Endogenous retroviral elements as proof of common descent

My thread, Most convincing evidence for evolutionary theory has been hijacked by this topic. While it is interesting and related to my topic, a prolonged discussion on it isn't required for that thread. So, I am moving the discussion to here.I shall first quote what iceage said to explain the topic in post 72. IamJoseph disagrees with this, as evident in post 75. I summarised in post 99, in a reply to IamJoseph, with this picture: and challenged IaJ with this: IaJ couldn't offer a retrovirus specifically, but given that some other viruses can have broad host ranges, I accepted the possibility that a cross-species retrovirus may exist (or have existed).Thus, I offered another investigation to distinguish between IaJ's opinion and my own: location of the retroviral elements: That's where it stands now. Further discussion, of which I'm sure there will be much, can now come to this thread, leaving my other one to do the job for which I created it.

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Thread moved here from the Proposed New Topics forum.

There is a good summary of some ERV based argumentation in the ERV's: Evidence of Common Ancestory thread, as well as some nice pictures of where some actual insertions occur in primate phylogenetic tree.TTFN,WK

Thanks Doddy
I am happy to shift discussion to this thread. I was not trying to hijack the topic on the "evidence" thread. I am learning about the subject. I initially heard it explained by a genetic scientist at Auckland University, I was intrigued and I would like to be able to use the information to explain evolution to creationists.

This is in reply to IamJoseph's reply to me in Message 110. No it wasn't, it was expressed as relating to 'lifeform transmission', whatever that means. Just look back at what you wrote, no evolution anywhere in that first paragraph. This has nothing whatever to do with the discussion. Why would you prefer me to acknowledge something that has never really come up between us? What your basis is for separating humans into a kind of their own is irelevant to the fact that you still then need to demonstrate the 'cross-kind' infectivity of whatever virus you think is responsible for the similar insertion sites. But your description of 'cross-species' is nonsensical unless you mean two species before an after anagenetic speciation. Given you say it relies on speciation and specify that speciation 'is a perishment of a life form.' the only concievable way this can be coherent is if you are talking about the anagenetic origin of a new species evolving, or elevating if you will, from an ancestral population. This is pretty much just gobbledigook. The premise of adaptation is not that organisms are perfect, so the fact that they are prone to disease and infection is not germane. The fact that traits often evolve which act to reduce the impact of a virus or even to ameliorate or obviate a disease show that adaptation does occur. The fact that viruses then themselves adapt to work around such evolved defenses, as they do around artificial defenses such as antivirals, is just further evidence for adaptation. This doesn't address anything in the paragraph it is supposedly responding to. A single host dying of a fatal virus has nothing to do with speciation and certainly noting to do with the lateral transfer of gentic material between hosts. Does my premise become dented? Not particularly, because as I pointed out before it isn't the mere existence of a retroviral sequence in the genome which is considered compelling evidence, it is the location of that sequence. The reason it was off topic is because it is a detailed discussion of the validity of one specific evidence for evolution when the point of the thread was to have people suggest lines of argument or evidence they felt were successful.TTFN,WK

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WK

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No it wasn't, it was expressed as relating to 'lifeform transmission', whatever that means. Just look back at what you wrote, no evolution anywhere in that first paragraph.

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Evolution is about the process of changes and graduations - namely transmissions in life forms.

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This has nothing whatever to do with the discussion. Why would you prefer me to acknowledge something that has never really come up between us? What your basis is for separating humans into a kind of their own is irelevant to the fact that you still then need to demonstrate the 'cross-kind' infectivity of whatever virus you think is responsible for the similar insertion sites.

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It is relevent. If one makes categories, then the issue concerns fulcrum difference separating the categories. Q: What separates humans from all other life forms?

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The fact that traits often evolve which act to reduce the impact of a virus or even to ameliorate or obviate a disease show that adaptation does occur. The fact that viruses then themselves adapt to work around such evolved defenses, as they do around artificial defenses such as antivirals, is just further evidence for adaptation.

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The issue here is whether the host can reject an alien component embeded by a virus in the host dna, or only the virus' 'harmful' effect.

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This doesn't address anything in the paragraph it is supposedly responding to. A single host dying of a fatal virus has nothing to do with speciation and certainly noting to do with the lateral transfer of gentic material between hosts.

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Speciation cannot occur with harmful factors being transmitted - it will destroy both the precedent and follow-up species. A factor embedded in a dna which accounts for a new species, is a harmful factor from the premise of its destruction of that species; it ceases being an adaptation of that species.

