Retrovirus infection of germline confirmed in vivo

_{April 8, 2008

Intelligent Design}

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There was some discussion here in the past year or so of whether retroviruses could indeed infect a germ cell and hence leave deactivated heritable fingerprints in descendents. Mike Behe mentions these retroviral markers as convincing evidence (to him) of common descent, at least in the primate lineage including humans and chimps. This experiment pretty much settles the question.

The testis and epididymis are productively infected by SIV and SHIV
in juvenile macaques during the post-acute stage of infection

Miranda Shehu-Xhilaga*1,2, Stephen Kent3, Jane Batten3, Sarah Ellis5,
Joel Van der Meulen1,2, Moira O’Bryan4, Paul U Cameron1,2,
Sharon R Lewin1,2 and Mark P Hedger4

Published: 31 January 2007
Retrovirology 2007, 4:7 doi:10.1186/1742-4690-4-7

Abstract

Background: Little is known about the progression and pathogenesis of HIV-1 infection within the male genital tract (MGT), particularly during the early stages of infection.

Results: To study HIV pathogenesis in the testis and epididymis, 12 juvenile monkeys (Macacca nemestrina, 4–4.5 years old) were infected with Simian Immunodeficiency Virus mac 251 (SIVmac251) (n = 6) or Simian/Human Immunodeficiency Virus (SHIVmn229) (n = 6). Testes and epididymides were collected and examined by light microscopy and electron microscopy, at weeks 11–13 (SHIV) and 23 (SIV) following infection. Differences were found in the maturation status of the MGT of the monkeys, ranging from prepubertal (lacking post-meiotic germ cells) to post-pubertal (having mature sperm in the epididymal duct). Variable levels of viral RNA were identified in the lymph node, epididymis and testis following infection with both SHIVmn229 and SIVmac251. Viral protein was detected via immunofluorescence histochemistry using specific antibodies to SIV (anti-gp41) and HIV-1 (capsid/p24) protein. SIV and SHIV infected macrophages, potentially dendritic cells and T cells in the testicular interstitial tissue were identified by co-localisation studies using antibodies to CD68, DC-SIGN, ??TCR. Infection of spermatogonia, but not more mature spermatogenic cells, was also observed. Leukocytic infiltrates were observed within the epididymal stroma of the infected animals.

Conclusion: These data show that the testis and epididymis of juvenile macaques are a target for SIV and SHIV during the post-acute stage of infection and represent a potential model for studying HIV-1 pathogenesis and its effect on spermatogenesis and the MGT in general.

