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


(Matthew Pevarnik) #208

It would be misleading to say a couple of things regarding ‘random’ insertions and what scientists are actually claiming about ERV evidence.
A) ERVs are known to have preferred locations to insert. Here is another paper discussing such: https://academic.oup.com/nar/article/42/16/10209/2903314
B) it is never truly ‘random’ anyways because of biochemical reactions that obey certain rules and laws
C) there is a very different signature that ERV bombardment causes vs. inheritance through common descent. Even with preferential site integration, you might find <5% of ERVs in similar locations in the genome when ERV bombardment is the mechanism (see Yohn et al 2005).

You are perhaps claiming that all 200,000 ERVs have inserted in afterwards via preferential site selection. However the body of research on ERVs demonstrates that this is decisively not the case.

None of this though depends on any side argument of what is actually ‘random’ in nature, not is it something where we just throw up our hands and say ‘there are mysterious forces at work with ERV insertions, therefore God must have done it supernaturally.’ (Side note: if there are natural mechanisms that we understand, that doesn’t mean that God isn’t involved- otherwise God is now doing very little and hiding his activity at the nanoscale compared to hundreds of years ago where He was in charge of everything in nature).


(Martin R) #209

you said: " … there are mysterious forces at work with ERV insertions, therefore God must have done it supernaturally"

what are you talking about? why supernatural ? Is chemistry something supernatural?

Why you guys talking to people like this? We are not stupid (some of us)

Professor Shapiro just told you ( but i am sure you were aware of it), that there are proteins which can recognize a DNA sequence… therefore, it is very possible, that ERVs can recognize AND CHOOSE where to insert to … TO CHOOSE … INTENTIONALLY… based on some rules… e.g. design rules… i don’t know… if i would, i would get a Nobel price… go and find out, you are paid for, not me…

So what is supernatural ?

again,

what is supernatural ?

as i have replied to the other guy, you just don’t know what is going on… not yet… will take much much longer…or never …it is getting more complex everyday… more questions than answers everyday…

and let me finish with this, i stole it from another website, but i like it:

‘There is nothing more deceptive than an obvious fact.’

Sherlock Holmes Quote

-The Bascombe Valley Mystery


Viruses intentionally choose how they infect
(Matthew Pevarnik) #210

My apologies for using that kind of language- there seems to be a range of perspectives for those who reject ERV evidence for common descent and I was trying to cover a few main perspectives in a single post.

It seems that your main argument is that ERV insertions into the genome can occur in homologous locations due to site preference by particular ERVs. However, it was discussed extensively earlier and I just mentioned it in my previous post, that we know what such an event looks like- you end up with less than 5% of the ERVs in homologous locations. However, 99.99%+ of ERVs are in homologous locations meaning that your explanation has already been rejected by the scientific community (Shapiro included).

It is already well known that ERVs have integration preferences. That is instead of having about a 1 in 3 billion chance to be inserted in a similar spot (in say the human vs. chimpanzee genome) some of the 200,000 shared ERVs have instead closer to a 1 in 10 million chance of occurring in the same spot- yet there are over 200,000 in homologous locations. One could of course come up with the odds of such a process, i.e. one in 10^1,400,000th. That number is silly, but it again goes to show why your idea for rejecting ERV evidence is a rejected hypothesis within the scientific community.


(Haywood Clark) #211

Sorry, maybe I was unclear. I don’t see how your linking to a video of a question and answer from someone with no expertise in retrovirology, who answers the question very vaguely, contributes anything to a productive discussion.

Do you know that there are literally thousands of published cases in which integration sites have been located, both natural and experimental?

So, it’s clear that neither you nor Shapiro knows, but it also seems clear that you aren’t looking for any real evidence for the distribution of integration sites. Is that correct, Martin?


(Chris Falter) #212

On the other hand, given an entire genome to infect, an ERV does not always “select” the identical location each and every time. In fact, such a coincidence is extremely low probability.

