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

RichardFry wrote (in #20):
"...a “simpler” form of DNA then the DNA we currently have could have, for example, 3 “letters” instead of 4. Is this not an simple example of a possible precursor to extant DNA?"
Actually, there is a strong possibility that the original genetic code may have consisted of as few as two nucleotide bases, rather than the current three that constitute an mRNA codon. This would mean that the original codon "lexicon" could only have coded for a maximum of sixteen amino acids, rather than the current twenty. That this was likely the case is supported by an examination of the current three letter codon lexicon and the amino acids it codes for. This lexicon is highly redundant, with many of the amino acids being coded for by only the first two bases in the codon (the so called "wobble hypothesis" originally proposed by Francis Crick). A few amino acids can even be coded for by six different codons (i.e. even the second base in the triplet can "wobble" a little). Only two of the amino acids are coded for by only one codon: methionine and tryptophan. It is likely that methionine has its "privileged" status by virtue of the fact that it is the "start" amino acid for all proteins (for stereochemical reasons that are two complex to describe here). Therefore, the codon for methionine (AUG) was probably among the original set of two-base codons, and only later was modified to its current three-base form. Tryptophan, by contrast, was almost certainly the last amino acid to be coded for. It is relatively rare in many proteins, and was therefore probably a kind of "afterthought" in the codon/amino acid lexicon. All of the foregoing can be tested by simply examining the codon/amino acid "lexicon" and comparing it with the known abundances of the different amino acids in proteins. In other words, the current codon/amino acid lexicon, rather than being "irreducibly complex", shows all the signs of having been modified from a much simpler system that consisted of a two-letter code specifying no more than sixteen amino acids. It may even be the case that the "ur" code consisted of only one-letter codons (and therefore could only specify four different amino acids), and that the two-letter and three-letter codes are later elaborations of this simplest of all codes.Allen_MacNeill_{April 9, 2008
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A more interesting question is how the RNA retroviridae evolved in the first place. All of the RNA retroviruses have an enzyme called reverse transcriptase. This enzyme allows the RNA viridae to "violate" the "central dogma of molecular genetics": it allows them to make a DNA copy of their RNA genome. This cDNA copy is then integrated into the genome of the host cell by another enzyme called integrase. This insertion, as you have pointed out, is essentially random. The RNA retroviridae are very pernicious disease-causing agents because they mutate very rapidly, thereby escaping surveillance by the host's immune system. This is because reverse transcriptase completely lacks the proof-reading and error-correction mechanisms normally found in DNA replication. Virtually every reverse transcription by these viruses produces several point mutations, meaning that a host that has harbored such viruses for many generations (i.e. a few weeks) has multiple independently evolving lines of these viruses attacking their cells. The random insertion of the cDNA copy of the RNA genome of these viruses can play hell with normal cell function. This is why most RNA retroviridae attack only cells that are either immediately replaceable (such as epithelial cells) or cells whose loss does not cause immediate impairment or death. Viruses that attack essential and non-replaceable cells (such as brain cells or muscle cells) impair or kill their hosts and therefore are generally eliminated by natural selection. Originally thought to be unique to these viruses, reverse transcriptase is now known to be a normal product of genes in eukaryotes, where it participates in the regeneration of telomeres at the ends of chromosomes. Perhaps the best hypothesis for the origin of RNA retroviruses is that they began as "rogue" reverse transcriptase genes. The gene for reverse transcriptase virtually is a retrovirus all by itself; all it needs to do is become detached from its normal position in the genome of a cell that contains it. This can happen as the result of several molecular genetic processes such as transposon "jumping" and chromosome fissioning. Even more likely would be the mutation of an mRNA transcript of the normal reverse transcriptase gene, allowing it to continue to exist outside the genome, but inserting a cDNA transcript into the host genome in random locations. This hypothesis is supported by the observation that the genomes of most RNA retroviruses are extremely small. HIV, for example, has a genome that consists of just nine genes: the genes for reverse transcriptase and integrase, a few proteases (which trim the coat proteins), a few coat protein genes, and a gene for G120, a binding protein that allows the virus to bind to the CD4 receptor on the plasma membrane of T4 helper lymphocytes (and a few other cells with similar receptors). The combination of the genes for