Comments

Perhaps the designer, introduced new information so that the lungless frog could breath out of it's skin.DeepDesign_{April 10, 2008
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What does this finding do to ID? http://www.hindu.com/thehindu/holnus/008200804101021.htmDeepDesign_{April 10, 2008
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bFast, why is everybody verifying the evolutionary hypotheses? It's not interesting and there is plenty of opportunity to falsication nowadays. That's how the scientific method supposed to work. What counts is the details. I looked into the details of the human chromosome 2 fusion; It is only superficially in accord with evolution. You can find the details here: http://www.volkskrantblog.nl/bericht/150215 There is too much talking and too little science.peter borger_{April 10, 2008
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RichardFry, 5-10 million years is the max. The actual time span could have been much less but we have no way of measuring it to that detail. If there are several more Cambrian finds then the numbers could change. I am not sure how much you know about the Cambrian Explosion but there was a time period for which very little was found and then a relatively short time later all the modern phyla of the world appeared. And there was zero evidence for a gradual transitions or any predecessors. What has happened in any 5-10 million year period? Usually not much. What has happened in the last 10 million years? Humans but what else? You may be able to point out a few interesting changes but most of the present species have not changed a lot. For example birds are still birds after 140 million years. There are lots of varieties but they are still birds.jerry_{April 10, 2008
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Allen MacNeil says "And once again, I would like to stress that the answer to this question is not natural selection, if one considers it to be a mechanism for generating new phenotypes. It isn’t; it only preserves a small fraction of all of the possible phenotypes that the “engines of variation” can produce. It is these “engines of variation” ...." The engines of variation are out there and incredibly powerful, got it. However, it seems the engines of variation never was the weak link, and we still have a problem. Picture a corporation. OK, the R&D Department (engines of variation) is extremely prolific, lets take that as a given. But also a given is that they are extremely independent, and work undirected, so they create all sorts of conceivable new product concepts. Now, every new concept, good or bad, must be deployed and tested in the marketplace, where natural selection takes place (customer purchases). So, what is the choke point, the critical path that takes the greatest amount of time)? It is not the R&D process that you seem to focus on with such great zeal! It is the assembly lines. An assembly line must be established for every new concept/variation. And then, depending on customer purchases (survival and reproduction), every assembly line must either be expanded or closed down. This is a logistical nightmare, to say the least!! Re: Haldane and others. Further complicating things, new concepts coming out of R&D cannot explain the products currently on the market. Rather, large groupings of assembly lines must somehow be integrated together, in perfect order, to explain the immense complexity of today's products. It's the irreducible complexity thing all over again. All this, and we are still focused on the brilliant but misguided minds/brains in R&D. Hmmm. Is this any way to run a business, or your local biosphere for that matter?Ekstasis_{April 10, 2008
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bFast (#44): Believe me, I have absolutely no religious reasin to reject common descent. My religious faith is perfectly compatible with it. Indeed, I do provisionally believe in common descent. And yet, I believe that the issue should remain open to discussion because the evidence, though certainly substantial, is not really strict. And above all, admitting common descent does not necessarily mean admitting "universal" common descent. There is at least one major step which can in no way be explained by "descent with modifications", and that's OOL. Allen MacNeill may choose not to consider it, but I think that all of us in ID are, justly, very interested in it. There is no reason, neither logical nor empirical, to believe that OOL is not a fundamental issue to understand successive evolution. After all, the principles, forces or whatever which have designed the first forms of life can well have been active in their successive evolution, and even some modalities, but not necessarily all of them, could be in common. And OOL has nothing to do with common descent. Moreover, the information issue is similar in both OOL and successive evolution, even if I believe it is a little bit tougher in OOL. Therefore, common descent is certainly the most reasonable hypothesis, at present, about one aspect of the modalities of biological information implementation: in other words, we can say that probably the new information necessary for macroevolution may well have been implemented "over" existing forms of life. There are certainly evidences for that. But the issue, and its unknown details, should remain open. Regarding Allen MacNeill's "engines of variation", I can only restate what I have already said many times: they are either "variations of random variations", adding nothing to RM + NS, or obscure references to unknown organizing principles, much more metaphysical than the hypothesis of a designer. It is significant, however, that Allen MacNeill, with all his openmindedness (which I certainly am more than willing to recognize), still does not feel like including, even hypothetically, the action of a designer among his "engines of variation". In the end, the real ideological problem is always there: the most likely explanation is not even considered.gpuccio_{April 10, 2008
