But of course we weren’t talking about “a genetic element” were we?
Ouch. These Epicureans are a rough bunch.
Except that the authors are saying no such thing. Of course endemic infectious retroviruses were present in the common ancestor. They quickly dispose of the alternative. And of course “purging” does not necessarily entail purifying selection. And of course they didn’t propose natural selection and deletion, they wanted a specific mechanism to explain why the other primate species had endemic infectious retroviruses but we didn’t.
You can always posit any just-so story you want and claim victory. What the authors are looking for is something with an element of realism.
Of the 203,000+ human ERVs, only about 100 are NOT found in the chimp genome at the same position. The other 202,900 are found at the same position. The article at ENV is simply misleading its readers.
Right now I’m looking at the reasonableness of the idea that the ERVs are the result of common descent. I’d rather you address that question. If the theory requires a 40 fold drop in ERV formation after separation I think that needs further justification.
Just for the record, this is from the article at ENV:
“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?” Do Shared ERVs Support Common Ancestry?
This was written in 2011, 6 years after the chimp genome paper demonstrated that we share over 200,000 ERV’s with chimps which is more than 99.9% of the total ERVs in the human genome.
We can directly observe retroviruses producing new ERVs in host genomes. That is the justification for concluding that ERVs are the result of retroviral insertion. Inserting into the host genome is necessary part of their life cycle. There is also no justification for believing that insertion rates are going to be the same through time, and every justification for believing that retroviruses come in waves, as we see with HIV in modern human populations and historically with PtERV insertions in the chimp and gorilla genomes. There were hundreds of PtERVs that appeaed in the chimp and gorilla genomes over a very short amount of time, perhaps as little as a few hundred thousands years or as much as 2 million years.
It’s not ERV formation that you are asking about but rather the fixation of ERVs- that is an ERV insertion that not only is present in an individual, but such a fixation would occur in the population as a whole until as members have the ERV insertion in the same location in their genome.
So maybe it is just that members of a population we’re all impacted by some ERV (let’s say an endemic one like those mentioned above). However, we see a very different type of signature when the genome is being bombarded by ERV integrations vs. a more gradual fixing of ERVs. The Yohn et al paper we discussed above demonstrates that you might get less than 5% ERVs in the same spot if a bombardment is the main mechanism but ERV spreading via mechanisms similar to how alleles spread results in a very different signature (over 99.99%+ similar locations for ERVs in a population).
So it is very well established that such ERVs that we share in the same locations as chimpanzees share the same signature as the common descent (99.99%+ similar locations) and not a separate bombardment (<5% similar locations). So now we are prepared to take a look at your concern over changing rates of ERV fixation.
Your argument initially was ‘if the rate of 100 insertions per 6 million years is interpolated backwards and assumed constant- this would require many billions of years worth of such a process.’
My question still is- what reasons do you have to assume a constant fixation rate of ERVs for billions of years? I will provide some reasons and already have that the rate should decrease over time and certainly not be constant at the very least.
Reasons already provided:
@Cornelius_Hunter brought up the fact that humans ‘purged’ some endemic ERVs that fellow primates share- this matches well to the ERV fixations that chimpanzees have had since we split ~6 million years ago. They have had three times as many in the same time span. With such a purging event, we would expect the fixation rate to decrease.
In Summary for part 1 of my response, ERV fixation occurs via either genetic drift with neutral selection or due to providing a positive selection advantage due to increased immunity against other ERVs. This paper discusses this in much more detail:
There are a total of 112,000 ERV-class I, 8,000 ERV-class II, and 83,000 ERV class-III insertions in the human genome for a total of 203,000 total insertions that make up approximately 4.6% of the human genome. MaLRs are a parts of the viral genome that have latched onto a transposon and jump around the genome through transposon activity, so I am not including them in our calculations.
We then go to the chimp genome paper which listed the number of lineage specific ERVs. These are the ERVs that aren’t shared at an orthologous position between the two species:
Out of the 203,000 ERVs found in the human genome, there are 5 ERV class 1 and 77 ERV class 2 insertions that are not found in the chimp genome at the same position. This means that all the rest of the ERVs are shared. In the chimp genome, there are 234 ERV class 1 and 45 ERV class 2 insertions that are not found at the same position in the human genome. Therefore, chimps share nearly 203,000 ERV insertions with humans while having just under 300 that are not shared with humans.
Are you aware of BioLogos’ mission statements on just this crucial point? You don’t seem to have an accurate awareness of it:
Here is an augmented image… and below it a copy of the text, so that a SEARCH might find it in the future! Perhaps you will revise many of your old “chestnuts” which seem directed at various audiences not oriented towards God or the Christian faith.
(6) We believe that God typically sustains the world using faithful, consistent processes that humans describe as “natural laws.” Yet we also affirm that God works outside of natural law in supernatural events, including the miracles described in Scripture. In both natural and supernatural ways, God continues to be directly involved in creation and in human history.
(7) We believe that the methods of science are an important and reliable means to investigate and describe the world God has made. In this, we stand with a long tradition of Christians for whom Christian faith and science are mutually hospitable. Therefore, we reject ideologies such as Materialism and Scientism that claim science is the sole source of knowledge and truth, that science has debunked God and religion, or that the physical world constitutes the whole of reality.
(8) We believe that God created the universe, the earth, and all life over billions of years. God continues to sustain the existence and functioning of the natural world, and the cosmos continues to declare the glory of God. Therefore, we reject ideologies such as Deism that claim the universe is self-sustaining, that God is no longer active in the natural world, or that God is not active in human history.
(9) We believe that the diversity and interrelation of all life on earth are best explained by the God-ordained process of evolution with common descent. Thus, evolution is not in opposition to God, but a means by which God providentially achieves his purposes. Therefore, we reject ideologies that claim that evolution is a purposeless process or that evolution replaces God.
Depends on what you mean by random. If you mean a uniform distribution across every location, well then rain doesn’t fall randomly. A lot more rain falls in Seattle than in Tempe, quite predictably. But which city in Washington state will get the most rain on October 19, 2018? That’s basically random.
Similar reasoning applies to the insertion locations of ERVs.
as Shapiro said in his lecture, there are proteins which can recognize DNA sequences … these things INTENTIONALLY looking for a place where to insert … they use ‘sensors’ to find the right place … unlike the rain you have mentioned… can’t wait when you come up with the snow flake…
I don’t know, perhaps there are exact spots where to insert … and, as time goes on, all the spots are taken one by one… and then it looks random to you… i don’t know…
Anyway… 200,000 virus insertions? Honestly, i am afraid, there is something totally unexpected going on …