Why Aren't the Twin Locations of >100k+ ERV's (human vs. chimp) Discussed More?

(Cornelius_Hunter) #127

Ouch. It’s bad enough to be misrepresented. But then the touche at the end.

(Matthew Pevarnik) #129

Thanks Chris. The warning was somewhat appropriate as my stomach started to do that one thing it does when I check my stock investments every morning.

@Cornelius_Hunter its going to make me grumpier than usual I think for you to keep bringing up this Klaussen paper as evidence against CD as it seems the paper isn’t quite all that you’re making it out to be. I do appreciate your ERV engagement earlier though it seems you consider it an ‘anomaly’ in light of massive evidence against CD like the Klaussen paper which is not massive evidence at all. Perhaps we can keep this thread focused on ERVs and if you find a really good topic that CD fails on, you can start another thread. I would still be curious to hear some non-CD engagement with ERVs.

(Cornelius_Hunter) #130

Well it is unfortunate that problematic evidence is thrown out on the basis of an erroneous, misrepresentation, and no defense is allowed. Chris Falter apparently did not read, or does not understand. But I got it–stick to ERVs here.

(Chris Falter) #131

You defended yourself in multiple posts in the thread I linked to. Interested readers may follow the link.

(Matthew Pevarnik) #132

Cornelius, go defend your interpretation of the Klassen paper in the other thread that you posted several times in. Is the Klassen paper problematic for CD? No it’s not and stop this persecution complex nonsense: you can correct any erroneous misrepresentations and make a defense.

He read it, many others read it, I read it. And the conclusion I’ve come to unfortunately (as I really take what you say seriously: I was reading a paper in my pajamas late at night when my kids are sleeping- that is precious time for me :sweat_smile:) is well something like this:

Appreciate it!


That’s a non sequitur. No one is saying that ERVs are evidence for common ancestry and evolution because they are non-functional. Also, you need to show that the cost incurred by ERVs in the regions they are found would have been too high. You also need to show that there is a known mechanism for specifically removing ERVs. If there are no mechanisms for removing ERVs from the genome then you are left with the standard selection of alleles, substitutions and indels that reduce any cost incurred by ERVs. There are currently human ERVs that are heterozygous in the human population, and there doesn’t appear to be any strong selection against them.


ILS is a known and observed mechanism. If there were ERVs which were heterozygous in the common ancestor of gorillas, chimps, and humans then it is possible that ILS will fix the ERV in some lineages while they disappear in others which would create small incongruencies in the expected pattern. However, these should be exceedingly rare, and they are. Out of the 200,000+ ERVs that fit the expected pattern only a handful don’t, and this is what we would expect to see from common ancestry where ILS is possible.

You are projecting. More than 99.9% of the ERVs fit the expected pattern, and that pattern is consistent with common ancestry. You reject the evidence and stick to a lack of common ancestry. You are projecting your own unwillingness to dump a failed model onto others.


We do have retroviruses that infect us: HIV-1, HIV-2, HTLV-1, and HTLV-2.

“Four types of HTLV, type 1 to 4, have been described in humans and for 3 of them simian counterparts (STLV-1, STLV-2, STLV-3) have been identified in multiple NHP species. The majority of human infections are with HTLV-1 which is present throughout the world as clusters of high endemicity.”
[url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4289907/]Peeters, et al. (2014)

Arguments from incredulity don’t get far in science.


What we have is an observed mechanism that produces orthologous ERVs in different organisms. That mechanism is common descent. We observe that human relatives share the same ERVs because they inherited those ERVs from a common ancestor. We also have the observed mechanism of retroviral insertion, and we know from those observations that retroviral insertion is random enough that only very rarely should two insertions happen at the same base in the genome.

We have directly observed retroviruses inserting into genomes, and we have the data demonstrating that only a tiny, tiny percentage of insertions should occur at the same base in independent insertions.


again? see my comments above. we also observed the opposite (ervs parts can be created from host parts). so both options are possible. combine it with the fact that some creatures cant survive without some ervs and the best explanation is that these ervs are actually in the same spots because of common design.

