Creationist Arguments Against ERV's

[Loudmouth]

I have seen several creationist arguments against the ERV evidence for shared ancestry between humans and other primates. I thought it would be best to address them all in one thread instead of sporadically in other threads where they are off topic.

The basic argument for common ancestry is that retroviruses insert all over the genome, so the chances of two retroviral insertions happening at the same base within a 3 billion base primate genome is quite low. Therefore, finding a high percentage of ERV's at the same location in two genomes means that those ERV's had to be inherited from a common ancestor since independent insertions would produce insertions at the same base only on very rare occasions.

One of the arguments I keep hearing is that some ERV's are functional. How does this even apply? Why can't ERV's have function while also being the product of a retroviral insertion in the genome of a shared ancestor? Why must those be mutually exclusive? Afterall, the retroviral genome already has function outside of the human genome. The long tandem repeats (LTR's) function as strong promoters that cause the host to make tons of RNA copies of the retroviral genome. The other genes in the retroviral genome also have different functions that can be co-opted through evolution.

 

[Loudmouth]

Another argument that creationists make uses insertional hotspots. The creationists argue that since there are hotspots it makes sense that 99.9% of the 200,000 ERV's in the human genome have orthologs in chimps. However, that makes zero sense. They never tie the rate of insertion into hotspots to the percentage of human ERV's that have chimp orthologs. Instead, we get the argument of the untethered probability with references like this one:

"But although this concept of retrovirus selectivity is currently prevailing, practically all genomic regions were reported to be used as primary integration targets, however, with different preferences. There were identified 'hot spots' containing integration sites used up to 280 times more frequently than predicted mathematically."
Eugene D. Sverdlov, "Perpetually Mobile Footprints of Ancient Infections in Human Genome," FEBS Letters, Vol. 428, Issues 1-2, May 22, 1998, p. 1-6

280 times more frequent than what? The odds of winning the Powerball lottery are around 1 in 150 millions. If those odds were reduced to 280 in 150 million (i.e. 1 in about 500,000), would you think that winning would be assured 99.9% of the time? No. So lets follow their references, and see if their argument holds up. If we go to the paper cited above it turns out that it is not the original source for those findings. Instead, Sverdlov cites this primary research paper:

http://genesdev.cshlp.org/content/8/12/1473.full.pdf+html

So let's see what the real probabilities are. From the paper:

"A pool of 10 ug of infected TEF DNA (from -5x l0^6 cells) would therefore contain -1-1.5 x 10^7 integration events. If integration occurred at random throughout the genome (size 2x 10^9 bp) we would expect to see about two to three integrations, in each orientation, within the 500-bp stretch of DNA."

The fully random rate of insertion is 2-3 insertions per 15 million insertions. For their hotspot that has an increased rate of 280 times that, we are looking at about 900 insertions happening in that hotspot out of every 15 million. That is a probability of 1 out of every 16,000 insertions.

If we further assume that every single ERV is found at such a hotspot (which they aren't, but just to make this as favorable for creationists as possible), how many ERV's should be found at orthologous positions between the human and chimp genome if those insertions were independent events? Just 1 out of every 16,000. There are 200,000 ERV's in the human genome, so this would mean that we should see about 12 out of those 200,000 ERV's that are shared with chimps, or just 0.006%.

So how many do we share? We share nearly 99.9% of those ERV's with chimps, not 0.006% as the creationist argument would predict. Obviously, the creationist argument doesn't work.

 

[AV1611VET]

Would anyone like to tell me what ERVs are in words that my great-great-great grandmother would understand, so I can argue against them too?

 

[Loudmouth]

Would anyone like to tell me what ERVs are in words that my great-great-great grandmother would understand, so I can argue against them too?

Retroviruses are a special kind of virus. They replicate by inserting themselves into your DNA. Once in your DNA, they take over the cell and force it to make more copies of the virus. Those copies move to the outside of your cells, bud off, and then infect other cells where the process is repeated again. Here is a more complex picture of what happens.

