Philosophy Discussion Forums | A Humans-Only Club for Open-Minded Discussion & Debate

[JamesOfSeattle]

Because any genetic material would have to be sequestered into the human genome and directed into either a human egg or sperm without disrupting its code.

Not sure “sequestered” is the right word here. I think “incorporated” would be better. Yes, the genetic material would have to be incorporated into a cell of the host genome. That’s what retroviruses do. It’s their modus operandi. If that host cell happens to be a germ line cell, there you go.

This would have to happen randomly.

Again, modus operandi.

Maybe you have another mechanism in mind for the human genome acquiring viruses?

So the most likely time/place for a virus to infect a germ line cell would be when it is most exposed to the environment. I’m fairly certain the target would not be a sperm, mostly because 1. the sperm DNA is not in a form in which the retro viral DNA can be inserted (it’s super-compacted), and 2. the odds of any given sperm cell reproducing are minuscule (so sperm are almost always a dead end for the virus). So the most likely target would be the egg after it has been released into the Fallopian tube up until a short time after it has been inseminated and undergone several cell divisions. The germ line cell(s?) would still be exposed to the external milieux until the outside layer of the blastocyst is formed. And for what it’s worth, we know for sure that the “milieux” is full of material from an external source, because that’s what the sperm is, plus whatever viruses might be in the fluid.

Let’s say for now the virus infects the zygote. The viral DNA would get inserted randomly into the host DNA, as you say. Actually, the insertion is probably not completely random. It is most likely to happen where DNA is somewhat exposed, i.e., where the DNA is actively being used by the cell. Now you mention that the insertion has to happen where it doesn’t disrupt the host code. This is true, but given, as mentioned in the video, that the human genome is about 90% “junk”, which just means non-coding for protein, there seems to be a lot of room for safe insertion. If the viral DNA destroys a vital function, that cell dies and is thus selected against.

So now if the viral DNA finds some innocuous spot, it just sits there and the host apparatus makes lots of copies of it, one for each cell.

Now if the viral DNA turns out to be somehow useful to the host, that host will be selected for survival, and the important viral DNA will be preserved, and possibly tweaked. The non-important (for the host) DNA will come along for the ride but will get mutated without effect on the host species.

How’s that?

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[ThomasHobbes]

Because any genetic material would have to be sequestered into the human genome and directed into either a human egg or sperm without disrupting its code.

Not sure “sequestered” is the right word here. I think “incorporated” would be better. Yes, the genetic material would have to be incorporated into a cell of the host genome. That’s what retroviruses do. It’s their modus operandi. If that host cell happens to be a germ line cell, there you go.

No it would have to be successfully incorporated into a host egg or sperm and still result in a successful outcome.
Now all you have to do is ask how the **** foetus managed without the working placenta before the wonderful retrovirus made it all possible.

[ThomasHobbes]

...
Now if the viral DNA turns out to be somehow useful to the host, that host will be selected for survival, and the important viral DNA will be preserved, and possibly tweaked. The non-important (for the host) DNA will come along for the ride but will get mutated without effect on the host species.

How’s that?

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Complete bollox.
Mush more likely that the genetic material originated billions of years ago, and the virus came FROM its original.

[Mark1955]

Yet the anecdotal evidence that the source of all human-like viruses is in fact originally from humans is vast.

Setting aside the lack of value of anecdotes to a scientist, would you like to provide this evidence, then we can criticise it.

[Mark1955]

Note: This post was made by LuckyR


The build up to this can be seen here: viewtopic.php?f=12&t=15797&p=321710#p321710

Moved due to an inappropriate thread title (which cannot be editted once posted.) If anyone would like any particular posts above thread placed here please PM me and I’ll copy and paste where appropriate. Anyway, back to LuckyR’s post:

Prove it!

Here is an entertaining synopsis geared to the lay public:

The Virus and the Placenta
Boston in the mid-1990s was humming with the activity of the Human Genome Project. Sequencing technologies had advanced to the point where scientists were incorporating gene discovery into even the most basic research. Since the American courts had thus far allowed companies to patent the genes they discovered, companies like the Genetics Institute (now a part of Pfizer) saw a chance to cash in. There, molecular biologist John McCoy was looking for proteins secreted by cells since they seemed good targets for developing potential drugs.

All was going as planned until McCoy’s bioinformatics specialist Steve Howes rushed into his lab in 1997 to show him the sequence of a gene they called syncytin, which their work showed was secreted by placenta tissue.

Before McCoy could go public with his discovery, he needed to figure out exactly what syncytin did, a job he passed to bench scientist Sha Mi, who everyone called Misha. Misha’s experiments seemed to be going as planned until, a few months later, she, too, rushed into McCoy’s lab with findings of her own.

