For Chris

I reply to you, Chris, a poster in a Facebook "intelligent design" group, on the subject of endogenous retroviruses (ERVs). Your own comments are in black and indented. Mine are in red.

Evolutionists claim that ERV is a strong evidence for common ancestry. However, their logic is full of holes. I have only looked into a couple of areas, and they are already sufficient to derail the entire hypothesis. My main arguments fall into two categories, (1) a lack of an evolutionary mechanism, and (2) double standards.

I don't know what the oft-used-by-creationist word "evolutionists" is doing in an "Intelligent Design" post. Are there "atomisits"? "gravitationalists", "germists"? Each of these is a well-established branch of science.  The truth is that you have satisfied yourself that you have "derailed" a large branch of virology and genetics, and, as we will see, you have used your 'arguments' to excuse yourself from looking at large sways of evidence you do not like to look at.

1. No Evolutionary Mechanism

1.1 Background

The gist of the evolutionary story for the ERVs goes something like this: Viruses infect primates and insert themselves into at different genome locations. We see in humans about 200,000 ERVs, most of which are at identical genome locations. Further, many of them share corresponding genome locations with chimps. Therefore, the common locations are best explained by shared common ancestry. 

This is hardly an adequate summary of the proof* of common descent among us primates. A summary of it can be found here. 
 
* I use the word "proof" in the quasi-legal sense of "proof beyond reasonable doubt rather than the axiomatic sense. Sufficient proof, when presented in court, to convict, or acquit, someone accused of murder.

This may sound nice, but as with most evolution ideas, it lacks a plausible evolutionary mechanism. It's like saying since the gift I received matches exactly the description in the letter I sent to Santa, therefore Santa is real. In both cases, the lack of a mechanism will invalidate the conclusion. The mechanism is not a sufficient condition for the outcome but is a necessary one. Unfortunately for TOE, there isn't even a plausible one.

I think that if we received gifts exactly matching our letter to Santa, it would be reasonable to conclude that someone read the letter and bought us the gifts. The exact 'mechanism' by which they were obtained and delivered would not be relevant to the conclusion. This is a very bizzare paragraph. And by the way, the conclusions from virology and genetics are  based not on an 'evolutionary mechanism', but on observations in virology and genetics. The 'mechanisms' are endogenization (the integration of retrovirally-derived DNA into germ-line cells) and genetic inheritance, in which genetic elements are inherited into the same locations as the genetic elements of the parent. Neither of these mechanisms in any serious doubt by virologists and geneticists, because, evidence.

Consider a single viral infection. Since the genome location where it inserts itself is unpredictable, then, initially, the infected population should carry the viral strain at various genome locations. In fact, this is what we are seeing in the KoRV infection in koalas [1]: 

// Of the 39 endogenous KoRVs (enKoRVs), only one was present in the genomes of both the sire and the dam, suggesting that, at this early stage in the retroviral invasion of a host germ line, very large numbers of ERVs have proliferated at very low frequencies in the koala population. //

This is from the abstract of the paper, "Proliferation of Endogenous Retroviruses in the Early Stages of a Host Germ Line Invasion". It seems that you are at least implicitly agreeing to the conclusion, derived also from a whole host of other lines of evidence, presented in this FAQ, and this site, that ERVs are indeed derived from retroviral activity. Certainly, the fact that these ERVs appear in various loci in different individuals, or not at all in some isolated populations, shows that they cannot be examples of some imagined "designer's" handiwork.

This paragraph refers to sampling on a sire-dam-progeny triad. The genome distribution is something like this (letters denote genome locations):

Dad: a, b, c, ...

Mom: a, c, d, ...

Child: a, b, d, ...

This means every individual has a different set of infection locations, which is very different from what is claimed in humans, where for the most part, every individual carry them at the same genome locations.

This can't be right. If the 'c' allele is fixed between the sire and dam, the progeny will necessarily inherit it.  