Endogenous retroviruses, ERV's, are the viruses that have inserted into the host DNA and have remained there.

 

[AV1611VET]

Endogenous retroviruses, ERV's, are the viruses that have inserted into the host DNA and have remained there.

Wow! Thank you! 'Preciate it!

So now, what are you asking in the OP exactly?

 

[Loudmouth]

Wow! Thank you! 'Preciate it!

So now, what are you asking in the OP exactly?

This is the analogy I usually use.

Let's say there are two people in two separate rooms, and they each have a copy of the Oxford unabridged dictionary. We ask them to randomly flip through the dictionaries and put their finger down on a random word, and to do this for 100 words.

When we compare the randomly chosen words from each person, what do you think the chances are that 99 out of the 100 words would match? Those chances would be pretty astronomical, right?

The same applies to retroviruses. Your genome has more than 2 billion bases that retroviruses can insert into, comparable to the thousands of words contained in the dictionary. The chances that two separate insertions will happen at the same base is not that great. The chances that 99 out of every 100 will happen at the same base aren't even worth considering.

Therefore, when we see two genomes with the same ERV's at the same bases we know that those were not produced by separate events. Instead, there was a single event in a common ancestor and the two genomes are descendants of that common ancestor.

 

[AV1611VET]

This is the analogy I usually use.

Let's say there are two people in two separate rooms, and they each have a copy of the Oxford unabridged dictionary. We ask them to randomly flip through the dictionaries and put their finger down on a random word, and to do this for 100 words.

When we compare the randomly chosen words from each person, what do you think the chances are that 99 out of the 100 words would match? Those chances would be pretty astronomical, right?

The same applies to retroviruses. Your genome has more than 2 billion bases that retroviruses can insert into, comparable to the thousands of words contained in the dictionary. The chances that two separate insertions will happen at the same base is not that great. The chances that 99 out of every 100 will happen at the same base aren't even worth considering.

Therefore, when we see two genomes with the same ERV's at the same bases we know that those were not produced by separate events. Instead, there was a single event in a common ancestor and the two genomes are descendants of that common ancestor.

Okay, thanks.

Good analogy!

Do you teach microbiology or something?

 

[DogmaHunter]

I have seen several creationist arguments against the ERV evidence for shared ancestry between humans and other primates. I thought it would be best to address them all in one thread instead of sporadically in other threads where they are off topic.

The basic argument for common ancestry is that retroviruses insert all over the genome, so the chances of two retroviral insertions happening at the same base within a 3 billion base primate genome is quite low. Therefore, finding a high percentage of ERV's at the same location in two genomes means that those ERV's had to be inherited from a common ancestor since independent insertions would produce insertions at the same base only on very rare occasions.

One of the arguments I keep hearing is that some ERV's are functional. How does this even apply? Why can't ERV's have function while also being the product of a retroviral insertion in the genome of a shared ancestor? Why must those be mutually exclusive? Afterall, the retroviral genome already has function outside of the human genome. The long tandem repeats (LTR's) function as strong promoters that cause the host to make tons of RNA copies of the retroviral genome. The other genes in the retroviral genome also have different functions that can be co-opted through evolution.

The strongest argument against ERV's is in my signature

 

[Loudmouth]

Okay, thanks.

Good analogy!

Do you teach microbiology or something?

I have taught undergrads how to do microbiology in a lab setting, if that counts.

 

[Loudmouth]

The strongest argument against ERV's is in my signature

Such is the explanatory power of "God did it".

 

[Loudmouth]

I have used these references in other threads, but it is probably a good idea to get all the cards out on the table early in any ERV thread. I say that there are over 200,000 ERV's in the human genome because that is how many were found as part of the human genome project. Here is Table 11 from the human genome paper:

Notice that the header says "number of copies (x1000)". Between ERV classes I-III there are a total of 208,000 ERV's.