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RichardFry, "Again, 5-10 million years is not abruptly." That's contextual, isn't it? If development was proceeding over a period of time measured in the hundreds of millions of years, and then in 5-10m (or even longer) we see tremendous development, that seems abrupt to say the least. Besides, 'standard evolution'? The whole point of the cambrian, even among people who happily accept that evolution can accomplish a tremendous amount of things (like myself), is that the established trend was apparently bucked, in a big way. Unless 'standard timescales' are 'whatever timescale it takes for evolution to work, be it hundreds of millions of years, or tens, or less.'nullasalus_{April 10, 2008
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DaveScot:
Making matters worse is that almost all modern phyla and all extinct phyla appeared abruptly over a span of 5-10 million years in the Cambrian period some 500 mya.
Again, 5-10 million years is not abruptly. Are you saying that one of the things that can be infered about the designer is that it takes 5 to 10 million years per design? If so, it seems it works on similar timescales to standard evolution!RichardFry_{April 10, 2008
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You could also make it mathematically rigorous by comparing the number of endogenous retroviruses in the genome (6% for humans as I understand it) to the number we share with other species. Say we have 30k retroviruses in our genome and only share 7 with chimps. The natural conclusion is that we acquired 29,993 of them AFTER our split with the chimps, and only 7 before. But given the fact that most of our evolutionary history is alleged to have been SHARED with the apes, we would expect this to be the reverse — most of our ERVs should be a shared, and only a few different.
And here's where some knowledge of the area you're pontificating about might be useful. Your argument assumes that the evolutions of ERVs is sufficiently slow. If they evolve quickly enough, then any phylogenetic signal will be drowned out by the noise. If you look at any textbook on phylogenetics, you'll see they discuss this w.r.t. sequence evolution. Contrary to what Dave asserts, this is fully rigourous. Here's the rigour with full jargon: You have a stochastic process where all states intercommunicate. Therefore the process has a stationary distribution. The implication is that the historical signal will eventually be degraded. ERVs are a bit more complex, because they aren't single bases, but as long as we condition on their extinction not having occurred, the same result can be found: it's just a consequence of having a stochastic process. The questions then mainly become empirical - for example, how fast is stationarity achieved? What are the particulars of the stochastic process (and then we can return to mathematical rigour by trying to model them)? Amongst the many books I really should read is Mike Lynch's on genome evolution, which tackles these sorts of problem. It's not an area I've had to deal with much, so I'm not up to date on the literature.Bob O'H_{April 9, 2008
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Allan_MacNeill:
And so, I agree once again: the real question is not “has evolution (defined as descent with modification from common ancestors) occurred, but rather how has it occurred
Recently on ID the Future, Casey Luskin argues that the human chromosomal fusion does not necessarily support the theory of common descent. His case seems flimsy to me. He seems to suggest that, though it is evidence consistent with common descent, it could possibly be otherwise. I have seen no evidence that causes me to question common descent. It appears to me that the rejection of common descent by some is wishful thinking, or religious thinking, not evidence based. I wish that the ID community would truly take the position of being ID evolutionists, adopting common descent as a tennet. However, I know that such a position would alienate even more of the religious community than is already alienated. Sometimes philosophy just seems to get in the way.bFast_{April 9, 2008
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DaveScot wrote (in #42):
"The so-called “overwhelming evidence” of evolution is in fact restricted to evidence of common ancestry. If we use a very broad defintion of “evolution” - common descent with modification - there’s compelling evidence that common descent is true and modifications did indeed occur."
Hear, hear! This is precisely the position that the majority of the naturalists of Darwin's generation adopted within about a decade of the publication of the Origin of Species, and remains so today. And you are correct that most of the controversy over evolution within the scientific community has centered on the mechanism(s) by which "descent with modification has taken place. This controversy continues today, with partisans for neutral molecular evolution squaring off against "pan-adaptationists" against "neo-lamarkians", etc. etc. etc. And so, I agree once again: the real question is not "has evolution (defined as descent with modification from common ancestors) occurred, but rather how has it occurred, and how do we know? And once again, I would like to stress that the answer to this question is not natural selection, if one considers it to be a mechanism for generating new phenotypes. It isn't; it only preserves a small fraction of all of the possible phenotypes that the "engines of variation" can produce. It is these "engines of variation" that are the most likely place to find the source of the variations that are so amply recorded in the empirical evidence, some of which is chronicled in this thread. That will be the job of the next cohort of the fomenters of the next episode of the "evolution revolutions".Allen_MacNeill_{April 9, 2008