reverse transcriptase and integrase would immediately function as a "coatless" virus, and given the extraordinarily high mutation rate that is a feature of reverse transcription, the combination could easily pick up a few other genes via repeated insertions and lysis cycles. In other words, viruses like these are not "external" agents; they are products of our own molecular genetics, gone "rogue". If they do not kill their hosts before they can be transmitted, they will increase in frequency over time; that is, natural selection will favor their further reproduction and modification. If they (as some recent research suggests) occasionally benefit their hosts, they will be even more likely to survive and reproduce in future hosts. Evolution by natural selection in action.Allen_MacNeill_{April 9, 2008
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Allen I mistakeny said canker sores when I meant to say cold sores. Cold sores are caused by a strain of herpes virus. My confusing herpes, a dsDNA virus, with a RNA-RT virus is however, inexcusable. It's a good thing an organic coin collector like you was around to correct the misclassification which is akin to putting a Liberty Head dime into a Roosevelt dime collection. P.S. This does nothing to detract from the point about RNA-RT viruses being a perfectly suited, material vector for an intelligent designer to employ to cause quick, widespread, appreciable genotype change. Maybe that's the way we as budding intelligent designers finally defeat malaria. Not wipe out the mosquito or battle the parasite in the human host but rather make a retrovirus that infects mosquito gametes and inserts a gene that ruins the ability to host the malaria parasite but doesn't otherwise harm the mosquito. The mosquito will thank us for it too. DaveScot_{April 9, 2008
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DaveScot, Good to hear then you don't disagree with my assessment that direct molecular manipulation was/is required to create CSI structures. I did not realise that there were claims that DNA and ribosomes self assembled. I presume that they exibit IC and so could not have evolved? If so, it stikes me that a "simpler" form of DNA then the DNA we currently have could have, for example, 3 "letters" instead of 4. Is this not an simple example of a possible precursor to extant DNA?RichardFry_{April 9, 2008
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Furthermore, Herpes Simplex I, like all of the Herpeseviridae, does require physical contact to spread. The HSV particle is enclosed within a pseudomembrane, which it "steals" from its host cell during lysis. This pseudomembrane is relatively fragile, and can be destroyed by dessication and contact with disinfectants such as bleach and alcohol-based sanitizers. The Herpeseviridae are are very interesting group of DNA viruses. All of them are infectious in humans, causing such nasty diseases as chickenpox (caused by Herpes varicella), shingles (an adult form of chickenpox usually seen immune compromised people), mononucleosis (caused by Epstein-Barr virus), cytomegalovirus (caused by a close relative of Epstein-Barr virus), and Herpes Simplex II, which mainly affects genetalia. Epstein-Barr virus has also been implicated in chronic fatigue syndrome and a rare form of cancer called Burkitt's lymphoma. Nearly everyone reading this post has had one or more of the herpes viruses at some point in their lives. I have had all of them except Herpes Simplex II. Most people are exposed to the viruses during childhood, and therefore test positive for the antibodies against them. However, I contracted CMV at the age of 33, and had a very severe case of atypical mononucleosis, followed by a four-month bout with Guillon-Barré syndrome, a form of autoimmune paralysis that results from one's immune system attacking the myelin sheaths insulting one's motor neurons. This left me paralyzed from the chest down for almost two months; thankfully, like most cases of BGS, I eventually fully recovered. It is always best to check what one writes about before committing it to public view.Allen_MacNeill_{April 9, 2008
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Correction to my post: to be the most reasonable of the three scenarios. changed to to be the most reasonable of the three scenarios with respect to viruses that don't bestow any survival advantageungtss_{April 9, 2008
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Richard Of course it is unlikely to the point of impossiblity that complex structures like the bac-flag can self assemble from a bunch of proteins, but nobody is claiming that are they? More or less, that's exactly what they're claiming but I avoid the bac-flag as an example as there's a better example in DNA and ribosomes which are both universal in all forms of life and strictly required to be in place before Darwinian evolution can even get started. If a plausible pathway absent intelligent agencdy can be shown capable of creating DNA and ribosomes ex nihilo then I'll concede that everything that follows needs no intelligent agency either. DaveScot_{April 9, 2008
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DaveScot wrote (in #6):
"Oral herpes (which causes canker sores) is a retrovirus and it spreads without direct physical contact."