Now we go over to the chimp genome project which finished after the human genome project. As part of chimp genome paper, they compared the chimp genome to the human genome. In so doing, they were able to find the species specific ERV's. These are the non-orthologous ERV's which are ERV's that do not have a match at the same base in the other genome. Here is Table 2 from the chimp genome paper.

As you can see, there are only 82 human specific ERV's. This means that out of the 208,000 ERV's found in the human genome only 82 do not have a match in the chimp genome. If people prefer percentages, this means that 99.959% of the ERV's in the human genome have a match in the chimp genome. For the chimp genome, there are 279 chimp specific ERV's in addition to the 208,000 that they share with humans.

This is in stark contrast to the claims made by creationists, such as this article from the Discovery Center's blog "Evolution News & Views":

"Out of tens of thousands of ERV elements in the human genome, roughly how many are known to occupy the same sites in humans and chimpanzees? According to this Talk-Origins article, at least seven. Let's call it less than a dozen. Given the sheer number of these retroviruses in our genome (literally tens of thousands), and accounting for the evidence of integration preferences and site biases which I have documented above, what are the odds of finding a handful of ERV elements which have independently inserted themselves into the same locus?"
http://www.evolutionnews.org/2011/05/do_shared_ervs_support_common_046751.html

That article was written in 2011. The chimp genome paper, which clearly demonstrates how many orthologous ERV's there are, was published in 2005. There is absolutely no excuse for such poor scholarship on the part of the Discovery Center.

 

[AV1611VET]

I have taught undergrads how to do microbiology in a lab setting, if that counts.

Close enough.

 

[SteveB28]

I feel that I can hear a number of ostrich heads being quickly thrust into sand....................

 

[Loudmouth]

I feel that I can hear a number of ostrich heads being quickly thrust into sand....................

I didn't even get to the humorous attempts. There is one creationist who claims that ERV's can't be evidence of common ancestry because they are foreign DNA. It's like saying that fingerprints can't be used as evidence because they aren't found on fingers.

 

[SteveB28]

I didn't even get to the humorous attempts. There is one creationist who claims that ERV's can't be evidence of common ancestry because they are foreign DNA. It's like saying that fingerprints can't be used as evidence because they aren't found on fingers.

Or that a town of people infected with measles isn't an epidemic, because they're infected with foreign material.....?

 

[The Cadet]

Excellent thread. Keep 'em coming.

 

[SteveB28]

The silence is quite telling isn't it?

 

[Loudmouth]

The next topic is . . .

"Who made who?"--AC/DC

Some creationists argue that exogenous, infectious retroviruses originated from ERV's instead of the other way around. Overall, this argument is rather irrelevant and misguided.

First, we have the fact that the pro-virus (the DNA form of the virus that was inserted into the genome) can be considered an ERV, even if it is a young one. Post #4 has a good outline of the stages within the retrovirus lifecycle.

Second, we can observe exogenous retroviruses producing very real retroviral insertions into host genomes where there were no ERV's before. One famous example is this figure:

"The human chromosomes are shown numbered. HIV integration sites from all datasets in Table 1 are shown as blue “lollipops”; MLV integration sites are shown in lavender; and ASLV integration sites are shown in green. Transcriptional activity is shown by the red shading on each of the chromosomes (derived from quantification of nonnormalized EST libraries, see text). Centromeres, which are mostly unsequenced, are shown as grey rectangles."
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC509299/

[added in edit-- I wasn't sure if this was clear. The "lollipops" in the figure above represent new ERV's produced by retroviruses that were introduced to human cells in the experiment.]

Creationists like to argue that evolution or abiogenesis can't be scientific because we don't directly watch it happen in the lab. Well, guess what? We directly observe retroviruses making ERV's in the lab. They still won't accept it as true.

There is another argument that makes a much stronger case, IMHO. The creationist story goes that after the "Fall", mutations built up in the ERV's which transformed them into retrovirus producing factories. Evolution describes quite a different scenario. Evolution proposes that ERV's were as close to be infectious at the time of their insertion, and have only become less infectious since.