What you fail to mention is that the case of KoRV is powerful evidence for the origin of ERVs in retroviruses, and that KoRV could never have been part of an imagined "originally designed genome".

We also see the the similar thing in humans. For example, an HERV is found in 17 loci, with everyone carrying a different set among only a few cancer patients [2]:

// We found a total of 17 loci, and the frequency of their presence ranged from only 2 of the 358 individuals examined to over 95% of them. On average, each individual had six loci that are not in the human reference genome sequence. //

The above quotation is from "Unfixed Endogenous Retroviral Insertions in the Human Population", which was a study into HERVs that were NOT to be found in the human reference genome sequence, which catalogs the many thousands of ERVs and ERV fragments that are shared among the humans sampled. Yet more evidence that ERVs are not part of any originally designed genome. "Fixation" refers to the ubiquitous presence of an allele within a breeding population. There are no alternative alleles, so progeny will inevitably inherit it.

The obvious question to ask is how did infections starting at different location converge into identical ones. For this, the normal evolutionary mechanism of mutation-advantage-fixation is considered. The first question to ask is what advantage do viral infections bring to the host?

This confirms my suspicion that you do not understand what is going on, and it's very difficult to figure out where, exactly, he has got his wires crossed. "Infections" (integrations) do not "converge". Each one gets integrated at a separate, particular locs, which does not change. Sure, retroviruses, in the early stages of invading a genome, as we see with KoRV, will exogenise and re-endogenize, thus spreading in the genome. When an ERV is found at the same locus in two individuals,  it is highly probable that they are descended from common ancestors because, as you have rightly pointed out, "the genome location where it (a retrovirus) inserts itself is unpredictable". The more endogenizations that occur, the greater the chances are that some will go to fixation. This is from basic probability theory, discussed below. I discuss advantages (and disadvantages) below as well.

Unfixed ERVs are yet more evidence that ERVs are not part of any imagined originally designed genome, or they ought to be present in every individual. We go into advantages and disadvantages below.

1.2 No Advantages

1.2.1 Viral infections are harmful

The answer is clearly little, if any. Most viral infections are harmful. Most viral infections also do not attack germ-cells, the only type of cells that allow its genetic information to be passed down to offspring. Infections that insert germ-line cells are usually quite aggressive and serious. Both the HERV and KoRV infections cited above, for example, are linked to cancer.

Reverse transcription (the reading of retroviral RNA to produce a DNA version that can be integrated with  a host's DNA- is an error-prone process ). This is true whether the cell being invaded is a somatic one or a gamete. I have seen no evidence that integration with a gamete is more 'aggressive' than integration with a somatic cell. Remember that viral infections involve huge numbers of integrations by huge numbers of retroviruses with huge number so host cells. Retroviruses can 'afford' to reverse transcribe without great fidelity. It takes only a small number to be successful in order to replicate.

But indeed, most of the things that mess with our genomes are disadvantageous. This is hardly a surprise. Most, but not all. You have already been given the examples of placenta-forming syncytia and immunity from infection by other agents. Creationits and cdesign proponentsist literature is constantly hawking on about function in ERV elements. Take your argument up with them.

1.2.2 But how about co-option?

ERVs co-opted into the placenta, for example, is not only helpful, but essential. ERVs are also known to be co-opted to fight other viruses. Unfortunately, co-option is itself an evolutionary process that require chance, which means a sizable population. This means in order for co-option to occur, the infection must have already spread to the population. This essentially is trying to explain one magic with another.

Defence against infection  does not need to spread far for those who have it to be defended. Those without effective defense are likely to succumb and fail to pass their own genes, whereas the survivors will be the ones to recover the population and pass on their protective ERVs. Those with a reproductive advantage have a reproductive advantage.

"Exaptation" is the preferred term. It's a matter of chance and selection, the latter factor almost universally ignored by creationists and cdesign proponentsists. The idea is the one that prompted Huxley, Darwin's friend, to declate, "How stupid, not to have thought of that!"

