Why are there no human apes alive today?

You need to keep up with your own argument. You originally brought up the ptERV sequence as evidence against common ancestry as it was an ERV found in disparate old world (specifically African) monkeys and apes but not humans. If ptERV was transmitted vertically transmitted to these species through inheritance it would completely contradict our understanding of the relationships between primate species, including ourselves. But of course if they were transmitted they would be found in the same places of the genomes of all those species i.e. the sequences would be orthologous as Taq has repeatedly pointed out. Instead the ptErv sequences are inserted randomly inserted, as expected if these were separate infection events after the species had separated, so the sequences were NOT spread through inheritance. This is why ptERV is not used for evidence of common ancestry, because it did not originate in a common ancestor.Now ptERV is only one example of an ERV sequence. Many other ERVs do exist which can be used for evidence of common ancestry because they have been inherited from a common ancestor. We know this because the insertion points are shared across species. Your argument for this has been that separate infection events in different species have inserted in exactly the same position. But here ptERV can be used as an example of what to expect if your conjecture was true, but the pattern from infection as seen in ptERV is different from the pattern seen in inheritance. It also stands to reason that species with greater sequence divergence between species will also affect retroviral insertion sites. Of course Taq has also posted that excellent article on HIV insertions which shows the relative randomness in insertions.And just as an aside, I had a quick look over the link to the guinea pig article and could find no comparison to a human ERV, orthologous or otherwise. It is recommended that you read the links you are citing to make sure it says what you think it says, otherwise people will be more skeptical of other evidence you post.
As for the source of seven shared ERVs between humans and chimps, the link only leads to a deleted blog post so can't confirm the veracity. It could be referring to ERVs only shared by chimps and humans but not any other apes, so occurred after the human/chimp common ancestor split off from other ape species.

Table 11:Initial sequencing and analysis of the human genome | NatureFrom the 2001 human genome paper:Initial sequencing and analysis of the human genome | NatureThere are 112,000 class I, 8,000 class II, and 83,000 class III ERV's for a total of 203,000.In the 2005 chimp genome paper they only found ~300 ERV's in chimps that were not found in humans at an orthologous position, and ~100 ERV's in humans that were not found at an orthologous position in chimps. That is found in table 2:Initial sequence of the chimpanzee genome and comparison with the human genome | NatureOf the 2005 chimp genome paper:Initial sequence of the chimpanzee genome and comparison with the human genome | Nature

Which ERV are you referring to? And . . ? ERV's transmitted horizontally are non-orthologous. ERV's transmitted vertically are orthologous. I have said this multiple times now. No, it won't. There are billions of hotspots. The chances of two viruses inserting into the same hot spot is 1 in 1.5 billion for HIV. Remember those calculations you keep ignoring? This is where they come in. You have yet to show how PTERV1 insertions are inconsistent with the consensus phylogeny. PTERV1 insertions are non-orthologous which is consistent with HGT. The real number is around 200,000, not 7. Only a few hundred ERV's are non-orthologous between chimps and humans. Over 200,000 are orthologous. Links can be found in my post above. You haven't cited one yet. PTERV1 insertions do not falsify common descent because they are non-orthologous. I have said this time after time and you refuse to deal with it. If PTERV1 insertions were orthologous then that would falsify the ERV evidence, but they aren't.

I stand corrected. My research was obviously not thorough enough. This leaves me with three questions.1. Is there any mechanism that would allow HGT to take place between relatively complex species without the action of an intermediary, as you describe?2. What happens to those gene fragments in translation? Do they end up in the same place in the genome of the last species in this chain as they were in the first?3. Could this happen with anything like the frequency necessary to account for all the exact ERV correspondences we see between, say, humans and chimps?ABE: I now realize the my third question is kinda stupid. HGT correspondences wouldn't be orthologous.Edited by ZenMonkey, : No reason given.

Not that I know of. Extremely unlikely. Extremely unlikely. And as noted in 2, even if they occurred with sufficient regularity they'd be in the wrong places.

