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Viruses that prove common descent

mark kennedy

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With all due respect Mark, you're not really in a position to criticize others of that.
On the contrary, I have done extensive reading on the subject and I know the difference between a dangerous germline viral infection and an adaptive molecular mechanism. There are a lot of good arguments out there, this is the bitter dregs of desperation.
 
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On the contrary, I have done extensive reading on the subject and I know the difference between a dangerous germline viral infection and an adaptive molecular mechanism. There are a lot of good arguments out there, this is the bitter dregs of desperation.
Try and present a coherent argument, Mark. Make an effort. Bear in mind that what we are asking for is any possible alternative interpretations of commonly located ERVs in what evolutionary science has identified as closely related species.
 
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TheBear

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Cognitive dissonance or refusal to accept the truth. Agreed.

DNA test jailed innocent man for murder - BBC News

But once people believe a story you can't convince them otherwise.

The Problems With DNA Evidence and Testing - The Atlantic
Your username has never been displayed in any of your posting patterns that
I've seen over the last 4 years. From practically day 1, your postings reveal someone who has all the answers, with heels dug in to that position, and really isn't seeking the "truth" about anything.

That said, there are many factors that go into such cases. Faulty labs, shoddy forensic work, inexperienced technicians, contamination, detectives transferring blood, (via shoes), from a crime scene to a suspect's home, etc. But overwhelmingly, DNA forensic science works quite well. In fact, many homicide cold cases, occurring before DNA forensics was developed, have been solved, decades later. To suggest that since these anomalies, these exceptions to the rules take place, so therefore throw the whole thing out as unreliable, is akin to saying that since relatively tiny fraction of airplanes crash, we should abandon the whole aviation industry.

Further, unlike forensic DNA, which is limited to the particular labs and technicians, and has a specific result in mind, genetic research, (what the OP is about), is shared, studied and tested on an international level via journals and publications. So, you're comparing apples to oranges as your argument.

So, instead of talking about a handful of forensic DNA cases, how about trying to tackle the OP topic. Who knows? You just might find some "truth" and learn something new that will change your mind. That would be a good thing. Right?
 
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Your username has never been displayed in any of your posting patterns that
I've seen over the last 4 years. From practically day 1, your postings reveal someone who has all the answers, with heels dug in to that position, and really isn't seeking the "truth" about anything.

That said, there are many factors that go into such cases. Faulty labs, shoddy forensic work, inexperienced technicians, contamination, detectives transferring blood, (via shoes), from a crime scene to a suspect's home, etc. But overwhelmingly, DNA forensic science works quite well. In fact, many homicide cold cases, occurring before DNA forensics was developed, have been solved, decades later. To suggest that since these anomalies, these exceptions to the rules take place, so therefore throw the whole thing out as unreliable, is akin to saying that since relatively tiny fraction of airplanes crash, we should abandon the whole aviation industry.

Further, unlike forensic DNA, which is limited to the particular labs and technicians, and has a specific result in mind, genetic research, (what the OP is about), is shared, studied and tested on an international level via journals and publications. So, you're comparing apples to oranges as your argument.

So, instead of talking about a handful of forensic DNA cases, how about trying to tackle the OP topic. Who knows? You just might find some "truth" and learn something new that will change your mind. That would be a good thing. Right?
Excellent response. Thanks, Bear. The length these people go to, to deny the bleeding obvious, is truly astonishing. We only get one chance to live in reality. What's the point of pretending it isn't real? So sad.
 
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mark kennedy

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Try and present a coherent argument, Mark. Make an effort. Bear in mind that what we are asking for is any possible alternative interpretations of commonly located ERVs in what evolutionary science has identified as closely related species.
I did, you never addressed it in our formal debate and your debate tactics haven't improved in all the time since.



zpq0330457530001.gif
(Initial sequence of the chimpanzee genome and comparison with the human genome. Nature 2005)

Seems like we did this before, you want everyone to believe that almost 8% of the human genome is the result of dangerous germline invasions.

