I don’t follow you. If retroviruses infect a gamete cell they can be passed on to the next generation. This is not considered contentious by anyone in the field so far as I know.
-Tim
true. but do you hear about a real time case? more then that- we know that a lots of ervs parts are functional:
so its possible that those ervs are an integral part of the human genome, and not the result of infactions. more then that- ervs origin is problematic, because retroviruses need a host in the first place to survive. so they need to evolve from the genome itself.
Yes, I have a real-time case. Not sure why that’s necessary but here you go: Insertion of a bacterial gene into the mouse germ line using an infectious retrovirus vector - PubMed
As far as functionality, yes, some ERV’s can have parts that are “functional.” But we do not identify them as ERV’s based on any status of complete absence of function, but rather that they have very, very clear tell-tale markers of retroviral structures. And as I noted earlier, we’ve even managed to reactivate one of them.
-Tim
thanks tim. i actually know about this example. remember that this case control by designer and not a natural process. but lest say that indeed in a rare case its possible naturally.
now here is some problems with ervs:
1)ervs need a host to pass to the next generation. if so- how ervs evolved in the first place?
2)we know that ervs can infact by the genome. one such example is the v-src gene from the r-sarcoma virus:
so we have at least 2 evidence that those ervs are actually created from the genome and not the opossite.
To be honest, I’m completely befuddled by this conversation. We observe in real time retroviral insertions in host DNA. We know what that looks like. We know what the structural fingerprint of those insertions contain. Yet somehow for the rarer insertions into germ lines, you demand direct observational evidence. Although the mechanics of that are well understood, and follow directly from the exact same process of retroviral infection of any other cell, somehow this raises an objection for you. So I provide a laboratory example of where they engineered a retroviral insertion method into germ lines and the process works exactly as retroviral insertions have worked for any other infection into any other cell. Yet since this was engineered it is considered invalid? This seems to be just throwing up objections for their own sake. I can discern no reason behind it.
As far as the v-Src example you gave, again, I am completely at a loss as to your point. Yes, there exists retroviruses that can by virtue of their infection cause cancer, and that cancer can spread and thus create additional copies of those viral genes to further infect the host or any other organism that comes in contact with that tumor. Yes, that happens. So what? Infections that once began as retroviral infections can spread in other ways. In far rarer circumstances. But we can observe their origin as retroviral and the dominant means of infection as retroviral.
This is all starting to sound like the same logic I hear employed by AIDS denialists. That the HIV retrovirus is not the source of the infection but the product of an immunodeficient person. As difficult as it may be to discuss evolutionary denialism, AIDS denialism is something that I think most have now long given up reasoning with. Certainly I don’t know that I’m better equipped.
As to your question of how retroviruses evolved in the first place, I would imagine much the same way as any virus evolves. Viruses employ enzymes to infect their host. And yes, viruses require hosts. Retroviruses employ an enzyme called reverse transcriptase. Which allows for a different mode of infection. Do I personally know how this all arose in a stepwise fashion? Maybe tracing it all the way back to the last common ancestor? Or abiogenesis before that? Or the Big Bang before that? Or whatever caused the Big Bang before that? And so on? No. I don’t. But neither does a forensic expert examining a crime scene need to know how guns are manufactured and how the factories were built etc. ad nauseum to trace a ballistics trajectory and demonstrate that Suzy shot Tom. If you were to accept the same standards of evidence as you would if serving on a jury with an exceptionally well forensically proven case, I think you would find the source of many of your objections no longer very relevant.
-Tim
hey tim. im with you. i dont have a problem with ervs infactions and i said that in rare cases it may be possible. my argument is that we have seen a virus that infacted by the host himself. again- the v-src gene was taken by the virus from the host. not the tipical opossite:
“The src gene was taken up by RSV and incorporated into its genome”-
so we have evidence for both kind of infactions. remember that a tipical rtrovirus is about 3-4 genes. so its likely that the origin of retroviruses its from the host itself.
even according to some scientists virus origin its from the host itself:
“Some viruses may have evolved from bits of DNA or RNA that “escaped” from the genes of a larger organism. The escaped DNA could have come from plasmids (pieces of naked DNA that can move between cells) or transposons (molecules of DNA that replicate and move around to different positions within the genes of the cell).[48] Once called “jumping genes”, transposons are examples of mobile genetic elements and could be the origin of some viruses.”
so again- how do we know what possibility its true?