Oral herpes is not caused by a retrovirus. It is caused by a DNA virus called Herpes Simplex I, a member of the Herpesviridae (see: http://en.wikipedia.org/wiki/Herpesviridae). Herpes Simplex I reproduces completely differently than the RNA retroviridae. Specifically, it does not insert a copy of its genome into the genome of its host cell. Instead, the large DNA genome of the Herpes Simplex I virus remains within the cytosol of the host cell, directly the assembly of multiple copies of itself using the DNA replication machinery of the host cell. Furthermore, Herpes Simplex I virus does not cause canker sores. Also known as aphthous ulcers, canker sores are not caused by viruses at all, but rather are most likely a form of autoimmune disease (see http://en.wikipedia.org/wiki/Canker_sore)Allen_MacNeill_{April 9, 2008
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DaveScot: Thank you for your kind and patient response. Identical integration points [are why ERVs imply common descent]. Identical ERV’s are found scattered all over the genome. While there may be preferred insertion points there’s no evidence of any preference. 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. The way I see it, there are three scenarios for how ERVs could have spread to an entire population: a) The virus provided some survival advantage, such that it spread throughout the population via natural selection; b) The virus provided no survival advantage, but its appearance on a single chromosome in a single common ancestor managed to spread it throughout an entire population. c) The virus provided no survival advantage, but different individuals within the population were infected at identical insertion points; Scenario A (advantageous ERVs) screams ID to me, as it seems to for you, also. Scenario B (no survival value, spread from a single ancestor) seems highly improbable to me, for two reasons. FIRST: if the virus initially infected only a sperm cell, it would be passed on only in ONE of the relevant chromosal pair. In order to spread to an entire population, first two of that individual's descendents carrying the ERV would have to breed, and then the 1/4 of their descendants that are homozygous with respect to the ERV would have to breed, and their descendants would have to be the common ancestors of the entire population we see today (meaning everybody else died off) SECOND: Without any survival advantage to this new addition, genetic drift is going to wipe the new ERV off the map in time, unless you're looking at a population bottleneck of some sort where only the carriers survived an epidemic of the virus. In any event, the whole scenario looks rather implausible to me. c) That leaves us with c -- multiple initial infections at identical insertion points. While there's certainly no proof that it occurred, it seems (to my untutored mind) to be the most reasonable of the three scenarios. Viruses can have preferred insertion points. CONCLUSION: If we grant that the most plausible scenario is multiple infections at identical insertion points within the human population, I don't see why it's particularly Earth-shattering to say that multiple infections at identical insertion points is plausible across species as well. What do you think? If you need this explained your knowledge of genetics leaves an awful lot to be desired. I would hope we'd all be humble enough to realize that this statement is true for all of us in the face of the enormous complexity of the topic. Those of us with relatively more to be desired thank those of you with relatively less to be desired for your help.ungtss_{April 9, 2008
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DaveScot:
One is the entirely speculative self-assembly of complex machinery and abstract codes that specify their construction and operation.
What about if you replace "complex" with "simple"? In fact, do you consider there to be a difference at this level between "complex machinery" and "machinery".
Intelligent design is the current best explanation as that is the only demonstrated way that codes and machines even remotely approaching that level of complexity can be created ex nihilo.
Of course it is, however I think this is where ID has a serious failing for me. Of course it is unlikely to the point of impossiblity that complex structures like the bac-flag can self assemble from a bunch of proteins, but nobody is claiming that are they? So in my opinion that's an argument that should be put into the "do not use" section! Your milage may vary.
The fossil record is a record of saltation of new species. New species fully characteristic of their kind appear abruptly in the fossil record, exist largely unchanged for an average span of 10 million years, then just as abruptly disappear from the record.
Even so, those timescales are ones that I would hesitate to apply the label "quickly" to. To help me understand your POV on this problenatic issue what in your opinion was the duration of "abruptly"? A day? A year? 10,000 years? At these timescales decimal points matter!