The “sensors” do raise the probability of inserting at some locations and diminish the probability of inserting at other locations. Just as atmospheric conditions raise the probability of rain clouds in some locations and diminish the probability of rain clouds in other locations. But the probability of independent insertions at identical locations in two different genomes is still vanishingly tiny.

Peace,
Chris

P.S. I’m pretty sure viruses don’t have intentions, so I would recommend against using the word “intentionally” in your argument. :slight_smile:


(Matthew Pevarnik) #213

A post was merged into an existing topic: Viruses intentionally choose how they infect


(Matthew Pevarnik) #214

27 posts were merged into an existing topic: Viruses intentionally choose how they infect


(Martin R) #215

( i see you split some of my posts… sure, i apologize for the mess. )

How well known are the integration preferences of the ERVs ? In my other posts i have mentioned, that i am an engineer, so basically, i am a layman, so please be patient with me…

I have noticed, that today’s science has a lot of troubles…

“This is officially becoming a trend: Springer is pulling another 64 articles from 10 journals after finding evidence of faked peer reviews, bringing the total number of retractions from the phenomenon north of 230.”

you go to google, and you get tons of similar articles… to be honest, i am even not surprised… people cheat…even scientists… moreover, scientists are expected to deliver results… in your jargon: “there are very strong selection pressures”

However, to learn, that it becomes a trend, is something, which is very disturbing…

Don’t get me wrong, i am not saying that this is the case with ERVs, however, how confident you guys are about these insertion preferences? How confident you are, that you are able to mimic the right conditions for your experiments? Is it even possible to mimic the right conditions?

the other day i have noticed:

CRISPR genome editing… a big thing, a revolution … and then i read “DNA Damage from CRISPR Has Been ‘Seriously Underestimated’”.

Anyways, ERVs, 200,000 insertions? Some other guy on this forum pointed out, that the insertion rate dropped 40-fold … i have noticed one thing… the most interesting biology stuff always happens in the deep past and then never again… moreover, you guys still don’t know where viruses come from…


(Matthew Pevarnik) #216

That’s part of the scientific process. There is a retraction watch leaderboard:

I’m not sure what you are trying to get at. On one hand you are using some of the results of science to argue your point, but then questioning whether the same science of site preference integration is actually a valid result.

What is your point?

Yes we know how these things integrate into the genome. We can replicate it over and over and over again in our studies. We can figure out where they are integrating and find that some ERVs have a preference depending on their sequence.

Yes in the history of the lineage that eventually led to humans there are at least 200,000 such ERV integrations into the genome over a time span of at least 100 million years. That’s about one fixation every 500 years. The insertion rate DID NOT decrease by a factor of 40. The rate of fixation tends to decrease over time because as was posted many times retroviruses already in the genome help fight of the integration and potential fixation into the genome. The rate will decrease over time, not to mention a specific mechanism was provided that helped the lineage that led to humans experience a two fold decrease of fixation compared to chimpanzees.

Well you’d be wrong. The same laws and mechanisms are present today.

Which has absolutely nothing to do with the ERV evidence for common descent.


#217

We understand it just fine. The main point is that retroviral insertion rarely occurs at the same location independently in two genomes. We have multiple experiments demonstrating this fact. Therefore, the only rational explanation for finding more than 99% of 200,000 ERVs in the same location in two genomes is common ancestry. Retroviruses simply don’t insert at the same base at a high enough rate to produce that many identical insertions.


(George Brooks) #218

Excellent summation!


(Martin R) #219

sure i do … i am using those scientific results that make sense… on the one hand, you confirm that retroviruses have insertion preferences, on the other hand, you say RV insert randomly.