Nuggin says I think you need to stop making baseless accusations. If there are more then name them. The article said 7. It doesn't matter if it is out. The person that wrote the article is a science head and likely knows as much as you guys.It is not about just the number of ERV's idenitifed to promote ancestry with chimps. It is about the fact that Horizontal Gene transfer as well as epigentic inheritance are other forms of non-vertical transmission of genes. This opens the doors to non verticle inheritance of ERV's and their 'ghost relics' being found n certain places within the genome.You do not have to believe little creationist me. This is from your body of research. The fact that you may be totally ignorant
of it is not my responsibility.Horizontal gene transfer in prokaryotes - Citizendium
http://www.mindfully.org/GE/2003/Junk-GenomeNov03.htm
Horizontal Gene Transfer Accelerating Evolution - ScienceAGoGoNot only can HGT and epigenetic information reach the germ line, some ERV's have been found to actually be required and functional. With time you are going to see more and more of this as has been the case since the articles above were written.Here is another article you may find interesting:The Perils of Dogma"IT WILL TAKE YEARS, perhaps decades, to construct a detailed theory that explains how DNA, RNA and the epigenetic machinery all fit into an interlocking, self-regulating system. But there is no longer any doubt that a new theory is needed to replace the central dogma that has been the foundation of molecular genetics and biotechnology since the 1950s.The central dogma, as usually stated, is quite simple: DNA makes RNA, RNA makes protein, and proteins do almost all the real work of biology. The idea is that information is stored in the twisted ladders of DNA, specifically in the chemical bases (commonly labeled A, T, G and C) that pair up to form the rungs of the ladders. A gene is just a particular sequence of bases on one side of the ladder that specifies a protein."
http://www.mindfully.org/GE/2003/Junk-GenomeNov03.htmHere is a bit more..."In the past, mathematical models of evolution have focused largely on how populations respond to single mutations, the random changes in single nucleotides on the DNA chain. Other theories have focused on recombination, the process that occurs in sexual selection when the genetic sequences of parents are recombined.The new mathematical model, developed by Rice's Michael Deem and visiting professor Jeong-Man Park, attempts to find out how HGT changes the overall dynamics of evolution. In comparison to existing models that account for only point mutations or sexual recombination, Deem and Park's model shows how HGT increases the rate of evolution by propagating favorable mutations across populations"
Horizontal Gene Transfer Accelerating Evolution - ScienceAGoGoThis article I believe won an award. At the moment your researchers are scurrying to invent models that are meant to address these confounding variables. Good luck to them.So it appears it is OK for Taq to swear at me and you to baselessly call me a fibber. You had best stop and try to mount some decent refute.The point I have made is that there is more than enough contradictions eg ERV's connecting humans to guinea pigs whilst not all mammals, ERVs not in humans but in other primates. tens of thousands of ERVs with few that are actually examples and many that are contradictions. This along with the possibility of HGT and ERV preferences opens the door to other ways in which ERV's can end up where they are, is more than sufficient evidence for skepticism.Additionally much of these results involve population sizes and bottlenecks. Your researchers have no idea of population size. It is based on probabilities etc. Rather they make the population size fit their model to arrive at the result they require. As for population bottlenecks they are basically fluff. TOBA and KT have much the same representation of species after the event as prior to the catastrophe. If you want links for verification because you are not up to date with the latest research just say so and request and I will provide plenty to amend any ignorance.There is also research that suggests the major sweep models your evolutionary research has been based on for the past 35 years is erraneous and simplistic.
http://www.sciencedaily.com/...ases/2011/02/110217141307.htmAll you evos pay out on creationists when we have a dig at your theory. You say your theories are backed by results that support the theory and that makes it reliable and as good as factual. Well, here is the big news. Much of data is contradictory. It is sufficiently contradictory that is is now not reliable. It has not continued to be supported and as far as I, and many other creationists believe, it has been falsified.There are no levels of falsification as just one example is sufficient to falsify any theory. There is no just a little falsified, a theory either works all the time or it does not. The fact that you continue to 'mend' your initial bases with more and more theoretical assumptions is hardly a faith changing paradigm. In fact the more a creationist learns and delves into your research, the less ignorant they are of it, all the more reasons are found for skepticism.So basically I maintain that ERV's are not a reliable, consistent determinor of common ancestry anymore, if they ever were. It is a matter of faith that you continue to regard them as a valid.I am not trying to disprove evolution. It is based on theory and assumptions as are my and any other creationists propositions. I am suggesting that there is more than one hypothesis that runs along side the theories you have re intermedites extinction.