That actually makes for a testable prediction. If we were to create a consensus sequence of recent HERV-K insertions, what does each predict? Creationism predicts that a consensus sequence, which removes accumulated mutations, should not produce infectious viral particles. Evolution predicts that a consensus sequence can produce infectious particles since it is closest to being the original viral sequence.

What do we see?

"Human Endogenous Retroviruses are expected to be the remnants of ancestral infections of primates by active retroviruses that have thereafter been transmitted in a Mendelian fashion. Here, we derived in silico the sequence of the putative ancestral “progenitor” element of one of the most recently amplified family—the HERV-K family—and constructed it. This element, Phoenix, produces viral particles that disclose all of the structural and functional properties of a bona-fide retrovirus, can infect mammalian, including human, cells, and integrate with the exact signature of the presently found endogenous HERV-K progeny."
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1665638/

That in silico sequence was a consensus sequence derived from an alignment of several HERV-K insertions. The consensus sequence shows us where the mutations are, and when they reconstructed the DNA sequences without the mutations they got a retrovirus.

Another win for Evolution.

 

[lasthero]

Sheesh, nothing? Not even a few drive-by posts?

 

[Loudmouth]

Another interesting creationist argument I have run across involves PtERVs (Pt for Pan troglodytes since it was first found in chimps). This family of retroviruses is represented by 100's of ERV's in chimps and gorillas, but is not found in humans and orangutans. Here is a nice reference that I will be using later:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1054887/

First off, beware of creationists bringing "the same retrovirus". It is grammatically correct to say that chimps and gorillas have ERV's from the same retrovirus. However, they skip over a very important factor. Are these PtERV insertions found at the same base in the chimp and gorilla genome? They simply don't mention that. In most cases on forums like these, I think this is due to the fact that they don't understand the argument for common ancestry. If they did understand the argument, then the first thing they would look at is whether these PtERV insertions are at the same base (i.e. orthologous). However, the supposed creationist experts who write blogs claiming to be experts should know better. For example, this blog written under the auspices of the Discovery Center.

Second, this specific example, PtERV, is actually one of the better pieces of evidence for evolution because it allows us to test creationist predictions against evolutionary predictions. As we have often heard from creationists, hot spots and multiple insertions at the same positions is what explains the orthologous ERV's, not common ancestry. Therefore, creationists would predict that 99.9% of PtERV insertions in chimps and gorillas should be orthologous since that is the percentage of ERV's shared by humans and chimps.

Evolution makes the opposite prediction. According to the proposed evolutionary relationships between humans and other apes, humans and chimps share a more recent common ancestor than chimps and gorillas. Here is a nice cladogram showing the relationships.

As you can see, if chimps and gorillas inherited those ERVs from a common ancestor then humans should have them too. We don't. Therefore, those PtERV insertions had to occur independently in gorillas and chimps which means that they should be found at non-orthologous positions.

So we have creationism predicting orthologous PtERV insertions and evolution predicting non-orthologous insertions. So what's the verdict? We go back to the paper referenced earlier.

"Based on an analysis of 1,467 large-insert clones, we mapped 299 retroviral insertion sites among the four species (Figure 3; Table S2). A total of 275 of the insertion sites mapped unambiguously to non-orthologous locations (Table 2), indicating that the vast majority of elements were lineage-specific (i.e., they emerged after the divergence of gorilla/chimpanzee and macaque/baboon from their common ancestor).

Within the limits of this BAC-based end-sequencing mapping approach, 24 sites mapped to similar regions of the human reference genome (approximately 160 kb) and could not be definitively resolved as orthologous or non-orthologous (Table S3)."

The "limits of this BAC-based end sequencing mapping approach" is a bit technical to explain, so suffice it to say that the BAC based approach can only tell you if they are within ~100k bases of each other. It can't tell if they are at the same base. Later in the paper, they were able to take some of those unambiguous results and resolve them down to the base level. None of those results showed an orthologous PtERV insertion.

What we have is yet another defeat for creationist predictions and a full on victory for evolution.