An interview with Tavian Oladapo.

INTRODUCTION A bit of background information about who you are and what attracted you to this subject.
I'm a retired Englishman. I was a schoolteacher and a software engineer. I retired early. I wanted to study. Evolution has always interested me. I wanted to learn more about human nature, because I think such knowledge is very important. I discovered that many people, especially in America, hated and opposed the idea of evolution. This was news to me. I got involved in creationist-evolution discussions. I came across endogenous retroviruses and how they provide such clear and irrefutable evidence for common ancestry among all us primates - humans, chimps, gorillas etc. 1. What are ERVs? Acronym. What a retrovirus does. Germline cells. Inheritance.

ERV is an acronym for Endogenous RetroVirus. A retrovirus (HIV is an example) gets into (or integrates with, in the jargon), the DNA of its target organism. This fools the target into making and releasing more copies of the virus. When a retrovirus integrates with the DNA of a sex cell, an egg or sperm cell, it becomes heritable. It can be passed down to the offspring, and to their offspring, and so on. It becomes part of the genome - within the genome, hence the term, "endo-genous". Some more useful terminology: A provirus is a retrovirus integrated within a somatic, or non-reproductive cell. These cannot be inherited.

Retroviruses in the environment, or present as proviruses are called "exogenous", meaning outside of the heritable genome. Orthologous genes are homologous genes where the genes diverge after a speciation event.

2.What is the genetic evidence that ERVs come from ancient viruses? Same genes and structure. Codon bias. Phoenix. Repeated host DNA. There are several lines of evidence for this.

a) Same structure and detail as retroviruses. KoRV. Retroviruses, whether loose in the world or integrated with a target's DNA, have a distinctive type of structure, featuring a specific set of genes and other genetic elements oriented to their means of replication in target cells. These are found in ERVs. Not all of them are complete. Older ERVs get eroded by mutation or chopped up by recombination, but they all, however complete or incomplete, feature retroviral genetics - genetics that make no sense in a non-viral context. 

b) Codon bias ERVs have the same codon bias as exogenous retroviruses, retroviruses found in the environment, not embedded in DNA. A codon is a triplet of DNA bases, from A, G, C and T that 'codes' for a particular amino acid (which are then chained together to make a protein). Now, there are different codons that code for the same amino acids. Viral DNA tends to use certain codon triplets. Non-retroviral DNA tends to use other, equivalent codon triplets for the same amino acids. We call the differences codon bias. ERVs have a viral codon bias, whereas the DNA they are embedded in exhibits non-retroviral codon bias. 

c) Phoenix The "Phoenix virus" was the result when experimenters took a bunch of human ERVs from different loci in the DNA that looked very similar. They were all inactivated by mutations at different points, but they figured that if they "ironed out" these mutations by taking a "majority vote" from each ERV as to what base should be at any given location, they might resurrect a fully working provirus (a complete, undamaged retrovirus integrated in host DNA). They succeeded. The result was a fully functional retrovirus that could cause the host cell to make copies of it and release them into the environment. They could see that those released retroviruses could reinfect cells just like any naturally occurring retroviruses in the environment today.
d) KoRV

More evidence that ERVs are of retroviral origin is the case of an exogenous retrovirus endogenizing today. There is a disease among koala bears. It is getting into the heritable genome of koalas.

