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This seems prity relavent, any comments in reference to the Comment:

http://creationevolutiondesign.blogspot.com/2006/12/neanderthal-genome-my-testable.html

Hi

Because we share some alleged ERV's with chimps. It is thus suggested as proof for our common descent, that we both must have originated from a specie that was infected by this virus. The first problem with this argument is that it's hard to tell what an ERV is when you meet one. It doesn't come with a tag attached saying: "This is an ERV". It could be that some genes which we expect to be ERV's aren't ERV's but something completely different, or it could even be junk genes, byproduct. That is because a virus will rarely be embedded in it's complete form. To explain this, let my use a simplified example. Imagine a woman who has a flu and the virus gets embedded and passed on to a fertilized egg cell. This is of course unlikely because the common flu virus is usually not located near the ovaries, but indulge me for the sake of argument and simplicity. The child would have a flu in every single cell of his body. His cells would constantly reproduce this virus, and spread it throughout it's body. You can imagine this fetus doesn't have a fighting chance from the start on. No, for an ERV to be passed down trough generations, it has to be rendered harmless first. So how do you recognize it as a virus after this rendition to harmless junk then?

 

A second problem of the argument, is it's slippery slope. What if both chimps and humans were infected by the virus, and both got ERV's in a similar fashion? After all, given their similar physiology, that seems reasonable enough right? Well the reply from evolutionists is, that the ERV is specific in a certain locus (place on the genes) and it is improbable for both chimps and humans to create an ERV at the exact same spot. However, I disagree. There is a recent discovery at the university of Pennsylvania US that shows a human DNA-associated protein that would dictate where on the DNA AIDS is to be inserted. The protein called LEDGF would travel along with the retrovirus in it's mantel and then modulate where in the human genome the virus is inserted. So if retroviruses can be locus specific, then loci-specific ERV's is no longer a problem for creationists. It is then a matter of simple causality. Not only similar results by common design; but also similar results by similar processes of viruses become endogenous.

Hi Guys,

Here is a quote from the original post;

First and foremost, Of a genome that is 6 billion bases long, what are the odds that a ERV will be inserted into the same place? 1 in a 6 billion, right? Now, if there are 2 such ERVs, the odds are 1 in 6 billion times 1 in 6 billion for both being inserted into the same places by chance. If there are 3, you must multiply by another 1 in 6 billion. Now, since you have 12 such insertions in humans compared to the common ancestor, you have just passed the creationist number for it having occured by chance! By creationism's own criterion, their argument is invalid. The only creationist rebuttal to this is that there are hot spots, where the odds of a virus being inserted are slightly higher than other places, but there are still a great number of hotspots throughout the genomes, and given the above points, there is no reason why multiple infections would result in the same ERVs being inserted in the same locations with the same crippling errors and showing the same pattern of change with time. Again if there are multiple hotspots and multiple infections, there is no reason that there should not be ERVs that do not match the phylogenetic tree. again we see no deviances from expected inheritance patterns.

In respect to the insertion selection site. Does this recent scientific discovery have any relavence to this subject:

http://www.nytimes.com/2006/07/25/science/25dna.html?ex=1311480000&en=34d8e6ced8d42f47&ei=5089&partner=rssyahoo&emc=rss

A small snippet:

Biologists have suspected for years that some positions on the DNA, notably those where it bends most easily, might be more favorable for nucleosomes than others, but no overall pattern was apparent. Drs. Segal and Widom analyzed the sequence at some 200 sites in the yeast genome where nucleosomes are known to bind, and discovered that there is indeed a hidden pattern.