NewCreature wrote:Sure I agree that is true. With respect however to a proviral integrations and ERVs, which much of the endogenous material is assumed to be, they would functionally be the same. IT would appear that what you are asking is which would change faster a proviral integration or the retroviral particles that the infection is creating.
No this is not what I am asking, how can I make this more clear?
![Smile :)](./images/smilies/icon_smile.gif)
*I'll use an example.
Several things to keep in mind when answering this question.
Remember the frame of time we are speaking of is within the period of integration
in this scenario.
As a reminder the hypothesis is that the
ERV's are a result of multiple insertion events in a single cross species pandemic.
All insertions mutations etc, are to be interpreted by the conditions to be expected
if the hypothesis were true.
Lets say a virus infects host 1, then host 1 creates viral particles which infect host 2. Let's say it continues on down this way up to host 10,000. The virus somehow became integrated into host 1's germ cell and was passed down to his child. Are there likely to be more differences between the virus which infected host 1 and host 10,000, than there are between the integrated material between host 1's germ cell and the ERV of his progeny?
The two measurements are summarized below.
![Arrow :arrow:](./images/smilies/icon_arrow.gif)
Difference in sequence between the original virus which infected host 1 and host 10,000.
![Arrow :arrow:](./images/smilies/icon_arrow.gif)
Provirus in host 1's germ cell, the ERV sequence of all his/her descendents
at the time the last host (host 10,000) is infected.
Which one is expected to show more discrepancies?
Please be aware of the timeframe, I cannot stress this enough.
P.S. I don't think I can clarify this question any further, whatever answer you give to this will be used in the analysis to follow.
NewCreature wrote:The only benefit of the ERV sequence, above treating it is a standard proviral integration, is that heredity is another mechanism whereby mutations will accumulate in the ERV sequences (proviral integrations). Ignoring ERVs for a moment it would seem if we can show that proviral integrations mutate faster than the retroviral particles in the population it would leave no doubt that ERVs, with their added mechanisms whereby they change, change faster than a retroviral population.
We'll return to this once the questioning section is over.
NewCreature wrote:What do you think about this question?
You did not respond to this point.
We'll return to this once the questioning has been completed. Suffice it to say the evidence shows that virl material changes at a much faster rate than endogenous material. But please do not respond to this until we have completed the groundwork.
NewCreature wrote:Thankfully the viral ... by which the can be changed.
All very well and true, but not pertinent to this discussion as we shall see once we have completed this part of the discussion.
NewCreature wrote:
And the integration of these disparate(separate and unique) infections are the same. We are therefore only concerned with what must have happened. That the virus in question no longer exists doesn't matter, and in fact it isn't even sensical to compare the mutation rates (of ERV's since the dissapearance of the exogenous version of the virus to the mutation rates of the originating virus), because as you said there is nothing to compare.
No they won't be the same. They will be similar. I am not roped into one idea and during the course of investigation it is important to keep in mind that for most ERVs we don't see exogenous material in the environment capable of yielding the endogenous material. There is no reason to decree that all the reverse transcribed matter in the human genome is retroviral in origin.
You are right, they might not be. But we must examine each hypothesis critically and alone. This way we can remove each possibility. The hypothesis we are examining here is
multiple insertion events within a single pandemic. Remember this problem began when you were using the solutions of multiple hypothesis to answer the various questions.
NewCreature wrote:You where the one that asked which changed more an ERV sequence or a population of retroviruses. I was simply pointing out that changes in the ERV caused the retroviral population to stop changing, and to stop even being coded for. This is likely to be what happens in many cases of immunity.
But how can that be if a single population of virus infected multiple species? Obviously here within the context of your hypothesis the virus integrated into the genome of multiple species. The most likely scenario is a sequential integration. Don't you concur? If so then the virus must have infected the various populations for some time even after integrating into the genome of one species.
NewCreature wrote:So, lets stay on topic. The question is, does the viral material passing from host to host change at a faster pace than endogenous material passed from parent to child or is it the reverse? This is the question I have been trying very patiently to pose to you. Please, if you could, answer this question.
What is your answer to this question and why Much of the endogenous material that is passed from parent to child shows huge deletions. Heredity can account for the accumulation of mutations in the provrial integration, which is what we assume the ERV to be. Wouldn't the accumulation of mutations in the father's genome be copied into the gamete? While the female egg is a preexisting gamete from very early in a woman's life, the sperm from an older father contains the mutations in the ERVs sequence. The ERV would also be mutated by the combination of the gametes into a unique individual at conception as well.
I am sorry but this does not address the
comparison at all. I have reworded the question above marked with an *. Please send me a private message to discuss the question so we don't have to continue with this dance.
![Smile :)](./images/smilies/icon_smile.gif)
I would like to move on, as I am sure you do as well.
NewCreature wrote:
If I were to infect a chimpanzee and a human with the same retrovirus how much of the sequence of the insertions will be modified due the type(species) of cell it has infected?
I don't know.
The initial insertion would be the most similar between the two species because it would be carried out mostly by proteins within the virus itself. The propagation of the proviral sequence and course of infection will be less similar. The proteins involved will be different, and the two species may not both yield an infection, one could be immune.
Also what do you think about this?
Ok good answer I will address this once all the questioning is complete.
**Bear in mind I did not counter every point, because I did not want to bog down my post. There are many points in this post I must address later.
The focus of this post is to clarify the question which still need to be address by NewCreature.
As you have addressed one question I will pose the next question which needs to be addressed.
In your scenario, how long does it take for a single integration event to propogate, into the entire population(of a species)?Bear in mind that the scenario is multiple insertion events within a single cross-species pandemic.
I want to add that I appreciate the time you put into this discussion.