With more than 100 members, CERV 1/PTERV1 is one of the most abundant families of endogenous retroviruses in the chimpanzee genome. CERV 1/PTERV1 elements range in size from 5 to 8.8 kb in length, are bordered by inverted terminal repeats (TG and CA) and are characterized by 4 bp TSDs...The age of each subfamily was estimated by calculating the average of the pairwise distances between all sequences in a given subfamily. The estimated ages of the two subfamilies are 5 MY and 7.8 MY, respectively, suggesting that at least one subfamily was present in the lineage prior to the time chimpanzees and humans diverged from a common ancestor (about 6 MYA). This conclusion, however, is inconsistent with the fact that no CERV 1/PTERV1 orthologues were detected in the sequenced human genome. (Retroelements and the human genome: New perspectives on an old relation)
This indicates the Chimpanzee is being inundated by ERVs with over a million base pairs becoming permanently fixed right at the time of the split. ERV germline invasions are rare at best and to have so many, many with open reading frames is a formula for extinction. Which means you ignore the differences and overstate things in common. What you are attempting to do is evade in the inverse logic. It really is nothing more the another homology argument known as,

What they found in the Initial Sequence of the Human Genome. Their estimates apply only to the human genome, comparisons wouldn't come for several years:

112,000 ERV class 1 79.2 Mb 3.69% of the genome
8 ERV class II 8,9 Mb .31%
83,000 ERV class III 39.5 Mb 1.44%
Table 11. Number of copies and fraction of genome for classes of interspersed repeat.

These would not be compared to the chimpanzee genome until 2005. They found 73 human-specific insertions of the HERV-K and 45 chimpanzee-specific insertions, leaving ~9 human-specific insertions before dying out. This comparison put's the amount of DNA from retroviruses at 5.44%. In the Chimpanzee genome it's almost 8%, 'With more than 100 members, CERV 1/PTERV1 is one of the most abundant families of endogenous retroviruses in the chimpanzee genome.' (Nature 2005).

Against this background, it was surprising to find 234 ERV class 1 > then a million base pairs in the Chimpanzee genome but absent in human DNA:

nature04072-t2.jpg

Notice the ERV class 1 and this discussion from the Chimpanzee Genome paper:

Against this background, it was surprising to find that the chimpanzee genome has two active retroviral elements (PtERV1 and PtERV2) that are unlike any older elements in either genome; these must have been introduced by infection of the chimpanzee germ line. The smaller family (PtERV2) has only a few dozen copies, which nonetheless represent multiple (~5–8) invasions, because the sequence differences among reconstructed subfamilies are too great (~8%) to have arisen by mutation since divergence from human.

retrovirus.gif

Figure 4.4.1. Human endogenous retrovirus K (HERV-K) insertions in identical chromosomal locations in various primates

There are at least seven different known instances of common retrogene insertions between chimps and humans, and this number is sure to grow as both these organism's genomes are sequenced (see Prediction 4.5: Molecular evidence - Endogenous retroviruses)​

The essence of the argument is the strongest argument against germline invasions in the first place. They are rare and they are pretty much random. Once they hook you with the assumption that they must be the result of a germline invasion they use the probability argument for common ancestry. The only way it would be possible for mutations and insertions to be in the same place is a common ancestor. It's just another homology argument buried in highly technical viral research but it really comes down to a false assumption and some anecdotal comparisons.

The odds of a single germline invasion from an ERV is itself, astronomical. The very statistical argument my opponent is trying to make is the reason the first assumption is patently false.
 
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I did, you never addressed it in our formal debate and your debate tactics haven't improved in all the time since.



zpq0330457530001.gif

(Initial sequence of the chimpanzee genome and comparison with the human genome. Nature 2005)

Seems like we did this before, you want everyone to believe that almost 8% of the human genome is the result of dangerous germline invasions.