Hi Mazzy,Normally I wouldn't see the need to call attention to the fact that Nuggin was suspended for 24 hours, but you frequently mention to me in email that you are experiencing difficulty viewing messages and so maybe you can't tell that Nuggin is suspended, so I thought I'd mention it. Suspension is indicated by a circular red icon next to the member's name. If you hover your mouse over the icon a hoverbox will appear with the time remaining in the suspension. If you click on the icon the reason for the suspension will appear.Rule 5 of the Forum Guidelines requests that you post no bare links, that you make your point in your own words and describe how the links support your point. Could you please supply this information for these links? I have examined them and do not see how they support your position. A couple of these links are to long articles, so you may want to identify just where in the article you found the supportive information: It wasn't clear how the remainder of your post addressed the topic, which conerns the details and validity of the classification system that places chimps, gorillas, humans, gibbons and orangutans in the same group. The rest of your post seemed to consist primarily of criticisms of other areas of biology.There are less than 90 messages left before discussion in this topic will end. Time is growing short. I think it is time to make progress on the ERV discussion, and if this hasn't happened within another 20 messages or so then I will constrain the topic further to exclude ERVs and focus exclusively on classification based upon morphology, i.e., Linnaean classification.I don't see how the other participants can make any progress on the ERV subtopic if your position is that if someone wrote something (in this case, that there are only 7 ERVs held in common between chimps and humans) then you're going to believe it despite quotes of and citations to the technical research indicating that whoever wrote it was mistaken. It is because of what seems like the unlikelihood of progress on ERVs that I'm going to limit further discussion on them to around 20 more messages.