e) Host repetition

Retroviruses leave a telltale trace of integration in the form of a repeated host sequence either side of the integrated provirus. These are also evident in ERVs.   3.How does this prove common descent or ancestry? In every cell in the same position. Inheritance, not infection. ERVs are found in the DNA of every nuclear cell of your body. They are always in the same positions in the DNA, going from cell to cell. If they had come directly from the environment, they would not be in every cell, and they would not be in the same position in each cell. Integrase, the retroviral enzyme that inserts the retroviral genetics, cannot choose where to make the insertion. This means that ERVs are inherited. They are copied from the single cell you started out as. Cell reproduction duplicates the same DNA every time including each ERV, in its unique position. Mostly common to all humans, so they come from common ancestors. The vast majority of ERVs are common, in common locations, among all humans. This means that we have all inherited the same common ERVs from the same common ancestors, each common ancestor likely having only acquired one new ERV and passed it on, much as Mitochondrial Eve bequeathed to all of us her mitochondrial DNA and Y-chromosome Adam bequeathed to all men his Y-chromosome. Mostly common to all humans and all chimps, so they come from common ancestors. The vast majority of ERVs are common to all humans and chimpanzees. This means that we have all inherited the same ERVs from the same common ancestors, each common ancestor likely having only acquired one new ERV and passed it on. 4.How many ERV insertion points do humans share with chimps,bonobos gorillas,and other hominins like neanderthals and denisovans, and what is the explanation for the gradient of shared ERVs? A few are found in humans and not in chimps. Even fewer differences between modern humans and other species of human. There are approximately 200,000 ERVs and fragmentary remains of ERVs in the human genome. Virtually all are common to humans and chimps. 279 are found in chimps, and not in humans. 82 are found in humans and not in chimps. As evolutionary history based on other criteria would predict, there are a smaller number of ERVs which differ from modern humans in other species of the genus Homo than differ between modern humans and chimps and gorillas etc. because we split more recently from other humans than we split from the other primates. There has been less time to acquire different ERVs. Neanderthal and Denisovan retroviruses in modern humans. ................................................. 5.Do humans share ervs with other primates and mammals? 6.Is there evidence of shared ervs between other animals? For example between dogs,other primates,do whales share ervs with each other and with hippos for example? 7.Do birds share ervs with each other and with crocodiles for example? TBA ................................................. 8.There is some evidence of the role of ERVs in the production of syncytin which is crucial in the pregnancy of placental mammals...Would you care to elaborate on that plz? Env genes in exogenous retroviruses and in ERVs carrying syncytia. Same relative position. In both, they fuse cells together. Different examples. A syncytium is tissue made of cells which contain multiple cell nuclei, formed by accumulating multiple cells. They exist in muscle tissue, and also in the placentae of placental mammals. They are indeed essential in the reproduction of placental mammals.

There are three interesting facts about this.

a) Syncytin genes are found in ERVs in precisely the same relative position in the ERV as the environment or "env" genes in retroviruses. Env genes are retroviral genes that allow retroviruses to breach target cell barriers and merge with them. b) Exogenous retroviruses such as HIV use their env genes to merge attacking immune system T cells and thus neutralize them. c) Syncytin genes are found, in different species of ERVs, in different chromosomes, in different evolutionary lineages. This is evidence that many have been co-opted (exapted is the technical term) from different retroviruses over time. 9.Would you care to tell us what you know about the resurrection of an erv that was found in the human genome? I think it was called the Phoenix virus. HERV-K majority vote. Made a fully functional retrovirus. A recent, therefore relatively intact type of ERV was identified. Its name is HERV-K, Human Endogenous RetroVirus type K. Our genomes have many copies of this ERV, each with different mutations to the others. Researchers figured out that if you take the most common nucleotide in each given position, that is likely to be the original nucleotide of the original retrovirus. So they constructed this "consensus sequence" genome, inoculated human cells with it. The result was a fully replication-competent virus. It could induce the human cells to produce new copies of the virus that could then, in turn, reinfect human cells. Creationists often say that we don't do observable, repeatable experiments in biological and related "evolutionist" sciences. This is just about the most slam-dunk proof there can be for the origin of ERVs in exogenous retroviruses. 10.What has been the response from the usual suspects? . You know -in particular,one branch of the invisible cloud people's fan club, and what has been their usual talking points and your rebuttals? These are gone into in considerable detail in my FAQ, but briefly, Function, target specicifity, 14, how did we survive? Presupposition. Circularity. VIGEs/design

a) ERVs serve useful functions for their carriers. This is the most common bleat and they think it is a show-stopper. "ERVs are not junk! Gotcha." They present a dishonest straw-man version of science that says that ERV genetics have to be junk, and they are valueless as evidence if they have function. My response is that it is only certain components of certain ERVs that perform useful functions. Some of them are even vital. But a complete ERV in a zygote, the single cell that a life starts out with, and whose DNA gets replicated at every cell division, wouldn't get the zygote very far in development. In addition, ERVs are implicated in many diseases, especially cancers that develop late in life and are therefore invisible to natural selection. ERVs have thrown in their lot with the host DNA. Their only route now, to replication, is the reproduction of the host's DNA with them going along for the ride. Good old natural selection will favour those genetic elements that make a positive contribution to that  

Target specificity b) Retroviruses target specific DNA loci, or have preferred loci. ERVs naturally target certain loci in the DNA of their target cells. This explains common loci in different species.

The first is false, and the second is grossly misleading. It is true that there is often a statistical tendency to integrate at certain types of regions. This has been studied quite intensively and reported in an attempt to find ways of combating retroviral diseases.