A perfectly plausible explanation for this is that the earth, as soon as was able to support organic life in any form, was purposely seeded with it (Francis Crick and Leslie Orgel’s directed panspermia).
I take it you disagree with the drubbing Dawkins has recieved for suggesting the same in "Expelled"?RichardFry_{April 9, 2008
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Richard you are pandering to their intrepretations Not really. "Their" interpretations are largely my interpretations as well. I'm a materialist to the point where my credulity is stretched beyond the breaking point. This basically occurs at two points. One is the entirely speculative self-assembly of complex machinery and abstract codes that specify their construction and operation. The genetic code, DNA, and ribosomes are the best example of this. Intelligent design is the current best explanation as that is the only demonstrated way that codes and machines even remotely approaching that level of complexity can be created ex nihilo. Another breaking point is the absurd untestable concept of an infinite multiverse. An infinite multiverse is self-defeating when it comes to biological ID in any case. In an infinite multiverse there must by definition be an infinite number of universes where an intelligent agency with vast material powers, including the ability to design organic forms of life, existed and was responsible for the design of life on earth. What I mean by that is that who says the changes had to be implemented quickly? The fossil record. The fossil record is a record of saltation of new species. New species fully characteristic of their kind appear abruptly in the fossil record, exist largely unchanged for an average span of 10 million years, then just as abruptly disappear from the record. 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. There are few if any predecessors to these in any earlier fossil records. Another troubling obstacle, this time for the origin of life instead of its diversification, is that life as we know it first appeared, arguably, some 4 billion years ago. That far back in time the earth barely had time to cool off enough for liquid water to exist which means that abiogenesis had very little time to occur. A perfectly plausible explanation for this is that the earth, as soon as was able to support organic life in any form, was purposely seeded with it (Francis Crick and Leslie Orgel's directed panspermia). The purpose of that was to terraform the planet so that it could eventually support oxygen breathing land animals. The first seeding culminated in the Ediacaran biota. A second seeding of modern forms of life took place in the Cambrian. 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. Eric Pianka, the notorious lizard expert at UT who caused all the stir by suggesting that the best thing for the planet is for something like the ebola virus to come along and kill 9 out of 10 humans on the planet, posed a philosophical question: "What makes humans more important than lizards?" I answered that if life is to continue beyond the time when our sun becomes a red giant and turns the earth into a cinder then a spacefaring species is required to do it. Lizards aren't building telescopes and spacecraft but humans are. If not for humans there is no way for life to relocate to a new planet. That's what makes humans more important than lizards. My general feeling is that life on the earth is just one link in a chain that extends indefinitely into the past and may extend indefinitely into the future. Young planets get seeded with life which by design matures into an intelligent form which is able to repeat the cycle by seeding other planets. This fits very nicely into the scheme of things here - a common attribute of all forms of life is to persist into the future. If earth-life is to persist it eventually has to find its way off this planet and there's really no other way to accomplish that other than through a high technology industrial species. This view is pretty hard-core materialism about as far removed from personal gods, special creation, and bible stories as one can get. I consider myself to be more of a materialist than the most ardent atheistic Darwin worshippers who for some inexplicable reason seem unable to accept the possibility that of continuity in intelligent life preceding ourselves. There is nothing in science which warrants that belief. DaveScot_{April 9, 2008
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gpuccio 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. It's possible that the infection prevents the spermatogonia from maturing into a viable sperm cell. They're detecting the infection by the presence of viral RNA in the cell which means it's an active insertion. Two possibilities exist from that point: the active viral DNA prevents maturation of the spermatogonia into sperm cells, thus there's still no demonstrated way for the insertion to be heritable or the maturation process deactivates the viral DNA load so it is still heritable. I'll agree that in order to be conclusive an infected spermatocyte needs to be observed maturing into viable haploid sperm cells and/or sequencing the DNA in a sperm cell and finding the specific, identical ERV sequence in it.DaveScot_{April 9, 2008
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DaveScot: I see.
The Darwinists I referred to are asking for an identifiable physical method by which purposeful genomic change can be made quickly in a large population.