However, you have ignored my previous question:

In regards to that research on retroviruses’ insertion preferences, how such a research looks like? Are you even able to mimic the right conditions? I do understand, these are complex things, so are you even able to mimic the right conditions to conclude it happened randomly? Perhaps you get those random insertions because you did not mimic the right conditions…

Look, i don’t think that these things were inserted independently, i just wondering, if you think, that the researchers can mimic the right conditions for such research.

Please don’t ignore this question again.


(Martin R) #220

alright, you guys like ‘thoughts experiments’.

so let me add one ( you will make jokes of it, but i will take the risk )

You do confirm that retroviruses have insertion preferences.

So lets say, there are 100 preferred insertion spots available in both genomes.

It is year 100,000,000 b.c.

first insertion … spot 5 is taken … another 500 years gone, spot 44 is taken … another 500 years gone… spot 7 is taken… another 500 years gone … spot 95 is taken…

Now let me refer to your lollipop-picture.

How would it look like? A random insertion pattern … would you agree?

Time flies, and 100 million of years are gone, and all the 100 spots are taken … in both genomes, because are so similar.

So, how does it look now? Same 100 spots taken in both genomes, now it looks like a common ancestry…

Of course, we assume, that human and chimp were created at the same time. Don’t forget, i am old-earth creationist.

I don’t believe that what i just demonstrated is the way it happened, but just for fun, so you can start joking…


(Martin R) #221

agreed, my bad.


(Martin R) #222

please provide some examples why i would be wrong…

don’t forget, i am a layman, but, if i got this right:

a cell evolved once… a photosynthesis evolved once … viruses evolved / escaped once … i am sure that there are tons of other things which coincidentally evolved once in the deep past and then never again … After 3.5 billions of years, i would expect that these weird coincidences happen again… or at least some of it … anything…


(Steve Schaffner) #223

Yeah, he said that because both statements are true.


(Steve Schaffner) #224

Okay, but let’s make your toy model a little more realistic. Instead of 100 preferred insertion spots, start with 100 million preferred spots. Now insert 200,000 ERVs over those 100 million years, independently and randomly in the two species. How many of the 200,000 will be in the same place?

Now make it even more realistic. The viruses that insert 100 million years ago are now from a different family than the viruses that insert 95 million years ago, which are different from those 90 million years ago, and so on.

What you will get in this model looks nothing at all like real ERVs.


#225

A better way to put it is that retroviral insertion is random enough that two independent insertions happening at the same base are very rare.

If you know of conditions where a retrovirus will insert into the same spot every time then you could be in line for a Nobel prize. The earliest gene therapies used retroviruses to insert the gene of interest into the host genome, but the retrovirus would insert all over the place would often cause big problems (e.g. cancers). If there were a virus that would only insert into one spot then this would be a huge step forward in medicine. Needless to say, no one has ever discovered any conditions or viruses that insert predictably.


(George Brooks) #226

I wanted to leave a record of the post below (from another thread) …

on THIS thread!

"The bars are the 22 human chromosomes and the X chromosome. The colored lollipops are the mapped insertions for 3 retroviruses: HIV, MLV, and ASLV. As you can see, they insert all over the place. Some viruses do show preferences for certain portions of the genome, but these portions make up a large percentage of the overall genome. For example:

For HIV the frequency of integration in transcription units ranged from 75% to 80%, while the frequency for MLV was 61% and for ASLV was 57%. For comparison, about 45% of the human genome is composed of transcription units (using the Acembly gene definition).
ibid

So HIV does show a preference, but that preference is to areas with active transcription which makes up 45% of the genome. So 80% of the time it inserts into a pool of about 1.5 billion bases, and 20% of the time it inserts into the other pool of 1.5 billion bases.

As you can see, the chances of a retrovirus inserting at the same base in two genomes is extremely slim. This is why independent insertions can not explain humans and chimps sharing 99+% of their 200,000+ ERVs at the same base in each of their genomes. The only explanation is common ancestry, the very same reason that you and your siblings and cousins share the same ERVs."


Definition of evolution and the distinction between micro/macro