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No I still disagree. The initial infection could happily take place in the cells from which the sperm and the oocyte are derived. If this were the case then my scenario stands and it still describes initial infection leading to huge infection in sperm or oocytes.
h2
you're talking about infection of the germ line cells early on in the organism's development?
__________________ MSci MSc ARCS DIC PhD..... yes, I am bragging.
No, that's true. But if you've got a viral infection are you really suggesting that only one cell gets infected? Multiple cells get infected and then spread to others, even in locally disease.
you are looking for a germ line cell that gets infected and then the infection breaks leaving you with an ERV, a much rarer occurance than a normal functioning infection which kills the cell - I haven't heard of any viruses which ultimately don't kill the cell, though granted many retroviruses do sit in the cell for a while. while I accept your point that a number of germline cells could be infected, 50% being left with an ERV seems rather too high. It would indicate either an extremely high failure rate of viral insertion, at the very least 50% if my thinking is correct and every single germline cell gets infected.
__________________ MSci MSc ARCS DIC PhD..... yes, I am bragging.
you are looking for a germ line cell that gets infected and then the infection breaks leaving you with an ERV, a much rarer occurance than a normal functioning infection which kills the cell - I haven't heard of any viruses which ultimately don't kill the cell, though granted many retroviruses do sit in the cell for a while. while I accept your point that a number of germline cells could be infected, 50% being left with an ERV seems rather too high. It would indicate either an extremely high failure rate of viral insertion, at the very least 50% if my thinking is correct and every single germline cell gets infected.
All this is still missing the point:
First we need an infection of a germ cell
That has to go on to produce offspring
That offspring has to ultimately become an ancestor of all members of that species.
That's all well and good, there are lots of retroviruses in the world, and there will always be somebody to whom all individuals can trace a lineage. Genetic bottle necks increase this tendency. It gets tricky when you start to explain homology of ERV's between species as due to anything other than common ancestry. Here are the factors:
Retroviral integration is an essentially random process. With 3 billion basepairs in the human genome, that's lots of places to insert
The chance of any specific germ cell leading to an offspring is also pretty rare.
The odds of any specific individual becoming a common ancestor to all members of his species is pretty low.
That trees drawn from ERV presence in different species would happen to match trees drawn from anatomical data, and pseudogene data, and protein data, and gene expression data, etc. just seems to make it too astounding to consider.
Compare that to common ancestry, where this result would be the natural, expected outcome, and see which explanation is more parsimoneous.
That offspring has to ultimately become an ancestor of all members of that species.
That's all well and good, there are lots of retroviruses in the world, and there will always be somebody to whom all individuals can trace a lineage. Genetic bottle necks increase this tendency. It gets tricky when you start to explain homology of ERV's between species as due to anything other than common ancestry. Here are the factors:
Retroviral integration is an essentially random process. With 3 billion basepairs in the human genome, that's lots of places to insert
The chance of any specific germ cell leading to an offspring is also pretty rare.
The odds of any specific individual becoming a common ancestor to all members of his species is pretty low.
That trees drawn from ERV presence in different species would happen to match trees drawn from anatomical data, and pseudogene data, and protein data, and gene expression data, etc. just seems to make it too astounding to consider.
Compare that to common ancestry, where this result would be the natural, expected outcome, and see which explanation is more parsimoneous.
oh I know the point, and of course you are correct, I am just enjoying picking biological nits with a proper biologist.... these creationists get so dull after a while.
__________________ MSci MSc ARCS DIC PhD..... yes, I am bragging.
you are looking for a germ line cell that gets infected and then the infection breaks leaving you with an ERV, a much rarer occurance than a normal functioning infection which kills the cell - I haven't heard of any viruses which ultimately don't kill the cell, though granted many retroviruses do sit in the cell for a while. while I accept your point that a number of germline cells could be infected, 50% being left with an ERV seems rather too high. It would indicate either an extremely high failure rate of viral insertion, at the very least 50% if my thinking is correct and every single germline cell gets infected.
Hi Jet, sorry for not getting back sooner but I was little caught up last night in another thread...
The reason I raised the 50% figure is this: each cell that the sperm originate from is diploid, however each sperm is only haploid.
So lets say the RV inserted into chromosome 14 (randomly chosen) of the original cell. Now the are two chromosome 14s in that cell, one from the organisms mother (call it Cr14i), one from the father (Cr14ii). Only one of those chromosomes will be present in each sperm, so statistically speaking that's 50% of sperm contain Cr14i and 50% contain Cr14ii . If the RV was inserted only into, lets say, Cr14i then only the sperm carrying this chromosome will carry the ERV.
However if the RV manages to insert itself into both Cr14i and Cr14ii then every sperm will carry the ERV regardless of which chromosome 14 copy it has.
Linear Mode