Taq says It turns out that the Guinea pig also shares a non-functioning GULO gene with a few of the same deletions found in the primate GULO gene. Although there are some differences noted as well, the similarities in the deletion areas raises some serious questions about the assumptions underlying the entire pseudo-gene argument for evolution. (see below diagram). Why would a deletion occur randomly in the exact same place in the Guinea Pig and the Primate? Obviously this is not evidence of common descent since the two lineages are so separated. So what is it evidence of? This suggests that these deletions are non-random, perhaps part of a regulatory mechanism, which is more aptly described as engineering mechanisms rather than with neo-darwinian mechanisms.http://open.salon.com/...vs_evolution_and_intelligent_designThere is no point in my providing links if you are not going to read them. You should be aware of the contradictions regarding ERV's without my having to spoon feed them to you. ...and they are not found in all mammals. Hence a contradiction to the simplistic response you provided.The loss of activity of the gene for L-gulonolactone oxidase (GULO) has occurred separately in the history of several species. The loss of this enzyme activity is responsible for the inability of guinea pigs to enzymatically synthesize vitamin C, but this event happened independently of the loss in the haplorrhini suborder of primates, including humans. The remains of this non-functional gene with many mutations is, however, still present in the genome of the guinea pigs and in humans.[4] The function of GULO appears to have been lost several times, and possibly re-acquired, in several lines of passerine birds, where ability to make vitamin C varies from species to species. In addition, GULO activity has also been lost in all types of bats, regardless of diet.[5]Loss of GULO activity in the primate order occurred about 63 million years ago, at about the time it split into the suborders haplorrhini (which lost the enzyme activity) and the more primitive strepsirrhini (which retained it). The haplorrhini ("simple nosed") primates, which cannot make vitamin C enzymatically, include the tarsiers and the simians (apes, monkeys and humans). The suborder strepsirrhini (bent or wet-nosed prosimians), which are still able to make vitamin C enzymatically, include lorises, galagos, pottos, and, to some extent, lemurs.[6]
L-gulonolactone oxidase - WikipediaBesides I only need one example. Besides PTERV1 there is also HERV-K that is not found in an orthologous region in mankind.
Page Not Found - HolySmoke! Is that so? Well then you had best spek to this reseach that disagrees with you."Retroviruses normally infect the somatic cells of their host and are transmitted horizontally, i.e., in an exogenous way. Occasionally, however, some retroviruses can also infect and integrate into the genome of germ cells, which may allow for their vertical inheritance and fixation in a given species; a process known as endogenization. Lentiviruses, a group of mammalian retroviruses that includes HIV, are known to infect primates, ruminants, horses, and cats. Unlike many other retroviruses, these viruses have not been demonstrably successful at germline infiltration. Here, we report on the discovery of endogenous lentiviral insertions in seven species of Malagasy lemurs from two different generaCheirogaleus and Microcebus. Combining molecular clock analyses and cross-species screening of orthologous insertions, we show that the presence of this endogenous lentivirus in six species of Microcebus is the result of one endogenization event that occurred about 4.2 million years ago. In addition, we demonstrate that this lentivirus independently infiltrated the germline of Cheirogaleus and that the two endogenization events occurred quasi-simultaneously."
Parallel Germline Infiltration of a Lentivirus in Two Malagasy Lemurs | PLOS GeneticsNow I have demonstrated multiple times that you are wrong. Remember my request to cruch numbers for the tens of thousand of ERVs present in the human genome that could end up in certain places due to site preferences and randomness, not to mention them being there due to horizontal gene transfer or epigentic inheritance. I have provided the information for you to ignore."In this light it is interesting to note that over 30,000 different ERVs are known within human genome. 37,43 The range of the total human genome occupied by ERV sequences is anywhere from 1% to 8% - depending upon the reference (with more recent references favoring 8% or greater). The same range is true for the chimp genome as well.41 In fact, more recent work suggests a 45% ERV origin for the human genome at large (Mindell and Meyer 2001) and 50% for mammalian species in general ( Link ). In any case, of these tens of thousands of recognizable ERVs, only seven are currently known to infect both humans and chimps at identical locations within the separate genomes ( Link ). Isn't it interesting that out of 30,000 ERVs only 7 of them are known to have inserted at the same site in humans and chimps? - What are the odds given the known preference of many ERVs for fairly specific hot spot insertions? "and"Although retrovirus integration can occur throughout the genome, local "hot spots" for integration exist where a strong preference for particular sites over others can be demonstrated statistically. Recent work with HIV and murine leukemia virus has implied that there is also a preference for integration into transcribed regions of the host genome, in the case of murine leukemia virus, near transcriptional start sites. The basis for these preferences is unknown, but they may reflect interaction of the pre-integration complex with specific proteins or with specific DNA sequences or structures that are associated with transcription."
Just a moment...
Pseudogenes I missed it, but will have a look. It doesn't matter even if you are correct. The point being it takes just one to thwart and falsify theory and HERV-K is one. It also makes a mess of your primate phylogeny and separates humans from chimps. HERV-K And what did it take to say it was orthologous....dating, rather than looking for and recognizing ghosts."We performed two analyses to determine whether these 12 shared map intervals might indeed be orthologous. First, we examined the distribution of shared sites between species (Table S3). We found that the distribution is inconsistent with the generally accepted phylogeny of catarrhine primates. This is particularly relevant for the human/great ape lineage. For example, only one interval is shared by gorilla and chimpanzee; however, two intervals are shared by gorilla and baboon; while three intervals are apparently shared by macaque and chimpanzee. Our Southern analysis shows that human and orangutan completely lack PTERV1 sequence (see Figure 2A). If these sites were truly orthologous and, thus, ancestral in the human/ape ancestor, it would require that at least six of these sites were deleted in the human lineage. Moreover, the same exact six sites would also have had to have been deleted in the orangutan lineage if the generally accepted phylogeny is correct. Such a series of independent deletion events at the same precise locations in the genome is unlikely (Figure S3). . .Several lines of evidence indicate that chimpanzee and gorilla PTERV1 copies arose from an exogenous source. First, there is virtually no overlap (less than 4%) between the location of insertions among chimpanzee, gorilla, macaque, and baboon, making it unlikely that endogenous copies existed in a common ancestor and then became subsequently deleted in the human lineage and orangutan lineage. Second, the PTERV1 phylogenetic tree is inconsistent with the generally accepted species tree for primates, suggesting a horizontal transmission as opposed to a vertical transmission from a common ape ancestor. An alternative explanation may be that the primate phylogeny is grossly incorrect, as has been proposed by a minority of anthropologists." [emphasis added] 42"Inconsistencies do exist with phylogenetic analyses and are often explained by ad hoc arguments without positive evidence." ( Link - last accessed 3/10/09)Not even precambrian humans are going to falsify your theory according to you.Endogenous retroviruses may arise within genomes by at least two different mechanisms: retrotransposition from a pre-existing endogenous retrovirus (intraspecific transmission) or infection and integration via an exogenous source virus (horizontal transmission). Many cross-species transmissions have been documented and frequently manifest themselves as inconsistencies in the presumed phylogeny of closely related species. During the 1970s and 1980s, Benveniste and colleagues identified, by DNA hybridization and immunological cross-reactivity, several retroviral elements that could be found among more diverse primate/mammalian species but not necessarily among more closely related sister taxa [12,13,14]. *** and colleagues, for example, reported the isolation of a particular class of type C retroviruses from a woolly monkey (SSV-SSAV) and gibbon ape (GALV) but not the African great apes [13]. These viruses shared antigenic properties with previously described type C activated endogenous retroviruses of the Asian feral mouse Mus caroli. Cross-species infection from murines to primates was proposed as the likely origin of the retrovirus. A related endogenous retrovirus was subsequently identified in the koala, suggesting a zoonotic transmission from placentals to mammals [15]. Evidence of horizontal transmission for other families of retrovirus has been reported among classes of species as distantly related as avians and mammals
Lineage-Specific Expansions of Retroviral Insertions within the Genomes of African Great Apes but Not Humans and Orangutans | PLOS BiologyPTERV1 remains a virus that is not found in Humans and Orangs. It is theorised to be non orthologous because when these researhcers went looking for it, PTERV1 had disappeared from the human genome and a stack of convolutions are required to explain it as always. The excuse is HGT.The major point being, just one example of inconsistency is suffient and info re HERV-K is one and makes a mochery of the entire concept. I need no more that this to allege the inconsistency and unreliability of these ERV's as support for common descent.Let's move on as requested.Edited by Mazzy, : No reason given.