Most any speculation for how retroviruses evolved may be fair game at this point, but you do not see the fully formed structures of a retrovirus in that order unless an infection originated from a retrovirus. If we find an embedded HIV sequence in your genome, we can be exceedingly confident it arose originally from an HIV infection. Not the other way around. We have no examples of a genetic sequence spawning retroviruses independent of an original infection somewhere. Whether that infection happened generations past and was reactivated in the genome, if it arose elsewhere from an infection within the genome and was duplicated to a new site, or if it was fresh from a site of infection. Whereas we have thousands of observations to the contrary.
-Tim
true. but again- its possible in both ways. myabe indeed some of the ervs are the product of infactions. but the whole argument is that ervs are only a product of infactions. and those 2 evidence i showed change this picture.
now lets assume that every erv is the product of infaction. even in this case it isnt evidence for evolution.
No, I’m sorry but the argument is not that ERV’s are only produced by retroviral infections but that they are only produced originally by retroviral infections. You can have a retroviral infection that is copied via a duplication event, transported by a tumor (itself typically caused by the retroviral infection), etc. But no, we do not have a single example of such a retroviral sequence (identifiable by your typical “fingerprint” of envelope, group antigen, reverse transcriptase, etc. elements) of genetic code arising independent of an original retroviral infection. Including the examples you provided, which themselves were instanced by an original retroviral infection.
-Tim
im not sure i understand you tim. if its possible that virus evolved from the genome (again- according to scientists) then its possible that all those ervs originally created in the current form and places in the genome (in ohter words: its not the result of infactions). and we have 2 evidence for this possibility.
Um, no. The two are unrelated, that’s a non sequitur. No one is proposing that a genome developed to the point that a fully formed retrovirus one day just sprung up from it. But rather, and this is under that very speculative hypothesis, that there was this core bit here…a component there, etc. that was maybe taken in pieces. To find a whole sequence together is something else entirely.
But I do have a way for you to test your idea. If retroviruses did spring up fully formed from genetic code inherited in our DNA, you would find at least some cases where the retroviral infection can be traced back to such a point in not just the infected patient but one of their parents as well. Same synteny. Outside of the rare freak case where a deactivated retroviral infection is reactivated by a mutation. If you think this is a significant source, which by every right it should be if ERV’s as you suggest are largely to be explained in this manner, then we should be able to trace these retroviral fingerprints hereditarily to a significant number of active retroviral infections today. Yet for some reason we don’t find them. But I welcome anyone to turn the science and medical community on its head and find these results. Imagine, someone like Ken Ham sponsoring this study and winning the Nobel Prize: I say go for it.
-Tim
first- the genes for retrovirus are all pack together:
http://www.cryst.bbk.ac.uk/PPS2/projects/CANTALE/cap1.html
so it may evolve in one step. even if not- this process can happan step wise.
im not sure what you mean by that. can you explain again? thanks.
also remember that this is not my idea but scientists one. and they are not creationists.
An analogy I could give is human evolution. As four-limbed land dwelling creatures we originally evolved from fish. But much more recently our last common ancestor was with chimpanzees. Or if you’re including extinct species the various homo species (e.g., homo Habilis) and australopithecines. What you are proposing is analogous to saying, “well, since scientists say we originally evolved from fish, why not in one step? Rather than stepwise? Both seem viable possibilities.” On a more macro scale the absurdity of this claim should be evident. Same for viruses. A bit of self-replicating RNA breaks off here. Transposable LTR elements there. Enzyme for reverse transcription. Envelope gene. And so on. And more likely across all those really fragments that are just pieced together over time. All the while you have various viruses that are doing their thing. Just like we had various amphibian and lizard and rat and lemur like creatures doing their thing before humans arrived on the scene. All with small genetic innovations.
As far as your other questions, I think I’m not sure I can explain better.
-Tim
all you need is a only about 4 genes. and remember that half a gene will not work. so even according to evolution its not a stepwise but a jumps of full genes. so i dont see a real problem. but even so- so its happaned in stepwise. what is the different if its still the result of human genome? all we need to show is there is a possibility that those ervs (not all of them) are not the result of infactions. and this is indeed what scientists claiming.