In that context then you are quite right to avoid supernatuural entities as a mechanism. However by giving that answer in a way you are pandering to their intrepretations. What I mean by that is that who says the changes had to be implemented quickly? Is that not placing constraints upon what the designer can and cannot do? In any case, my main point in response to your post is that I understand great progress has been made manipulating single atoms and striking progress has been made in general in that field in the last decade or so (for instance, atoms can be held in a criss-cross laser beam array and tuning the laser moves the atoms, I believe the interference patterns generated are the key). So, given that humanity is presumably are nowhere near the abilties of the designer in any way and if we assume that great strides will continue to be made in the future I believe that shortly as well as
The retrovirus vector is a perfectly workable material way for a designer to modify the natural course of evolution.
you can say that direct manipluation of matter can (and has) been proven to take place (by humanity for one!) with no supernatural intervention required at all. After all if we take humanities achievements as the absolute minimum that can be achieved by intelligent design(ers) then direct manipluation of matter is within all intelligent entities power (or will shortly be). After all, what was used to create irreducibly complex items except direct manipluation of matter? That right there is the key for me on this issue. To be clear, I'm not saying that "the designer thought it and it was so". If we can do it, so can the designer.RichardFry_{April 9, 2008
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Davescot: I agree with you that it is perfectly possible that, after spermatogonia infection, the retroviral genome could be permanently inserted in the genome of gametes; I just think that this paper does not observe that, so it remains a theorical possibility. Anyway, I agree that retroviruses could certainly be an instrument of intelligent implementationof information, playing a role similar to that of plasmides in bacteria. Indeed, all transposable elements in non coding DNA could act that way. But really, all that is at present speculative, and I think we need more facts.gpuccio_{April 9, 2008
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Richard The Darwinists I referred to are asking for an identifiable physical method by which purposeful genomic change can be made quickly in a large population. A highly infectious retrovirus is one demonstrated way it could be accomplished. What they're hoping to hear from us is the answer you gave - an omnipotent supernatural entity can do *anything*. The answer I give doesn't require supernatural powers but rather nothing more than the same means that human genetic engineers use to insert foreign DNA into living organisms. By so doing I deny them the chance to say that explanations invoking supernatural agency are outside the domain of science. The retrovirus vector is a perfectly workable material way for a designer to modify the natural course of evolution. Acknowledgement of endongenous retroviruses in common descent is double-edged sword. At the same time it lends strong support to common ancestry it also lends strong support to the intelligent design hypothesis by giving a designer a demonstrated physical means of altering the course of evolution. ERV's are generally deactivated quickly by random mutation. There's nothing preventing any one or any group of them from being reactivated in the future. Greg Bear did a lot of research into the possible reactivation of ancient ERV networks as a mechanism for saltation of new species. He used it as core plot element in his hard science fiction book "Darwin's Radio". Darwin's Radio was very favorably reviewed in Nature by prominent geneticist Michael Gold. He complimented Bear for thinking outside the box of usual genetic assumptions. I highly recommend the book. The sequel "Darwin's Children" I didn't think was anywhere near as good. DaveScot_{April 9, 2008
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gpuccio The abstract mentions that spermatogonia were observed to be infected. Spermatogonia mature into sperm cells. It isn't really surprising that mature sperm cells themselves might not have active retroviral insertion sites. The maturation process might serve to deactivate the viral DNA so it is no longer able to produce new virus particles. It may be as simple as endogenous retroviruses are incapable of producing new virus particles in a haploid cell. Expression of many genes not absolutely required for metabolism are repressed in gametes.DaveScot_{April 9, 2008
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DaveScot
When Darwinists ask me what possible mechanism might be used by the unknown designer to effect population-wide changes in species I’ve answered that a highly infectious retrovirus would be a really effective way.