A population being decimated by a disease will create a bottleneck where only the genes of the resistant will pass through. This will increase the chances that any heritable advantage will become fixed.

You seem to be arguing that ERVs can both be advantageous or deleterious, depending on what sentence you are writing. They can be both.
 

1.3 Unreasonable Fixation Rate

1.3.1 The necessary fixation rate and the observations

As explained earlier, since viral infections are supposedly random, but in humans, 200,000 ERVs are claimed to be in identical genome locations, the second obvious question is what mechanism caused this fixation, and whether it could have happened in a reasonable time frame.

Not "claimed", but found. The abuse of misleading weasel-words is yet another trait of creationists and cdesign proponentsists. 

This can be easily estimated. To be generous, consider the earliest primates fossils are dated about 50Mya. With viral infections starting from the onset, this means there are about 1 endogenization and fixation per about 250 years (50M / 200k). Using a standard 25 year generation time, this also mean 1 endogenization and fixation per 10 generations. Is this reasonable?

One estimate is that a beneficial mutation would take about 300 generations to fix in a mammalian lineage [3]. So, clearly 1 per 10 generations is not reasonable. Worse, since there are no conceivable benefits from a viral infection in the beginning, this fixation time is likely significantly longer, if at all.

The first thing to say is that the ERVs are there. You cannot doubt this because - reality. You have conceded (I think - is this an odd day of the week or an even one?) that ERVs are the result of retroviruses integrating their genomes with the genomes of the host species. How they come to fixation depends on their overall fitness value, because something that is deleterious will tend to be - um - deleted from the genome, generation upon generation. Something advantageous will tend to increase in frequency generation by generation. This is that basic evolutionary concept that Huxley remarked upon.

Secondly, You neglect the fact that the endogenization of retroviruses and the subsequent inheritance of their corresponding ERVs is going to be happening in a parallel fashion. 

Thirdly, reverse transcription is an error prone process. Of the many retroviral genes that each retrovirus integrates with a germline cell, a modification to one of those genes will 1) make it likely that the integration is survivable, by destroying the retroviruses replication capacity, and 2) make it more likely to produce an advantageous gene. Much more likely than a gene arising from scratch via DNA mutation.

Four.  Another factor to consider is that nobody else, even in the science-denial business or in science itself, as far as I am aware, after quite a bit of searching, has identified the fixation rate as a problem. Finding and investigating problems is the scientists stock-in-trade, and a route to career enhancement. Nobody but you sees this as a problem.

Five. Nobody knows the endogenization rate, nor the probability of a particular ERV going to fixation. This means that the probability of any number of fixations over any given time-frame is impossible to estimate.

Six. People are notoriously bad at dealing with probability. Many results of probability theory are counter-intuitive to humans. The "gambler's fallacy" is an example.

The probability that an allele will eventually become fixed in a population by genetic purely by genetic drift its frequency in the population at the time.

Each endogenization begins as a single allele (a single variant in a single individual). The probability of it's fixation is thus 1/N, where N is the size of the population. 

We don't know N.

The probability that 200,000 out of x endogenizations going to fixation depends, obviously, on x.

We don't know x.

The "time to fixation" argument is based on two values which we do not know. IOW, it is not a valid argument.

From HERV infection cited above [2]:

// Comparing the number of loci that we found to an expectation derived from a neutral population genetic model suggests that the lineage was copying until at least ∼250,000 years ago. //

Given that this estimate comes from a model, it should be taken with a grain of salt. However, it seems to indicate that this lineage had actually diverged since 250,000 years ago. In any cases, since the infection can be trace back to at least 250,000 years, using a standard 20-25 years generation time, it is simple to estimate that it has not been fixed in 10,000 generations.