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Does my premise become dented? Not particularly, because as I pointed out before it isn't the mere existence of a retroviral sequence in the genome which is considered compelling evidence, it is the location of that sequence.

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What this says is a new species has no control in its survival.

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The reason it was off topic is because it is a detailed discussion of the validity of one specific evidence for evolution when the point of the thread was to have people suggest lines of argument or evidence they felt were successful.

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Are these not directly inter-related: to arrive at what is successful, one eliminates what is not?

Hi, this is a reply to IamJoseph's reply to Coragyps in Message 147
I just thought it would be more on topic here. In your previous posts you have suggested that the existence of viral DNA in an apes genome means that the ape somehow lacked an immune system and therefore this virus should eventually kill the ape (I am unsure if you are referring to an individual ape or this ape population). However, as Coragyps was pointing out, even with a fully functioning immune system you can still be infected by a virus, still develop symptoms to the infection, without it being a long term detriment to your health or survival.Although the immune systems initial generic response to a virus can limit its ability to infect host cells, it takes time to mount a pathogen specific response to attempt to eradicate the virus. This takes the form of antibodies to bind to free viral particles to prevent the infection of new cells, and the priming of lymphocytes to locate and kill cells already infected, which are identified by viral proteins on their surface.Now usually this adaptive immune response is successful in removing the virus. However, some viruses are capable of becoming latent, they stop replicating and their DNA or RNA sits unexpressed in an infected cell effectively dormant. In this state there are no free viruses for antibodies to target, there are no viral proteins being presented on the infected cells. As far as the immune system is concerned, the virus is gone. Take cold sores for example, as mentioned earlier, which is caused by the herpes simplex virus (usually HSV-1). The cold sore heals as the immune system deals with the infection and the virus enters its latent phase, with its DNA hiding in nerve cells. If at a later date the immune system becomes depressed, the viral DNA reactivates and starts to create more viruses. A new cold sore forms and again the immune system moves in to bring everything to a halt. The infection comes and goes but the viral DNA will remain for life.Now herpes viruses don't integrate their DNA into the infected cells genome, it remains free-floating in the cytoplasm. Retroviruses, including HIV, do integrate directly into the hosts DNA due to their method of replication (look back at Doddy's post 99 on the other topic for more details), and they can also become latent. Latency does not only occur in the cells HIV targets (CD4+ T lymphocytes). Latent reservoirs can also occur in macrophages or microglia of the central nervous system, which is why HIV has been impossible to eradicate with conventional antiretrovirals.It is likely that a retrovirus became latent in the DNA of an ancestors gametes (sperm or egg cells). This DNA was then passed down through the generations from parent to child along with the rest of the genome. As this process continues, the viral genes acquire mutations which neutralise the it.
This is where your misunderstanding of speciation is causing problems with understanding. Speciation is a gradual process over many generations, yet you seem to think a new species somehow spontaneously appears, replacing the old species which dies out, and somehow these endogenous retroviruses jump to the new species. This is wrong, as endogenous retroviruses (ERVs) have been passed from ape to human the same way as you have inherited your genes from your parents.
(Sorry if I've misunderstood your position, I've just gone with my understanding of what you've written. If you want to understand speciation, I would suggest starting a new topic)
As for the ERVs themselves, they have been identified in our DNA through the human genome project. They have a standard structure of GAG-POL-ENV. The gag and env make the viral capsid and surface receptors, while the pol makes the enzymes necessary for replication. These enzymes have also allowed the viral sequences to copy themselves multiple times throughout our genome.Anyway, got to run. Hope this has helped in your understanding.

IaJ, even though the replies to your comments are clear and simple, you still seem to be missing the whole point of the "retroviral insertions" thread.
It is frustrating to those who want to discuss the topic with a common understanding being the background.
By the way, were you aware that about 8% of the human geonome consists of retroviral remnants?

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IaJ, even though the replies to your comments are clear and simple, you still seem to be missing the whole point of the "retroviral insertions" thread.
It is frustrating to those who want to discuss the topic with a common understanding being the background.
By the way, were you aware that about 8% of the human geonome consists of retroviral remnants?

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I was not intending to disrupt a good debate. I simply wanted to identify the parametres of evolution and its correct applications. I think a counterpart thread in the 'science' sector is needed, one which identifies anomolies and limits of evolution - else a faulty mindset can develop there are none! Creationism is thus miss-repped as non-science, and becomes a self-styled religion of its own. Evolution, science and medicine was introduced in a religious document - we tend to forget this!