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ungtss My thought is that evolution would predict that the overwhelming majority of ERVs would be shared by all humans and apes, commeasurate with the alleged “evolutionary distance” between them. The facts (at least as we have them today) appear to lean strongly against this. We really need to know how many are fixed in the human gene pool and how many are fixed in the gene pool of other primate species. Fixation for things with no selection value is a low odds event. For that matter fixation of stuff with a positive selection value is a low odds event too. So you'd really expect most of the ERVs are not fixed and are dwindling in frequency in their respective gene pools. Even just of few them that are fixed at identical insertion points in multiple species is strong evidence of a shared ancestor. Similar observations with psuudogenes and transposable elements makes the case even stronger. The vast similarity in function and sequence of active coding genes adds considerably more weight to the evidence for common descent. And that's just the molecular evidence. The fossil record generally agrees with the molecular evidence and so too do anatomical similarities in both living and extinct species. The so-called "overwhelming evidence" of evolution is in fact restricted to evidence of common ancestry. If we use a very broad defintion of "evolution" - common descent with modification - there's compelling evidence that common descent is true and modifications did indeed occur. What's missing is the root cause of the modifications. Ascribing all the modifications to chance & necessity is hardly more supportable than claiming it was one of the Gods in various and sundry revealed religions. Compare "God of the Gaps" to "Darwin of the Gaps". There's not a dime's worth of difference between the two of them. But rather than endlessly argue about whose speculative dogma, if any, is right about the diversity of life I prefer to focus on just one bit of molecular machinery common to all life - DNA and ribosomes. If someone can demonstrate how that code driven machinery came about without intelligent agency I'll concede that all subsequent evolution is possible and plausible without intelligent agency. But that's just me. I'll follow the evidence whichever way it leads. DaveScot_{April 9, 2008
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DaveScot: Thanks for the response. I am fascinated about with stuff and greatly appreciate the opportunity to bat ideas around. My thought is that evolution would predict that the overwhelming majority of ERVs would be shared by all humans and apes, commeasurate with the alleged "evolutionary distance" between them. The facts (at least as we have them today) appear to lean strongly against this. What do you think? I also found this interesting: only alpha, beta, gamma, epsilon- and spumaretroviruses have been found as ERVs. Deltaviruses and lentiviruses have not (http://www.retrovirology.com/content/2/1/50). HIV is a lentivirus (http://en.wikipedia.org/wiki/HIV). Therefore, it would be unprecedented for a lentivirus like HIV to actually make it into the genome. Of course, this study didn't actually show HIV making it into the genome.ungtss_{April 9, 2008
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ungtss Until we have more fully sequenced accurate genomes from many individuals within the same species it's impossible to say how many ERVs are fixed in the entire population and how many are not. A sample size of one individual from each primate species isn't a lot to work with. The race for the $1000 human genome sequence is on and is probably 5-10 years away. As it gets cheaper we'll have larger sample sizes to work with. AFAIK there are thousands of ERVs in both humans and chimps and only a very small fraction are at identical insertion points. Other classes of markers similar to ERVs are pseudogenes and transposons (thousands of those too) with at least some small fraction sharing identical cross-species insertion points.DaveScot_{April 9, 2008
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Look at HERV-k: Ten full-length HERV-K proviruses were cloned from the human genome. Using provirus-specific probes, eight of the ten were found to be present in a genetically diverse set of humans but not in other extant hominoids. Intact preintegration sites for each of these eight proviruses were present in the apes. A ninth provirus was detected in the human, chimpanzee, bonobo and gorilla genomes, but not in the orang-utan genome. The tenth was found only in humans, chimpanzees and bonobos.'' (http://www.ncbi.nlm.nih.gov/pubmed/10469592) 8 out of 10 of the HERVs found were HUMAN ONLY. Only 2 were shared. This indicates either that: 1) We have been distinct from the apes 5 times as long as we were related; or 2) There is a 20% chance that HERV-k can also infect apes at the same location But one thing this DOESN'T do is support the evolutionary conclusion that most of our evolutionary history is shared with apes.ungtss_{April 9, 2008