Yes. Some alleles go to fixation, some do not, and some disappear altogether. It is currently estimated that mtEve's mitrochondrial DNA and Y-Adam's Y-chromosome took, very roughly, 150,000 years to become fixed in the human species. (Though it is highly improbable that they ever met, or even that their life-spans overlapped.)
 

The observation from the koala study is similar [1]. It estimated the dawn of the KoRV infection to be:

// Within each of ten enKoRVs, the 5′-LTR sequence was identical to the 3′-LTR sequence, suggesting a maximum age for enKoRV invasion of the koala germ line of approximately 22,200–49,900 years ago, although a much younger age is possible. //

Using the lower range and a generation time of about 5- 

6 years (life span ~12 years) gives about 3700~4440 generations. The KoRV is still not fixed, some populations are virus-free, while as mentioned above, the ones that have it usually have it at different genome locations. All of these indication that, if the KoRV is ever going to be fixed in the koala population, it will be significantly longer. Even using the current 4000 generations, the required fixation rate calculated in primates, 1 per 10 generations, is very unrealistic.

Purely in your uninformed opinion. And why ignore the phrase, "a much younger age is possible"? Your opinion is based on -

A small sample size

A failure to factor in parallel inheritance

A failure to appreciate the possible effects of bottlenecks.

A failure to recognise the particular lifestyle of koalas, when you try to compare them with humans and chimps.

A failure to appreciate that not all retroviruses are the same and that they can produce different outcomes, including fixation rates.

And again, KoRV is extremely powerful evidence that ERVs derive from retroviruses, and that ERVs are not part of any original "designed" genomes.
 

1.3.2 What about bottlenecks?

Sure, disease may cause bottlenecks which makes fixation easier. However, having a bottleneck every 10 generations without wiping out the species in 50My is pure fantasy.

Again, you make the error of imagining that both endogenizations and spread to fixation occur in series, and you expresses an opinion without even trying to justify it. Of course you can't. The data to justify it or reject it simply doesn't exist (the number of endogenizations that must have become extinct.)

1.3.3 It may happen at an "enormous rate" in primates, right?

If so, we are not seeing it in either humans or primates, why? If there is indeed 1 fixation per 10 generations, we should see a significant spread every single generation. But are we? Further, vague statements like "enormous rate" means little in science. What exactly is an "enormous rate"? Is it reasonable? One can argue that Santa delivers gifts at an "enormous rate", and therefore Santa is real?

The ERVs are there, in our genomes. They are clearly of retroviral origin. Inheritance happens in parallel, not in series. You are asking people to believe that someone dedicated to fighting one of the best-established branches of science to accept your intuitions about what is "reasonable". even though you have no alternative explanation to offer.

1.3.4 How about parallel infection and fixation?

Parallel infections with each at multiple locations will make converging into identical locations even more difficult. This is because the probabilities of each fixing at its final location are now somewhat coordinated (not simultaneously). Since fixing even a single ERV has been proven difficult, fixing multiple ones concurrently seem to be, again, fantasy.

Again, this bizarre idea of "converging into identical locations". What could you possibly mean? The allele at each location is a separate issue from the allele at any other location. (Except for possible fitness factors that may result from the presence of one another). Broadly, each one will go to fixation, remain unfixed, or be lost independently, and can be expected to occur in parallel.    

1.3.5 What about the endogenization rate? We don't know that, right?

The endogenization rate must be higher than the fixation rate. The problem with it is even worse since endogenization does not require a large number of generations. It's just viral infections getting into the germ-line cells. If endogenization occurs at an enormous rate, we ought to see it in a large number of humans, since modern humans have a much larger population than any primates. We should be seeing this in a massive number of people, but are we? I doubt it.

Of course, the endogenization rate must be higher than the fixation rate. We have seen examples of ERVs that have not gone to fixation. We don't know the endogenization rate, because, surely, ERVs will be going extinct. Endogenization happens to a single germ-line cell in a single individual. If that individual does not pass the ERV on, it will be lost without trace. Again your intuitions are leading you astray. Your doubts are neither here nor there. 
 