 Surveys of retroviral loci reveal no repetition within 500 cell samples. Retroviruses would need to be able to target precise host DNA loci, down to single base-pair resolution, to account for commonly located ERVs in different species. Phoenix is discussed above. The fact that the same ERV is found in multiple loci in the DNA is yet more evidence that retroviruses cannot target specific loci. 14

c) Humans and chimps only share 14 ERVs in common loci. There are so many ERVs that this figure could easily be a coincidence. False. There are articles that report only 14 known, complete ERVs, but these predate the sequencing of the genomes of the great apes. Such is the desperate confirmation bias of creationists, this is the figure that many of them still cling to, and they won't be persuaded that it is completely out of date. There are some 200,000 ERVs and ERV fragments in the human and chimp DNAs How did we survive? d) Viral invasion on such a massive scale should have driven us to extinction. No. The historical death toll from viruses is enormous, but many survive pandemics and go on to produce progeny, often with enhanced resistance. Bear in mind that retroviral replication is rather error-prone. Reverse transcription has no error detection or correction. This means that viruses that become endogenized are frequently faulty, and are not replication competent.

Presupposition e) It is just supposition, or assumption or (favourite word), a presupposition that ERVs come from retroviruses? No. it is a conclusion arrived at for several reasons, reasons that we have just been into. Circularity f) This is circular reasoning. You are assuming evolution to prove evolution.
ERVs have the same detailed structure as retroviral proviruses. This fact does not require us to assume evolution.

Retroviral integration does not target specific loci in DNA. This fact does not require us to assume evolution.

Inheritance places the same genetic material in the same locations in DNA. This fact does not require us to assume evolution.

VIGEs e) ERVs could have been designed into the genomes originally to generate genetic variation. They produce exogenous retroviruses that re-enter the host DNA.
Simple parsimony dictates that you do not offer explanations for things that have no evidence for them. It is a simple waste of time. Retroviral integration is very error pprone and haphazard. The integration site is practically random, and reverse transcription is error prone. Not a clever way for an intelligent designer to tinker with our DNA, and still fails to explain the common loci of re-integrated ERVs. 11. I actually find the discoveries that show our kinship with other animals quite exciting and humbling,what do you think is driving the almost rabid and hysterical response from creationists,especially in america? Secular but many old denominations. Distrust of intellectual elites. No or poor education. Paranoia (communism). Despite the U.S. being a formally secular state, European immigrants were often from denominations and sects that predated Darwin. Many Americans were anti-intellectual and anti-authority and still are. In the early days there was practically no education, and it is still sub-standard today. They are bombarded with misleading false propaganda and smear campaigns against science. Darwin showed that all humans are related and of the same species. That went against the received ideas of the time. But he went further, and showed that all life is related. As Darwin wrote, There is grandeur in this view of life, with its several powers, having been originally breathed into a few forms or into one; and that, whilst this planet has gone cycling on according to the fixed law of gravity, from so simple a beginning endless forms most beautiful and most wonderful have been, and are being, evolved.

12.How often do you get communication from those sitting on the fence who appreciate what you do,and how does it make you feel? Not aware of any fence-sitters. There are those who accept, and those who never will. I'm not aware of anyone sitting on the fence over ERVs. Either people understand what strong evidence they are for evolution, or they will cover their eyes and stick their fingers in their ears and reject it come what may. I feel sorry for the latter. They are stuck in a mental trap. A few have said that my work has helped them out, but not all will own up to the fact. I have received messages from supporters, expressing appreciation for my work, and some of them use it themselves, which they are always welcome to do. But very few bother to comment. Human nature, I expect. It's taken for granted, the work people do to promote and defend knowledge. 13.I often tell people that the evidence for evolution is overwhelming,and even if this was not the case,it would say absolutely nothing about the truth of one religious claim amongst thousands...Would you agree or disagree?

Unfalsifability vs falsified claims. Honest about faith.

Most religious claims are unfalsifiable, which means that there are no tests that can either show that they are false if they fail, or give us some confidence in them if they pass. I have no interest in them. Believe what you like. The exception regarding religious claims is the claims of the creationists, which are falsifiable, and falsified.

14.I am sure you are as fascinated by our microbial squatters as i am, what are you hoping we discover in the future? Role in diseases, more positive functions and how they work, history of life-speciation. The unknown. I'm sure we will learn much more about their role in diseases, but also in their role in shaping our evolution, and their positive contributions. ERV genetics can be bad, but also good. We will also be learning much more about the history of life in general, deepening our knowledge of relationships between species and details of how and when and where speciations occurred. Most of all I'm excited about what we are yet to discover. That's the exciting thing about science.