With more than 100 members, CERV 1/PTERV1 is one of the most abundant families of endogenous retroviruses in the chimpanzee genome. CERV 1/PTERV1 elements range in size from 5 to 8.8 kb in length, are bordered by inverted terminal repeats (TG and CA) and are characterized by 4 bp TSDs...The age of each subfamily was estimated by calculating the average of the pairwise distances between all sequences in a given subfamily. The estimated ages of the two subfamilies are 5 MY and 7.8 MY, respectively, suggesting that at least one subfamily was present in the lineage prior to the time chimpanzees and humans diverged from a common ancestor (about 6 MYA). This conclusion, however, is inconsistent with the fact that no CERV 1/PTERV1 orthologues were detected in the sequenced human genome. (Retroelements and the human genome: New perspectives on an old relation)
Which means you ignore the differences and overstate things in common. What you are attempting to do is evade in the inverse logic. Orthologs assume a common ancestor, they do not prove one. It really is nothing more the another homology argument known as, 'Sequence homology' which includes Paralogy, Ohnology, Xenology, Gametology. (see Homology) If we are going to be using terms like orthologous then it should be understood that it is a homology argument used in comparative biology. It is orthologous if and only if two species share a common ancestor. Currently I am aware of only a handful of orthologous ERVs in the human and chimpanzee genomes. It's just another homology argument and a poor one at that. Just like all Darwinian theater if it's something in common is proves common ancestry and if it's not it's called natural selection. The inverse logic is never considered because common ancestry was already assumed a priori.

That's right, they found in the Initial Sequence of the Human Genome. Their estimates :

112,000 ERV class 1 79.2 Mb 3.69% of the genome
8 ERV class II 8,9 Mb .31%
83,000 ERV class III 39.5 Mb 1.44%
Table 11. Number of copies and fraction of genome for classes of interspersed repeat.

These would not be compared to the chimpanzee genome until 2005. They found 73 human-specific insertions of the HERV-K and 45 chimpanzee-specific insertions, leaving ~9 human-specific insertions before dying out. This comparison put's the amount of DNA from retroviruses at 5.44%. In the Chimpanzee genome it's almost 8%, 'With more than 100 members, CERV 1/PTERV1 is one of the most abundant families of endogenous retroviruses in the chimpanzee genome.' (Nature 2005).

Against this background, it was surprising to find:

nature04072-t2.jpg

Notice the ERV class 1 and this discussion from the Chimpanzee Genome paper:

Against this background, it was surprising to find that the chimpanzee genome has two active retroviral elements (PtERV1 and PtERV2) that are unlike any older elements in either genome; these must have been introduced by infection of the chimpanzee germ line. The smaller family (PtERV2) has only a few dozen copies, which nonetheless represent multiple (~5–8) invasions, because the sequence differences among reconstructed subfamilies are too great (~8%) to have arisen by mutation since divergence from human.
Addressed, but you didn't like it. Busy right now. I'll be back to put you straight - again.
 
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mark kennedy

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Addressed, but you didn't like it. Busy right now. I'll be back to put you straight - again.
No you won't, I doubt you even bother to do the background reading, let along discuss the actual evidence.
 
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dad

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(Initial sequence of the chimpanzee genome and comparison with the human genome. Nature 2005)

Seems like we did this before, you want everyone to believe that almost 8% of the human genome is the result of dangerous germline invasions. .

That does seem a stretch.
 
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Larniavc

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Some beliefs are very strange, and may be worse off perhaps for it,
but
no, I think many problably believe what is posted....
the world science teaches what is false, as if it is truth,

just as YHWH says in Scripture,
and who can resist it ? 'Educated' men must go along with it, in order to maintain such a system... while YHWH permits it to go on.
Word salad.
 
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mark kennedy

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Confirmed.

How so?
Deleterious effects Barry, a virus in the germline and you can't fathom that there will be a problem? That's not just unscientific, it's insane. We know what happens because of HIV, it gets into the code and just replicates itself beyond the ability of the cell to support itself. The resultant, full blown AIDs, leaves the individual without an immune system. What happens is the T cell is attached to by the ERV and plugs into a receptor on the exterior of the cell. Once injected it gets into the DNA and when it makes it's way to the Lymph nodes it proliferates to the point where a cold can kill you. That's a somatic invasion, on a germline level this is orders of magnitude more dangerous.

Like all these arguments, it's riddled with basic fundamental misconceptions.

HIV disrupts this process by directly infecting the helper T-cells. Your initial immune response does get rid of a great deal of HIV, but some of it manages to survive and infect these important cells. Once the infected helper T-cells are activated, they work to create new viruses instead of doing the job they are supposed to do in your immune system. In addition, many helper T-cells are destroyed in the HIV replication process. (Immune System 101)
That's all viruses really do, they replicate, they are degenerative and there is no reasonable way the Chimpanzee line could have survived being inundated by such massive ERV germline invasions. This is a terrible argument.
 