2. Double Standard

By double standard, I mean certain reasoning are only used when it is advantages to TOE, but dismissed when it is not. This is a classic case of heads I win, tail you lose, or more technically, an unfalsifiable hypothesis.

2.1 The Placenta Syncytin

The placenta syncytin is often used as evidence for common ancestry for primates, since supposedly it came from a viral infection and is very similar in primates. However, placenta syncytins are very different between mammalian clads. The current understanding is that it "evolved" independently six times [4]. If similarities of the placenta syncytins imply common ancestry, then differences of the same imply non-common ancestry. On the other hand, if both similarity and differences support common ancestry, then it is not possible for it falsify common ancestry. Then, neither can it serve as a supportive evidence.

Therefore, if the placenta syncytin is a piece of evidence for common ancestry in primates, then it is also counter-evidence for common ancestry in mammals.

Syncytia are not "supposed'" to come from "viral infections". They are embedded in ERVs in exactly the same position as you find retroviral env genes in exogenous viruses and in integrated proviruses. See "ERVs are essential in reproduction (syncytin and the formation of the placenta). How can this be?" That different ones are to be found in different lineages supports the evolution of each lineage. That they are the result of different endogenizations is not a surprise. What would be difficult to explain is, if the were designed into our genomes by some "intelligent designer", why would they be so different in each lineage?
 

2.2 Probabilities

It is ironic that the bulk of the ERV argument hinges upon the low probability of so many of them being in identical locations, while Evolutionists have been dismissing probabilities for eons. So, which is it? Does probabilities work in biology? If it does, then the virtual impossibility of generating a new protein fold (1 in 10^74) [5], and the incredible long wait time for just 2 mutations must also hold [6], making the TOE impossible. Given that the latter are confirmed, if only indirectly, by real observations, their cases are much stronger that ERVs.

The problem is that Evolutionists always want it both ways. When it is to their advantage, they parade it, when it is not, they dismiss it with vague assertions like "unlikely things happen", which is a non-sequitur.

These arguments always rest on a schoolboy errors in the application of probability theory. The phase space of proteins is immense. Why pick on particular examples and claim that they, and not any others, must be improbable? They rely on the erroneous calculation that a bunch of events is always the product of the probabilities of each individual event. I prove that this is incorrect with this simple routine, where the probability of an outcome, incorrectly calculated as being 10^-9, but is, in reality around 1/1500. But endogenizations are independent events. Chris, you fail to understand the essential difference in these two cases. Pascal must be spinning in his grave.
 
But the main error is even more basic than this. To calculate or reasonably estimate the probability of a simple, particular type of event happening is necessary to determine how many times it happens, divided by the total number possible of events. Thus the probability of scoring five or six on a six-sided die is 1/3. But on a disdyakis triacontahedronal die, the probability is 1/60. You cannot know the probability of a singular independent event happening if you don't know how many possible events there are in total. We have a good idea of how many endogenizations go to fixation in our species, but we have no idea how many endogenizations have not, and have become extinct. What we can say is that viruses can invade cells in utterly huge numbers and with great rapidity.  

Conclusion

In science, no amount of hypothesis, models, or math can argue against real observations, since explaining observations is the objective. As we have seen, in order to converge 200,000 ERVs from random initial genome locations to fixed ones, a truly enormous and unrealistic fixation rate is needed.

However, in reality, no such thing is observed. The analysis from koalas shows that a single KoRV has not been fixed after 4000 generations. Similarly, the analysis of the HERV in humans shows that it has not been fixed in 10,000 generations. We also do not see a massive number of endogenization and fixation in humans and primates. Why? Is it another case of it only happens in the past where we cannot observe? Evolutionists seem to think so, but that is mere speculation, not supported by real observations.