Hi Percy. I read your message and guess there is no point putting up the rest of the response to Taq, as I do not want to waste post space. I'll post the rest at your request if you deem it appropriate to do so.I did not see the suspension, so thanks for the info.There are inconsistencies in ERV research and this alone is suficient to provide my basis for refuting ERV's as a consistent and reliable method to determine the common descent of man and chimp. This does not disprove evolution but opens the back door to other possible explanations re ERV's being what they are and where they are in the genome.__________________________________Moving on re morphological support for creationist and evolutionary claims:Well I suppose to move on I will repost my basis for refuting Homo Erectus as an ancestor of mankind.I have posted side views of Turkana boy and comparisons for Turkana Boy to Eragaster, Rulolfensis and reconstructions. I am suggesting that their skull morphology alone exludes them as being human or even on the road to humanity. I have cited 'Lluc' that is proposed by researchers as being a flat faced ape.I have used homobaramins, however taxonomic classifications is not what is on trial here.This being the case, as well as other flat faced pimates being around, that reduced facial morphology is not necessarily a sign of becoming human. Indeed Lluc cannot be a human ancestor as he is 12myo and is classed as just an ape.I have concerns with fossils that may be representative of various individuals found and reconsituted as one.I am aware that both creationists and evolutionists do not know what the first apes looked like, whether or not they had been created or evolved. Hence the length of arms and limbs are not necessarily proof of the rise to humanity as arm and leg proportions may have lengthened or reduced in response to adaptation and future knucklewalking capability that 'evolved' independently.I suggest that assertions in relation to possibility of bipedalism as being demonstrating the rise of ape to humanity has been shown to be unrelaible, and inconsistent.I found this as a starting point:The exact criteria for membership in the Homininae are not clear, but the subfamily generally includes those species which share more than 97% of their DNA with the modern human genome, and exhibit a capacity for language or for simple cultures beyond the family or band.
http://www.sciencedaily.com/articles/h/hominidae.htmThe above article cites 97% makes a creature a memeber of homonidae. Initial findings cited somelike 99.2% similarity between hmans and chimps.The article below cites 95%.Biologist Roy Britten said that human and chimp genomes are only 95 percent similar, a slight drop from the 98.5-percent similarity previously reported. Britten based his estimate on a computer program he wrote that compared approximately 780,000 base pairs of chimp and human DNA found in GenBank.
Humans and Their Closest Genetic Cousin, the Chimp, May Not Be So Close After All | GenomewebThe article below speaks to a 6% difference.
Human-Chimp Gene Gap Widens from Tally of Duplicate Genes - Scientific AmericanTurkana bOy also has a reduced neural canal suggesting the inability of sophisticsted speach.There I say that not only is Homo erectus shown to be an ape morphologically, it also appears that your own taxonomic classification of homonidae has been brought into question.I hope to see Blevins pop in soon!Hopefully these points are sufficient for a kick-off.Edited by Mazzy, : No reason given.