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Deleterious effects Barry, a virus in the germline and you can't fathom that there will be a problem? That's not just unscientific, it's insane. We know what happens because of HIV, it gets into the code and just replicates itself beyond the ability of the cell to support itself. The resultant, full blown AIDs, leaves the individual without an immune system. What happens is the T cell is attached to by the ERV and plugs into a receptor on the exterior of the cell. Once injected it gets into the DNA and when it makes it's way to the Lymph nodes it proliferates to the point where a cold can kill you. That's a somatic invasion, on a germline level this is orders of magnitude more dangerous.

Like all these arguments, it's riddled with basic fundamental misconceptions.

HIV disrupts this process by directly infecting the helper T-cells. Your initial immune response does get rid of a great deal of HIV, but some of it manages to survive and infect these important cells. Once the infected helper T-cells are activated, they work to create new viruses instead of doing the job they are supposed to do in your immune system. In addition, many helper T-cells are destroyed in the HIV replication process. (Immune System 101)
That's all viruses really do, they replicate, they are degenerative and there is no reasonable way the Chimpanzee line could have survived being inundated by such massive ERV germline invasions. This is a terrible argument.
Oh, I do wish you could read my FAQ for comprehension. Veritas: ERV FAQ: How could a species survive a massive invasion of retroviruses into it's genome?
 
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mark kennedy

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Of course I read it and at least a dozen papers and articles on the subject Barry. I'm not misinformed, what you are pinning your hopes on is asinine.

First of all, 'How do we know the ERVs are of retroviral origin?', we don't. The link leads to a dead wiki link. Point two:

The observation that some individuals appear to possess resistance to HIV infection or its consequences has generated a host of epidemiologic investigations to identify biological or behavioral characteristics of these individuals. (Resistance to HIV Infection)
Which is an explicit reference to HIV, not germline mutations. So ERV infections can offer a defense to future ERV infections, still not seeing the point:

That is, some endogenous retroviruses are capable of enhancing the pathogenicity of exogenous retroviruses while others confer protection against infections with highly pathogenic exogenous counterparts. Most strikingly, envelope glycoproteins of endogenous retroviruses can confer protection against retroviral infections, but they have also been associated with a restriction in the ability of the immune system to combat such infections. (Interactions between Exogenous and Endogenous Retroviruses. Biomedical Science 1997)​

So what? This is saying there is even more barriers to ERV germline infects including the ERVs themselves. The rest are more of the same, anecdotal statements based on sweeping assumptions. It's not like I didn't read it, it's not actually saying anything.
 
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Of course I read it and at least a dozen papers and articles on the subject Barry. I'm not misinformed, what you are pinning your hopes on is asinine.

First of all, 'How do we know the ERVs are of retroviral origin?', we don't. The link leads to a dead wiki link. Point two:

The observation that some individuals appear to possess resistance to HIV infection or its consequences has generated a host of epidemiologic investigations to identify biological or behavioral characteristics of these individuals. (Resistance to HIV Infection)
Which is an explicit reference to HIV, not germline mutations. So ERV infections can offer a defense to future ERV infections, still not seeing the point:

That is, some endogenous retroviruses are capable of enhancing the pathogenicity of exogenous retroviruses while others confer protection against infections with highly pathogenic exogenous counterparts. Most strikingly, envelope glycoproteins of endogenous retroviruses can confer protection against retroviral infections, but they have also been associated with a restriction in the ability of the immune system to combat such infections. (Interactions between Exogenous and Endogenous Retroviruses. Biomedical Science 1997)​

So what? This is saying there is even more barriers to ERV germline infects including the ERVs themselves. The rest are more of the same, anecdotal statements based on sweeping assumptions. It's not like I didn't read it, it's not actually saying anything.
Wikispaces [bless and do not curse][bless and do not curse][bless and do not curse][bless and do not curse] on all users who trusted them to honour their promise of providing free space. The page you are looking for has been moved to Blogger. "The ERV FAQ" link links to all the FAQ pages. Here is the page showing why everyone but raving fundies conclude that ERVs are of retroviral origin. Veritas: ERV FAQ: Why do virologists and geneticists think that ERVs come from retroviruses? Isn't that just supposition on their part?
 
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