I've already debunked the erv hypothosis with factual data.
All you did was link to a video that I have already refuted. You haven't presented any data, so to claim that you believe in some mysterious non-existent data is simply dishonest.
Let's see if you can answer one question. How can you argue that ERVs are not the result of retroviral insertion when we can watch retroviruses produce ERVs both in the lab and in the wild. Here is more from another thread that you are still avoiding. You can't claim you have debunked anything until you address the actual hypothesis:
We identify them as retroviruses because ERVs have the usual complement of viral genes flanked by long tandem repeats (LTRs) at the beginning and end of the ERV.
On an interesting note, scientists have aligned these different ERVs, found the consensus sequence, and reconstructed a model ancestral viral genome. What they got was a functional retrovirus:
“Here, we derived in silico the sequence of the putative ancestral “progenitor” element of one of the most recently amplified family—the HERV-K family—and constructed it. This element,
Phoenix, produces viral particles that disclose all of the structural and functional properties of a bona-fide retrovirus, can infect mammalian, including human, cells, and integrate with the exact signature of the presently found endogenous HERV-K progeny.”
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1665638/
One important thing to note is that they had to remove the mutations from these sequences in order to get a functional retrovirus. This is NOT consistent with a scenario where widely shared ERVs are the source for new retroviruses. If ERVs were producing new retroviruses then you wouldn’t need to remove the mutations as part of a consensus sequence in order to get a functional retrovirus. The evidence is clearly in favor of ERVs being the product of retroviral insertions in the past which have accumulated mutations since insertion.
So why can ERVs be used as genetic markers, and a test for common ancestry? As stated earlier, part of the viral life cycle is insertion into the host genome. The human haploid genome is around 3 billion bases, as is the genome of other ape species. That’s 3 billion possible places where these retroviruses can insert. When viruses insert into the genome, they don’t insert at just one base. They insert all over the place. In this study, scientists infected cells with three different retroviruses: MLV, HIV, and ASLV. After infection, they mapped where the viruses inserted into the host genome. Below is map of where those viruses inserted, broken down in the 23 human autosomal chromosomes and the X chromosome.
Relationship between Integration Sites and Transcriptional Intensity in the Human Genome
The human chromosomes are shown numbered. HIV integration sites from all datasets in Table 1 are shown as blue “lollipops”; MLV integration sites are shown in lavender; and ASLV integration sites are shown in green. Transcriptional activity is shown by the red shading on each of the chromosomes (derived from quantification of nonnormalized EST libraries, see text). Centromeres, which are mostly unsequenced, are shown as grey rectangles.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC509299/
As everyone can see, the viruses inserted all over the place, into all chromosomes.
I can't really believe we have come to science to having to verify their hypothosis. Then how the neck do you believe in anything science stats. By your definition your erv argument is worthless. You can't verify thsts it's a fact because science doesn't verify.
The distribution and sequence of ERVs are facts, and they verify the hypothesis that humans and chimps share a common ancestor. That's how science works. You verify hypotheses with facts.