GULO is not an ERV. It is a pseudogene of an enzyme in the Vitamin C synthesis pathway. This is the third or fourth time I have told you this.So which ERV are you talking about? Remember, we are focusing on ERV's. How are these non-orthologous ERV's inconsistent with the consensus phylogeny? Remember that PTERV1 paper? It said the same thing. That's what all of the research says. Non-orthologous ERV's are the result of independent insertions in two different lineages after those lineages have split from their common ancestor. This is the case for both PTERV1 and human specific HERV-K insertions. Exactly, you can have both exogenous insertions which produce non-orthologous ERV's and insertions into a common ancestor which produce orthologous ERV's. Your quote agrees with me. I did crunch the numbers. Only 1 in 1.5 billion insertions will occur at the same spot. Using HIV as the example, 80% of the time it inserts into transcriptional units. Transcriptional units make up 45% of the 3 billion base human genome. Therefore, it takes 1.5 billion insertions, on average, for two insertions to occur at the same spot. Please show me where my math is wrong.And if retroviruses insert so easily into the same position in several species then why can't we find a single PTERV1 insertion at the same spot in any species? How do non-orthologous HERV-K insertions falsify the theory? Isn't it possible for HERV-K to continue to infect the human lineage after it split from our common ancestor with chimps? No, it took sequencing of the DNA flanking the inserts. And did you read this part?"Several lines of evidence indicate that chimpanzee and gorilla PTERV1 copies arose from an exogenous source. First, there is virtually no overlap (less than 4%) between the location of insertions among chimpanzee, gorilla, macaque, and baboon, making it unlikely that endogenous copies existed in a common ancestor and then became subsequently deleted in the human lineage and orangutan lineage."They point to the fact that PTERV1 insertions are non-orthologous to evidence horizontal transfer.Citing non-orthologous ERV's does not falsify the theory. Period. If humans and apes did not share a common ancestor then ALL of the ERV's should be non-orthologous. Using your criteria, all I have to do is point to a single orthologous ERV to falsify your baramins. I have over 200,000 such ERV's.