All you need is 4 genes, is that all? ;). No evolutionary scientist I know suggests we make a leap at once like that. My goodness. We do not observe evolution happening at within several orders of magnitude of that pace.
As far as merely showing that there is a “possibility” that ERV’s evolved within the genome to apparently produce modern day retroviruses, well, where do you see you’ve demonstrated that? What you’ve done is highlight the fact that some scientists have hypothesized that viruses may at some point originated in a rudimentary form from DNA (long preceding the emergence of humans and other mammals by the way), gaining new structures and capabilities over time. You’ve also highlighted that a retrovirus exists that causes cancer (which, by the way we know several retroviruses now can cause cancer and this is in fact one of the main limitations currently in gene therapy which relies on using retroviral shells for insertion). And those cancerous tumors can propagate copies of that virus as should be expected…as tumors propagate whatever is in their genome, inserted or otherwise. And of course there is an src gene found in human DNA that either got its origin from earlier retroviral insertions of the Rous sarcoma virus or was acquired by a retrovirus to form it (a process btw which is not uncommon, viruses pilfer DNA all the time, which can even on occasion result it horizontal gene transfer between organisms - not really relevant but an interesting tidbit).
So this is everything you’ve demonstrated. Which really ammounts to viruses acting like we’re used to seeing viruses act and retroviruses acting the way we’re used to seeing retroviruses act. In precise accord with every known mechanism of their behavior.
And as I mentioned earlier, if you disagree, test it. If ERV’s arose as you claim and produce retroviruses and not the other way around, then you should expect to trace a significant number of active retroviral infections today to one of the patient’s parents. Just as you can trace genetic markers for cancer. Or your genes responsible for giving you blue eyes or brown. All you need to do is sequence the retrovirus that the patient is infected with, sequence their genome, and then sequence the genomes of their parents. What you will look for are “ERV’s” with a matching genetic sequence to the retrovirus…and here’s the important part…a matching “ERV” in one of their parents with the same shared synteny (relative location) as you would find for any other inherited sequence of genes. Answers in Genesis once sponsored a geological dating “study.” If you really want to test your idea I suggest appealing to those creationist organizations with deep pockets such as AIG and ask them to fund such a study. Just keep in mind though, the medical and scientific community has never found what you would be looking for. But as a bonus, whoever found such a result would almost be guaranteed to win the Nobel Prize.
-Tim
we are not talking about evolution of genes but a stolen genes. its a different process. half of a gene will not work in this case. so the virus need to steal the whole gene\genes. here is a similar example:
1)with the fact that virus need a host and cant survive without it. all experiments so far support this conclusion. so why we need to believe against the scientific experiments?
2)we know that virus can steal genes.
3)we know that a lot of them functional. what is the chance that a virus infacted someone and it not just help him but also get fix in the entire population about 100,000 times for the about 100,000 ervs in the genome?.
4) we found ervs that contradict the animals phylogeny.
5) experts in the field claim this with their evidence:
so again tim- we have a good evidence for this possibility.
Dcscccc,
At a minimum, I usually understand what argument you are trying to make and how it relates to your position as a creationist. In this case, I am at a loss.
What exactly is your reasoning here and what goal is it supposed to accomplish? How does it relate to the question of common descent, let alone to the discussion about Vitellogenin? What is it designed to explain and how does it help your cause? Tim might understand what you are trying to get at, but for the life of me, I can’t see what the overall point is, regardless of lower level case that you seem to want to make (I think unsuccessfully, but it is irrelevant if it doesn’t support any meaningful overall argument). I would appreciate your clarification on this.
i think you should ask tim this question.
Why? You are the one who introduced the tangent by asking the first question, so I can’t imagine that Tim will be in a position to explain your motivation for getting into it. Were you just curious? If there is no overall argument that you were aiming at then my mistake!
Hey @DennisVenema
Looking at just VIT1 (or VTG1), your diagram showed it sitting alongside ELTD1. Of course the shared synteny extends much further than that. If you wanted to, you could have shown many more genes from that region in a diagram that looks like this
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