Personally I can't see why we could not equally say that the designer created the molecules directly, in situ, that made up the new changes. So a direct intervention rather then using things already created. To me I don't see why the designer could create from nothing originaly and then, for some unknown reason, starts to require things like retroviruses to do the same thing it did ealier. I mean, creating a living form from nothing must be harder then slightly modifiying one that already exists? Direct manipulation of matter must have happened at least once, no? Davescot, if we take it as read that the desiger can directly manipulate matter at the sub-atomic level then what is your opinion as to why retroviruses etc are needed at all?RichardFry_{April 9, 2008
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ungtss The question it settles is whether or not retroviruses can infect mammalian germ cells. It was argued that they cannot as there exist unique barriers to entry in germ cells that somatic cells generally don't have. There's still no experimental evidence that I'm aware of that mammalian egg cells are subject to retroviral insertions as there are additional barriers to entry there that sperm cells don't have. However, it needn't be able to infect egg cells in order to be integrated into the germ line so long as it can infect male gametes. This doesn't have any bearing on other arguments against retrovirus markers as evidence of common descent. That said I'll answer your unrelated questions to the best of my knowledge: 1) How can we presume that shared endogenous retroviruses indicate common ancestry, when many viruses (including SIV/HIV) can infect both lines independently? Identical integration points. Identical ERV's are found scattered all over the genome. While there may be preferred insertion points there's no evidence of any preference. 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. 2) How is it that all humans share SO MANY (thousands of) endogenous retroviruses — did our common ancestor or ancestor pool have all those viruses already? That appears to me to be the best explanation - integration into the germ line then spread through the gene pool in the same way that other alleles spread around and may become fixed. Again, changing allele frequencies and fixation of alleles in the gene pool aren't really disputed. 3) What are we to think of endogenous retroviruses that are not only beneficial but essential for organisms (like this one http://www.sciencedaily.com/re.....233630.htm) — is it possible that these retroviruses are actually intentional, designed mechanism for genetic engineering? Quite right. When Darwinists ask me what possible mechanism might be used by the unknown designer to effect population-wide changes in species I've answered that a highly infectious retrovirus would be a really effective way. In just one or several generations a designed genetic load carried by a retrovirus could spread the load through the entire population. It would happen so fast that in the fossil record it would appear as saltation. Indeed, we use retroviruses as vectors in genetic engineering ourselves. 4) Are to believe that ALL of the hundred-some-odd thousand endogenous retroviruses in the human genome were ALL transmitted via STDs that specifically target the gonads? HIV/SIV doesn't specifically target the gonads and we're lucky that it doesn't survive outside the body long enough to have much chance of spreading through the air like a common cold virus. Oral herpes (which causes canker sores) is a retrovirus and it spreads without direct physical contact. HIV/SIV isn't nearly as robust and generally requires direct blood-to-blood or semen-to-blood transfer. We're also lucky it isn't able to spread via mosquitos like the West Nile virus. 5) How did we come to be HOMOZYGOUS with respect to these endogenous retroviruses? Were both the Adam and the Eve infected? If you need this explained your knowledge of genetics leaves an awful lot to be desired.DaveScot_{April 9, 2008
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Ehmm... It should have been "common descent", I suppose...gpuccio_{April 9, 2008
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DaveScot: I have not yet read the whole article (lack of time), but from the abstract I would say that the subject here is infection of the reproductive system, not integration of the retrovirus in the trasmissable genome. So, I can't see the relevance to retroviruses in the genomes as evidence of uncommon descent. Please, correct me if I am wrong.gpuccio_{April 9, 2008
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I was wondering along the same lines as ungtss. Perhaps there are some presumptions making their way into the conclusions here?Gerry Rzeppa_{April 8, 2008
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not sure quite what question it settles. It certainly settles the question of whether germ lines can be infected by viruses. However, it doesn't answer the following questions: 1) How can we presume that shared endogenous retroviruses indicate common ancestry, when many viruses (including SIV/HIV) can infect both lines independently? 2) How is it that all humans share SO MANY (thousands of) endogenous retroviruses -- did our common ancestor or ancestor pool have all those viruses already? 3) What are we to think of endogenous retroviruses that are not only beneficial but essential for organisms (like this one http://www.sciencedaily.com/releases/2006/09/060911233630.htm) -- is it possible that these retroviruses are actually intentional, designed mechanism for genetic engineering? 4) Are to believe that ALL of the hundred-some-odd thousand endogenous retroviruses in the human genome were ALL transmitted via STDs that specifically target the gonads? 5) How did we come to be HOMOZYGOUS with respect to these endogenous retroviruses? Were both the Adam and the Eve infected?ungtss_{April 8, 2008
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so... isn't this good for evolution?WesleyP_{April 8, 2008
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