You may be smarter than the average bear but you are not smarter than the average human, that being me.Maz, do you understand that the frequency of ERV's ever attaching themselves successfully to genome is a very very rare event? You might as well try to dispute the lottery since no lottery winner has ever come from a laboratory experiment.
I believe that I can count the number of different ERV's between chimp and man with the fingers of one hand (of course I am smarter than the average bear so that number may be higher than you would first think). That makes it a very rare event since there were millions of years since the separation.
When you finally decide to actually address my post and the points and questions I present then you can reply to me.
For the moment this waffle, with NO research means you are a lazy quacker and will never win any point on a properly moderated one to one debate.
I can provide numerous examples of non shared and missing ervs. Why should I bother? I support each and every claim I make usually with peer reviewed researh and I have to put up with the likes of quackers like you and Dude providing nothing more than hot air that is usually outdated.
Here Dude is some support for a creationist paradigm.
Recent evaluation of the human genome sequencing data revealed that about 9% of the human genome is comprised of elements with long terminal repeats (LTRs)(LTR retrotransposons)(36, 43, 84) comprising over 200 families (30). The majority of these LTR elements, however, lack sequence similarity to retroviral genes within their internal region or constitute solitary LTRs.
Furthermore, there is evidence that transcription of at least some HERV families may be differentially regulated depending on the cell type. Characterization of promoter activities of HERV-K, HERV-H, HERV-E, ERV9, and HERV-W families, the most intensively studied HERVs, revealed specific cell type preferences for each HERV family, and even individual elements of one family showed significant variation in transcription pattern. In some cases, transcription factor binding sites that interact with cell type-specific nuclear factors could be identified, demonstrating that the expression of HERVs is regulated in a complex and diverse manner comparable to cellular genes.
What Made the Same ERV Transcribe Differently Among Different Cell Types Within the Same Organism? Design explains it, not evolution.
Why are there NO Examples of an ERV that Has Been Recently "Endogenized" or Examples of ERVS that Have A Direct Exogenous Counterpart?
Because ervs are not the remnants of past retroviral infections. If they were and if so many had endogenized so much evos should be observing numerous examples now and the fact is they are not.
Above is just one line of evidence that evos are grabbing at sraws using a crytal ball and in actual fact there is no evidence that retrovirus can or do endogenize at all.
Rather the data demonstrates functionality and genomic material being positioned right where it needs to be to perform the function evolutionists spent over a decade telling us they did not have.
Hence, again, creationist claims and predictions are being validated in time whilst evolutionary claims and predictions are gradually being falsified and reinvented.
Go get a life Subby. Your point score demonstrates you actually do not have one!