Taq, I can refute you further and had much more to say re your previous post.We have been requested by admin to move on. Hence..let's do it and not waste any more of our limited post space!This is already one wasted post space.I have posted a start in my recent post above.Edited by Mazzy, : No reason given.

Hi Mazzy,Are you still having trouble viewing posts? I'm only asking because you said this about ERVs: But I didn't request that you move on. I said I would allow 20 more posts to make progress on the ERV topic. If it doesn't happen within 20 posts then I'm going to insist discussion move on.And then in Message 1014 you wrote about Homo erectus, Homo ergaster, Homo rudolfensis and Turkana Boy, but back in Message 973 I ruled extinct species off-topic, here is the constrained topic description again:

• The details and validity of the classification system that places Homo sapiens in the Hominidae family (popularly known as the "great apes") along with chimps, gorillas, gibbins and orangutans. Extinct species should not be part of the discussion.

If you really are experiencing a great deal of difficulty viewing posts then I think it might be a good idea to fix that problem before continuing the discussion. There's no hurry.

You haven't refuted it yet, so what makes you think you can in further posts?Admin has allowed us 20 more posts.From the PTERV1 paper:"Our data support a model where ancestral chimpanzee and gorilla species were infected independently and contemporaneously by an exogenous source of gammaretrovirus 3—4 million years ago. "
Lineage-Specific Expansions of Retroviral Insertions within the Genomes of African Great Apes but Not Humans and Orangutans - PMCThe authors agree with me. The non-orthologous nature of PTERV1 infections points to an exogenous source that infected the chimp and gorilla lineages independently after they split from their common ancestor. So PTERV1 insertions are out.Let me put this in simpler terms for you. Let's assume you have a sister, just for this thought experiment. Both you and your sister were born with around 200,000 ERV's that are found in the same spot in each of your genomes. This is due to the fact that these ERV's are in the genome of you and your sister's common ancestor (your parents). Let's also say that you and your sister have a few kids. Let's also say that your sister suffers a retroviral infection that made its way into one of her eggs. That egg went on to become one of your nieces. That niece now has an ERV that is not found in an orthologous position (the correct term is paralogous for intraspecies, but never mind that) in your children. Does this mean that your children and your sister's children no longer share a common ancestor?

Sorry Taq, I thought the request was to stop immediately, perhaps I misread Percy's comment.Let me some up by reiterating my closing line in my previous post.It takes just one example of inconstency to blow a theory apart.You have it in HERV-K. The research provides inconsistent results in primate ancestry. That's it. No amount of crunching numbers or anything else will save the day.You know, kinda like being at court and being caught out in just one fib destroys all credibility.Besides it is facing off one theory against another for example below is research that suggest perhaps mutations are not so random after all.http://www.iscid.org/...rs/Borger_SharedMutations_061506.pdfHere is another link to verify the concept has been bought mutations being random into question..
http://classic.the-scientist.com/blog/display/56267/The link below shows that HGT genes can reach the germ line as can epigenically inhereted genes, but this is by the way side as one example of inconsistency is suffient to demonstrate the inconsistency of ERV's.
Parallel Germline Infiltration of a Lentivirus in Two Malagasy Lemurs | PLOS GeneticsI only need one example of inconsistency to refute you and I have provided one with HERV-K, so it ain't going to take 20 posts at all.Using ERV's to determine common ancestry is as much a matter of faith as a creationists belief in the bible.You faith in an idea is not deemed as support, let alone evidence, for ERV's and common ancestry.Edited by Mazzy, : No reason given.

For once, you are actually getting closer.So which HERV-K insertions are we talking about? Did you read this part?"Also consistent with the hypothesis of two independent germline infiltrations, the Southern blot (Figure 2) and PCR screening (Figure 5) of pSIV insertions in six Microcebus species and Cheirogaleus did not reveal any shared orthologous insertion between Microcebus and Cheirogaleus, as would be expected under the single ancestral germline infiltration model."Like PTERV1, these are non-orthologous insertions which indicates independent insertions in the two lineages that occurred after common ancestry.