The use of double standard makes TOE practically unfalsifiable. When both similarities and differences of the placenta synctins support the "theory", then neither truly supports it. Similarly, mathematical probability works, it works in communications, quantum mechanics, cryptography, it also works in biology when the proposed mechanism is inherently an stochastic process. If it works for ERVs, then it certainly works for proteins and coordinated mutations.

The case for ERVs supporting common ancestry is largely unfounded, both because it has neither a reasonable TOE mechanism nor observational support, and because the method it uses for validation will invalid it in other areas. In fact, real observations largely support the opposite in both cases. 

Again, this bizarre idea of ERVs "converging". What can you possibly mean?

Summary and after-notes

Chris, you offer no alternative explanation to the universally accepted scientific one, that only endogenization in common ancestors can account for enormous numbers of ERV elements that you (sometimes) acknowledge exist in precisely corresponding loci in the DNA of different kinds of organisms. You use a spurious, unevidenced "argument" for trying to excuse yourself from answering the questions that a design hypothesis raises, and for refusing to consider some of the most convincing lines of evidence for common ancestry that ERVs provide. You have made quite an effort, and it is a crying shame that it has all been for nothing.

Intuition.

Thomas Huxley said, "Science is nothing but trained and organised common sense, differing from the latter only as a veteran may differ from a raw recruit: and its methods differ from those of common sense only as far as the guardsman's cut and thrust differ from the manner in which a savage wields his club."

However, Dawkins says, "But Huxley was talking about the methods of science, not its conclusions. And those conclusions can be disturbingly counterintuitive. Quantum theory is counterintuitive to the point where the physicist sometimes seems to be battling insanity. We are asked to believe that a single quantum behaves like a particle in going through one hole instead of another but simultaneously behaves like a wave in interfering with a nonexistent copy of itself, if another hole is opened through which that nonexistent copy could have travelled (if it had existed)."

It used to be intuitively obvious that the world did not move, and that the universe revolves around it. Can you feel it move? Can you not see the universe revolving around us?

It used to be obvious that, if you measured the speed of light, your measurement would depend on the relative speed of the light source, and you, the observer. It doesn't.

So intuition can mislead us about what the world should be like. It can lead us into mistakenly thinking something cannot happen, especially when we feel that it supports an ideology that we desperately want to cling to. There is a name for this fallacy. Personal incredulity, (with more than a pinch of cognitive bias) in which, because you, personally, can't understand something, you think it can't possibly be true. But the endogenizations are there, in their many, many thousands, and you have no idea how they came to be there.

You are so sure that fixation rates are "impossible", but you utterly fail to support that assertion with evidence and reasoning.

You also utterly fail to offer an alternative hypothesis for the presence of corresponding ERVs in different kinds of creatures.

You will not put forward a "design" hypothesis, even in an intelligent design group on Facebook. You have nothing to offer but your personal incredulity, always refusing to tackle the questions a design hypothesis would raise, of which, a reminder: 

a) What is reverse transcriptase designed to do?
b) What is integrase designed to do?
c) Why were ERVs designed with a viral codon bias?
d) What is the design purpose of re-transcribable promoters?
e) What were the HERVs that produced the consensus sequence that generated Phoenix designed for?
f) What is the design purpose of both exogenous and endogenous KoRV? 
g) If chimps and humans have commonly located ERVs, what is the design purpose of giving these common ERVs common disabling mutations?
h) What is the design purpose of giving some people certain HERVs and not others? 
i) What is the design purpose of creating different syncytins in different placental lineages?

You talk about advantages and disadvantages, and ignore all the creationists' and cdesign proponetsists' bleating about function in ERVs. It is the only flimsy fig-leaf they offer to try and question virology and genetics and promote their design hypothesis. 

You also avoid, like the plague, powerful evidence. The astonishing 'Phoenix' result is a prime example.

Chris, you have nothing of any value whatsoever to offer.