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Although the immune systems initial generic response to a virus can limit its ability to infect host cells, it takes time to mount a pathogen specific response to attempt to eradicate the virus. This takes the form of antibodies to bind to free viral particles to prevent the infection of new cells, and the priming of lymphocytes to locate and kill cells already infected, which are identified by viral proteins on their surface.

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No dispute here. But the premise of not identifying a dna-embedded destruction of a species, which is the ultimate foundation of speciation, is the operable factor here, and not to be confused with accepted, garden-variety immunisation of a killer virus of certain effected apes. Its not about fighting a cold virus.

fair comment. No idea what you mean by that last bit, but as you say, it belongs somewhere else. Lets get back to the topic......

I think, IamJoseph, that you have cluttered up enough science threads with nonsense.Please refrain from commenting in areas that you no absolutely nothing about. Read what is explained to you much more carefully and ask thoughtful questions.In addition, you need to go back and support a large number of unsubstantiated assertions. I think you "accurate calendar" was about the first. We'd expect appropriate Biblical passages for that support in an appropriate thread.I'm giving you 24 hours this time. That will allow you to take the time to read more carefully and research those claims of yours that need to be supported.Enjoy the break.

Since you are just making up your own terminology here it would be helpful if you explained it a little. Are you using transmission here to mean any exchange of genetic material? A: Lots of things, the power of speech is only one such factor.Similarly there are many common features shared by humans and other life forms, and every species has something which separates it from all other life forms, in terms of classification. Unless that inserted viral DNA is itself harmful, such as in the case of a viral insertion causing cancer, then it hardly requires one.As it is there are mechanisms which appear to attack viral genetic material in the cell, but I am not aware of any which are proposed to act upon it once it is incorporated into the genome. If the incorporated material changes the cells physiology/morphology significantly then other areas of the immune system might well act upon it. If such an insertion occurred in a gamete/zygote it might well evade any immune response and unless it was detrimental to the host organism it would be propagated, as is thought to have been the case with endogenous retroviruses.So in brief I would say that the host is only likely to 'reject' alien DNA insertion to the extent that the inserted genetic material is harmful. This 'rejection' need not be active, it may simply be that the cell with the insertion fails to have any progeny or dies out without passing on the inserted DNA. That seems highly likely to me. Any species only has a say in its survival to the extent that its phenotype, dictated in large part by its genetic complement, allows it to survive in its environment. To a large extent the control is by the environment and changes in that environment. A population does not elect to become a new species.I can't quite see what this observation has to do with the patterns of retroviral insertions I'm afraid. The process of elimination only really works in such a context if you have an initial panel of suggestions to start with. The originating thread was more to elicit suggestions for such a panel rather than to discuss in depth the specific suggestions.Admittedly your contributions might also have been better received if they had been coherent either scientifically or grammatically.TTFN,WK

Speciation is not some kind of 'relay-race' where one species dies off and is replaced by another. Populations acquire changes over time until eventually they have become sufficiently different from the parent population to be considered a new species (bear in mind that the concept of 'species' is a human construct to aid in classification). Remember this gradual process of speciation can give rise to several daughter species, but this does not require the 'destruction' of the parent species to proceed.Endogenous retroviral DNA is not a mechanism for the process of speciation, this DNA has simply come along for the ride as it is inherited from parent to child. The reason it was put forward as evidence for evolution in the other topic is that the presence of this DNA, and its location in the genome, indicates how different species are related. For example the indentification of ERV DNA in human and other great ape genomes have shown how we are related, and indicates a common ancestor for this genus.The point I was trying to make in my last post was that the presence of this ERV DNA would have started out as a garden-variety immunity to a virus. An effective immune response forces some viruses to become latent i.e. stop replicating. This means they can hide from the hosts immune system, but it also means they are trapped in the infected cell.
Now in the case of retroviruses, as has already been stated, the viral DNA has already inserted itself into the infected cells DNA, but as it is in a latent state this DNA is unexpressed. If this infected cell is capable of duplicating itself, for example it is a stem cell for producing sperm, then it will copy the viral DNA as part of the duplication process, transmitting it to all daughter cells produced. If one of these sperm cells go on to fertilise an egg, the resultant child will also carry this viral DNA in every cell of the body. Of course as this ERV DNA has been repeatedly copied it has acquired mutations, inactivating it or at the very least reducing its virulence.

I confess I haven't read much of either topic, but I felt the need to ask if the content of What about those jumping genes? might have any relevance to this topic? At least superficially, it sort of looks like the "What you think happened" diagram in your message 1.More so, I need to go to bed.Moose