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You could also make it mathematically rigorous by comparing the number of endogenous retroviruses in the genome (6% for humans as I understand it) to the number we share with other species. Say we have 30k retroviruses in our genome and only share 7 with chimps. The natural conclusion is that we acquired 29,993 of them AFTER our split with the chimps, and only 7 before. But given the fact that most of our evolutionary history is alleged to have been SHARED with the apes, we would expect this to be the reverse -- most of our ERVs should be a shared, and only a few different. This appears to be the case. 6% of our genome is ERV, but only a very few are shared with the apes. More specific numbers would certainly make this more mathematically rigorous. Anybody have better sources for numbers on this stuff?ungtss_{April 9, 2008
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Ekstasis If the goal of the panspermia is to seed life that then develops, survives, and thrives, then why use individual organisms that possess consciousness, and die, fading to permanent black? Do we know for a fact that individual consciousness fades to black, never to return? How did *your* consciousness arrive in the first place and since it arrived once is it unreasonable to think that it might happen again? I think this is a question for philosophy not science.DaveScot_{April 9, 2008
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Chemistry and physics are mathematically rigorous natural sciences - historical biology is not. One way to make this discussion more mathematically rigorous would be to discuss exactly how many shared ERVs there are, the locations in which they are found, the degree of alteration of the ERVs, and the probability of the ERVs spreading throughout an entire population without any identifiable survival value, under the pressures of genetic drift.ungtss_{April 9, 2008
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William Nothing in prehistoric biology is mathematically rigorous. In any case modern biology, the study of living tissue, is the important branch of biology from which all practical benefit flows. Chemistry and physics are mathematically rigorous natural sciences - historical biology is not.DaveScot_{April 9, 2008
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RichardFry (#14) said: --- I take it you disagree with the drubbing Dawkins has recieved for suggesting the same in “Expelled”? --- Actually, there is a difference beetween Dawkins' view and DaveScot's view. Namely, before stating he could accept panspermia, Dawkins first said that Intelligent Design was complete nonsense. In other words, he says "There can't be an Intelligent Designer at all. But maybe aliens could have done it after all." When I saw "Expelled" in an advanced screening, everyone laughed at that comment because it showed Dawkins' hypocrisy perfectly. While I don't agree with DaveScot here, he's not being inconsistent. He's said that if aliens did it, that WOULD be Intelligent Design. Thus, he would not deserve a "drubbing" like Dawkins does for his [Dawkins] comments.Peter Pike_{April 9, 2008
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Interesting hypothesis, but it seems that a major inconsistency exists. If the goal of the panspermia is to seed life that then develops, survives, and thrives, then why use individual organisms that possess consciousness, and die, fading to permanent black? In other words, the micro level is totally out of sync with the macro. The only consciousness that presumably exists are a series of concurrent and sequential fragments. Forget the overall fire, we simply have a collection of sparks, each dying out. Seems rather cruel and pointless, does it not? Depends on the designer's purpose and values. Is it cruel and pointless to breed dogs, knowing that they will "live and ultimately fade to black," probably after experiencing some discomfort and probably fear? Maybe. But maybe the designer isn't as concerned with our feelings as we are. Maybe he/she/it is more concerned with something else, we know not what. Maybe we were created as servants. Maybe we were created as an experiment. Maybe we were created for aesthetic purposes (the same reason a man plants a garden). I wouldn't say the designer was cruel to give me 70 good years that end in nothing. Those were 70 good years, after all. Besides, it does not fit with empirical evidence. Near Death Experiences, with vast and mounting evidence that it is not simply a psychological phenomenom, too much to discuss here, points to the permanent consciousness of individuals. So, we are back to the permanency of the individual and the temporal nature of the cosmos, the very point at which human belief started!!! references to this empirical evidence?ungtss_{April 9, 2008
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Gerry: "Perhaps there are some presumptions making their way into the conclusions here?" In Darwinism presumption is the ubiquitous, fundamental flaw. It's always surprising to see those underlying presumptions ignored, nicely swept under the carpet of double talk. It is easy to make an assumption, build a complex argument over it with logic that, while being correct in itself, leads to erroneous conclusions. If no one notices the base assumption that itself lacks proof, the argument will seem right all the way from point B to Z (a being the assumption that is usually not even presented as the starting point). Something like building an equation that assumes that x = 3 when in fact x = 5. The equation may give a logically coherent answer but not a correct one.Borne_{April 9, 2008