Syncytin is produced only by certain cells in the placenta, and it directs the formation of the cellular boundary between the placenta and maternal tissue. Approximately one week after fertilization, the egg, now a hollow ball of cells called a blastocyst, implants itself into the uterus, stimulating the formation of the placenta, which provides the fetus with oxygen and nutrients while removing carbon dioxide and other wastes. It also serves as a barrier to prevent infection and keep maternal and fetal blood separate. (Mixing the two could cause a fatal autoimmune response.) The cells in the outer layer of the blastocyst form the outer layer of the placenta, and those in direct contact with the uterus are the only ones that made syncytin.

When the scientists looked closer at the DNA sequence of syncytin, they found that it was nearly identical to a viral protein called env that caused the virus to fuse with its host cell. In the placenta, syncytin performed helped the fetus fuse with its mother. At last McCoy, Howe, and Mi knew what syncytin did.

“This was a bona fide retroviral envelope protein that had somehow been captured during evolution and been trained to operate in human biology,” McCoy says.

The two other retroviral genes next to syncytin, gag and pol, were completely non-functional, McCoy says. Only env remained intact. “Everything else about that retrovirus had been trashed,” he says. The team published a paper in Nature in 2000.

“An important step in mammalian evolution was accomplished by capturing this viral envelope gene,” McCoy says. “There’s plenty of examples of viruses picking up human genes, but this is one of the first examples of the reverse.”

Humans aren’t the only species with a placenta, however. All mammals have placentas, including marsupials and egg-laying mammals. Although all of these mammals have a syncytin gene, they don’t all have the same syncytin gene. The syncytin produced by mice is completely different from the two syncytins found in humans and other primates. At numerous points in mammalian evolution, symbiotic retroviruses entered the genome and steered different groups of mammals along different evolutionary paths, according to a 2012 paper in PNAS by virologist Harmit Malik at the Fred Hutchinson Cancer Research Center in Seattle. Nor was syncytin the only driver

What bugs me about this is the use of words like trained and steered. This implies agency for which there is no evidence.

For those questioning the idea that it went from virus to human and not the other way round, the fact that mice have a different gene indicates our common ancestor didn't have a common gene. When the located gene can be shown to match a suitable virus and different virii have different gene the logic dictates transfer from virus to mammal. Otherwise a group of unrelated virii would have an approximately common geen they had inherited from different mammals.

[ThomasHobbes]

Yet the anecdotal evidence that the source of all human-like viruses is in fact originally from humans is vast.

Setting aside the lack of value of anecdotes to a scientist, would you like to provide this evidence, then we can criticise it.

I've no need, since the alternative offered is probabilistically impossible.

[JamesOfSeattle]

Humans aren’t the only species with a placenta, however. All mammals have placentas, including marsupials and egg-laying mammals. Although all of these mammals have a syncytin gene, they don’t all have the same syncytin gene.

What bugs me about this is the use of words like trained and steered. This implies agency for which there is no evidence.

The use of trained and steered doesn’t bug me because these are just the terms of design, but in this context we can assume natural design, i.e. natural selection. It would be awkward to have to say “naturally selectively trained” every time.

What bugs me is how they say all mammals have a syncytin gene but they don’t all have the same syncytin gene. Are the genes homologous? Which is to say, are the sequences similar enough to indicate that they started out the same but diverged thru evolution? If not, how could they both be called by the same name: syncytin?

For those questioning the idea that it went from virus to human and not the other way round, the fact that mice have a different gene indicates our common ancestor didn't have a common gene.

I can understand seeing a problem when someone says that everything with a placenta has a syncytin gene, but they didn’t all evolve from the same syncytin gene. It seems improbable that some mammals developed a placenta by co-opting a gene from virus X and others developed the placenta by co-opting from virus Y (or some other mechanism). That said, I can imagine that all mammals started out with a placenta and a gene that performed the syncytin function. Let’s call that version 0. If after many species have diverged, one of those species gets a viral DNA into it’s germ line, and a gene from that virus performs the syncytin function better than the version 0 gene, natural selection could select for the new version, say version 1, and the old version 0 could mutate into non-functionality without harm to the species.

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[Mark1955]

What bugs me is how they say all mammals have a syncytin gene but they don’t all have the same syncytin gene. Are the genes homologous? Which is to say, are the sequences similar enough to indicate that they started out the same but diverged thru evolution? If not, how could they both be called by the same name: syncytin?

Genes are named based on the function of the protein they code, so if it does the same job it gets the same name. We start by identifying the function, then we find the protein structure, then we work out the DNA sequence. If we find, as we generally do, that related species have related DNA sequences located then the gene and the species likely evolved together. If two fairly closely related species have very different DNA codes then we need to look for other ways the gene came into existence.

[Mark1955]

Setting aside the lack of value of anecdotes to a scientist, would you like to provide this evidence, then we can criticise it.

I've no need, since the alternative offered is probabilistically impossible.

Another statement without any evidence, why is it probabilistically impossible.