(Matthew Pevarnik) #138

Outrigger, did you understand the paper we’ve discussed extensively that demonstrates how one can potentially identify the difference between ERVs that are passed along to offspring vs. ERVs that separately bombarded different lineages? They produce extremely different signatures in the genome as the rest of @T_aquaticus 's quote that you left out for some reason demonstrates:


The normal life cycle of a retrovirus includes transcription of the inserted viral genome, so I’m not sure what you are getting at. That doesn’t put the origin of the insertion in doubt. We can directly observe the origin of new ERVs in the lab and in the wild.

(Cornelius_Hunter) #140

You just reinforced my point. Of course we have modern endemic infectious retroviruses. The point was in regards to natural history. The fact that we have modern endemic infectious retroviruses simply demonstrates that host restriction systems are not a viable explanatory mechanism. This evidence flatly contradicts common descent. Quoting from the paper which I posted, which I recommend reading:

(Cornelius_Hunter) #141

Actually, it is an argument from the current state of the art in biology.

To reiterate, the chimp-human DNA similarity is somethign like ~99%. What we know from biology indicates that 1% changes in the genome don’t even come close to traversing the enormous distance in phenotype space to get you from a primitive ape to a human. You can make all kinds of changes to a genome, and get little or no phenotype change. The mapping is robust. The science indicates that a 1% change will not go from a primitive, rudimentary primate to a human being.

Now can we prove this is the case? Of course not. One can always hypothesize that higher order (e.g., regulatory) changes will work this magic. But it really is, at this point, a complete unknown. You are arguing for an unknown–somehow a 1% genetic change brings on this enormous change. This is not indicated, and requires an unknown mechanism.

And when I point this out, you defend yourself by claiming I am making an argument from incredulity.

(Matthew Pevarnik) #142

Unless it’s those pesky tool using kind:

It’s only a matter of time until they become BioLogos forum moderators :nerd_face:

(Chris Falter) #143

Hello Dr. Hunter,

You probably missed the long and productive discussion that Richard Buggs, Steve Schaffner, and Dennis Venema had on Human Chimp Genome Similarity here on the forum. It ended only about a month ago. Schaffner (@glipsnort), a member of one of the world’s foremost primate genetics teams at Broad Institute, concluded that the similarity is actually about 95%. @DennisVenema agreed. @RichardBuggs accepted 95% as an upper bound, although he suspects the similarity measure will be lower when the genomes are fully sequenced.

Thus your critique of common ancestry among primates seems to be based on old, inaccurate estimates that have been overtaken by better data.


(Cornelius_Hunter) #144

Hence the tilde. Estimates are all over the map, depending on what is accounted for, etc.

(Matthew Pevarnik) #145

What is your point now? Very few ERVs are unique to the human lineage, as in 22 out of 200,000:

What does this have anything to do with contradicting common descent?

(Cornelius_Hunter) #146

The point is that the lack of endemic infectious retroviruses contradicts CD because they exist in other primates, and by CD inference, in our primate common ancestors. So they are in our ancestors but not us. You might say, "well, that is because Humans evolved some restriction systems. But that’s not true, because we have HIV now. So what we have is a violation of the expected CD pattern, and we need a new mechanism to fix the “anomaly.” This mechanism would, somehow, purge the early (earlier) human lineage of the endemic infectious retroviruses which we otherwise must have inherited from our primate ancestor. There’s always a fix, but with each fix, you have a parsimony cost.

(Matthew Pevarnik) #147

So your point is that humans gained some kind of mechanism to help us (at some point after we split from other primates in the CD model) and thus the ERVs were from before this point which is exactly the model that we’ve been repeatedly speaking of… those 200,000 ERV insertions occurred in a common ancestral population. Why would such a mechanism remove previous ERVs that had already been integrated into our genome?