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DaveScot: "It observed the active infection of cells that mature into sperm cells. The active infection means that the viral DNA load was inserted into the cell." 1) Correct me if I'm wrong, but doesn't "active infection" mean an infection that is producing new packaged virions, something that wasn't measured in this paper? 2) The "load" (genome) of the virus is RNA, not DNA. "It’s possible that the infection prevents the spermatogonia from maturing into a viable sperm cell." Wouldn't it be more accurate to conclude that it's likely, not merely possible? What other conclusion is more likely since they observed no infection of anything more mature than spermatogonia? "They’re detecting the infection by the presence of viral RNA in the cell which means it’s an active insertion." Doesn't that merely mean (assuming that they lack the sensitivity to detect input genomes) that they are measuring transcription of the provirus, and do not know if the newly-synthesized viral genomes are being packaged and excreted or not?Russell_{April 9, 2008
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Dave Scott, you say "If we suppose that rational man and an industrial civilization capable of repeating the cycle of directed panspermia was the ultimate goal more terraforming was required at least in as much as laying down large stores of easily accessable fossil fuels to power an industrial civilization. In order to repeat the cycle and ensure that life continues beyond the point where the earth is able to support it (the sun will eventually fry the earth into a cinder in another few billion years) there must be some means of identifying young planets able to support life (astronomy), the ability to transport life to them (space exploration), and the ability to customize forms of life suitable for the new environment (genetic engineering). We seem to be proceeding along all of those lines." Interesting hypothesis, but it seems that a major inconsistency exists. If the goal of the panspermia is to seed life that then develops, survives, and thrives, then why use individual organisms that possess consciousness, and die, fading to permanent black? In other words, the micro level is totally out of sync with the macro. The only consciousness that presumably exists are a series of concurrent and sequential fragments. Forget the overall fire, we simply have a collection of sparks, each dying out. Seems rather cruel and pointless, does it not? Besides, it does not fit with empirical evidence. Near Death Experiences, with vast and mounting evidence that it is not simply a psychological phenomenom, too much to discuss here, points to the permanent consciousness of individuals. So, we are back to the permanency of the individual and the temporal nature of the cosmos, the very point at which human belief started!!!Ekstasis_{April 9, 2008
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"Just hope you aren't like Gregor Mendel and have to be long dead before anyone notices you were onto something important." Things are even worse now, in that somebody who is onto something important might be shunned by "peer reviewed" journals.William Wallace_{April 9, 2008
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It's like saying: "How did that computer virus come into being?" "Well, there's a very similar section of Code in Microsoft Word 95 -- so it probably originated there and was subsequently modified." "Well that doesn't mean anything. How did it come to be in Microsoft Office in the first place!?"ungtss_{April 9, 2008
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Identical integration points in the same species are easily explained by inheritance. Common ancestry in the same species isn’t really disputed. The argument goes that identical integration points in different species is also due to inheritance via common ancestry only in this case the ancestor was common to both species.
I understand the argument you restated, Davescot, but note (and this is not directed against you) that it is rarely presented with the mathematical rigor. I do not claim to be an expert on retroviral markers as evidence of common descent, but, God willing, hope to become one. I suspect the argument is a house of cards. Until or unless I become an expert, though, it is interesting to consider other's discussing it. I hope the discussions become more mathematically rigorous.William Wallace_{April 9, 2008
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Allen: A more interesting question is how the RNA retroviridae evolved in the first place ... Perhaps the best hypothesis for the origin of RNA retroviruses is that they began as “rogue” reverse transcriptase genes. That just begs the question. "How did they evolve in the first place?" "While, they broke off from eukaryotes significantly more complex than themselves." "Well, how did the significantly more complex eukaryotes get the gene in the first place?" That question remains unanswered. To meaningfully answer the question, "how RNA retroviridae evolved in the first place," you need to explain how they evolved in the much more complex and impressive eukaryote ...ungtss_{April 9, 2008
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Allen Trust me, no one is ever going to compare you to Charles Darwin at this point in time but I won't say that will remain true as it's within the realm of possibility you'll come up with a general theory of biology as important as Darwin's. Just hope you aren't like Gregor Mendel and have to be long dead before anyone notices you were onto something important.DaveScot_{April 9, 2008
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Actually, like Charles Darwin, I collect stamps. I am closing in on a complete collection of all of the US commemorative issues, including those from the 19th century. And yes, I'm aware that this passion of mine plays right into the hands of Ann Coulter and other like genii. My wife is the numismatist in the family; indeed, she controls all of the money, currency, coin, and other forms of fiat money. And my kids collect their .99 fine silver "walking liberty", "peace", and "Morgan" dollars/thallers from the tooth faerie...Allen_MacNeill_{April 9, 2008
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