Producing Exogenous Retroviruses but None Have Been Proven to Directly Cause Disease?

A: Reverse transcription is a highly error-prone process. The "successful", disease causing ERVs tend to be eliminated. It is called "negative selection". Nevertheless, there are a number of retroviruses that do exist in exogenous and endogenous forms, and endogenous retroviruses are known to produce virions in koalas, for example, and in sheep.

Q: By Chance, What Made ERVS Evolve from Being the Cause of Exogenous Infection into Elements that Resist Exogenous Infection?

A: Not entirely by chance. Don't forget natural selection. And it's not only ERVs themselves that protect the cell from exogenous infection, but the ancient immune responses of the cells themselves to the original retrovirus that became endogenized.

Q: By Chance, What Made ERV Elements Change From Viral Activities to Cellular Activities and Create New Essential Genes?

A: Not entirely by chance. Don't forget natural selection. Reverse transcription is a very error-prone process. Errors in reverse transcription can disable the viral function. Any errors that happen to be useful to the host will tend to increase in frequency in the host population.

Q: How Could ERVS Create a Specie-Specific Regulatory Network that Controls the Expression of Cells in a Collective Manner?

A: Reverse transcription is a very error-prone process. Errors in reverse transcription can disable the viral function. Any errors that happen to be useful to the host will tend to increase in frequency in the host population by natural selection.

Q: By Chance, What Made Unrelated ERVS in Unrelated Species Create Almost the Same Gene (Convergent Evolution)?

A: Not entirely by chance. Don't forget natural selection. In the case of syncytins, syncytal formation is a "strategy" of retroviruses. It is accomplished with their env genes, which are similar in different retroviruses.

Q: By Chance, What Made Two Unrelated ERV LTRS Evolve Independently in Creating the Same Regulatory Roles for the Same Gene (Convergent Evolution)?

A: Not entirely by chance. Don't forget natural selection.

Q: By Chance, What Made ERV LTRS Immediately Turn into Essential Gene Regulators Upon Insertion?

A: Retroviral LTRs are essential regulators (promoters) of retroviral gene transcription. Without them, retroviruses would never get transcribed, and would become extinct. Drop a promoter in a genome, and there is a good chance that it will promote the transcription of some native genetics. But they certainly would not have been essential immediately upon insertion. See the Mullerian two-step. And it would not have been entirely by chance. Don't forget natural selection. Those variations that just happened to be useful increased in frequency in the population, eventually becoming essential by the process described in the link just given.

Q: By Chance, What Made LTRS Acquire Transcription Abilities for Essential Genes?

A: Not entirely by chance. Don't forget natural selection. LTRs are promoters. In functional proviruses, they are essential for getting retroviral genes transcribed. Drop a promoter at random into the DNA, and there is a good chance it will promote the transcription of anything downstream of it. Essential genes usually have several promoters. Some of them may be of retroviral origin, others not. See ERVs promote the transcription of host DNA. Doesn't this prove they are designed?

Q: Where is the Proof that ERV LTRS can “Self-Replicate” and Why Don’t We See them Doing it Now?

A: We do. Here's an example.

Q: By Chance, What Made the Same ERV Transcribe Differently Between Supposedly ‘Closely Related’ Species?

A: PtERVs are not found in humans. Related species can have unique ERVs, acquired after speciation, and differences due to incomplete lineage sorting, and differences due to post-endogenization evolutionary histories. Regarding ERVs we do have in common, remember that closely related species are not identical. ERV genes, just like 'native' genes, transcribe differently even in different tissues in the same organism. If that was not the case, your brain tissue would look and behave in exactly the same way as that of your lower bowel. And it's not all entirely by chance. Don't forget natural selection.

Q: By Chance, What Made the Same ERV Transcribe Differently Among Different Cell Types Within the Same Organism?

A: See above.

Q: Why are there NO Examples of an ERV that Has Been Recently “Endogenized” or Examples of ERVS that Have A Direct Exogenous Counterpart?

A: There are. Examples already given.

Q: If ERV Elements Deteriorate Rapidly, Why Did Only One ERV Remain Active and Continue to Infect All Placental Mammals Over a 70 Million Year Period?

A: Selection. Don't forget natural selection.

Q: Do ERV Elements Have Random Integration Sites?

A: They are not entirely random. There are some statistical tendencies towards certain types of regions, but this is inadequate to explain orthologous ERVs, which have an integration site specificity at individual base-pair resolution. This is what falsifies separate creation.

Q:What has the Presupposition of Evolutionary Science Done for Research on ERVS?

A: Conclusions drawn from evidence are not "presuppositions". Stop talking nonsense now.

To an extent, ERVs are!


  1. In regard to your 2nd paragraph:
    "Nowhere does the page address the evidence that ERVs are derived from retroviruses, ..."

    I'm not quite sure whose page you're reading, but please refer to the 2nd paragraph under ERV 101:
    "What makes retroviruses particularly interesting is that they are the only viruses that have the ability to splice foreign genetic elements into the host cell as well as they are the only viruses whose genome consists of RNA that reverse transcribes to DNA. The steps of retroviral infection are: ..."
    We claim that all ERVS are essential and beneficial genetic material. But, as true with all genetic material, ERVs can mutate and cause disease.

    1. The quoted text refers to retroviruses which typically integrate with the nuclear DNA of somatic host cells.

      Who are "we"?