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

Bob, At (97) you just doubled down:
[Quoting me] And you compare the plastic predictions of evolution on a grand scale with the plastic predictions of single atoms by statistical mechanics? [End quote] Yep.
Now, if you take the Einsteinian modification that E=mc^2, the First Law of Thermodynamics has no known exceptions. Granted that we can't test it all the time, but it has been tested multiple times with the same result, and its incorporation into multiple other theories yields consistent results. The same can be said for almost all instances of the Second Law, certainly all laboratory instances. While the behavior of any given atom cannot be predicted with accuracy, the activity of large ensembles of atoms can be predicted with amazing accuracy. Gases will mix irreversibly without energy input to separate them, a cold object will cool a warmer object while a warm object will warm a colder object, et cetera. Those are strong predictions, not to be violated. The examples I gave,
the ancestors of various Cambrian assemblages of organisms, the presence or absence of large quantities of “Junk DNA” in the genomes of large groups of species, the convergence or lack thereof of different ways of organizing entire phyla into a tree of common ancestry.
are where materialistic evolution didn't just hedge its bets; it got the facts grossly wrong. Now, I could have understood if you had challenged the idea that ME got these facts grossly wrong; disagreed, but understood. But the apparently cheerful acceptance of a theory that makes gross mistakes, after equating it to statistical mechanics, is breathtaking. You claim that a stochastic theory can make predictions. Fair enough; I agree with you. But then, what do you do with a stochastic theory that makes grossly wrong predictions? At this point the comparison between it and thermodynamic theory is distinctly unflattering to ME. I think I now see why you didn't regard what you were doing as literature dumping. You cheerfully did it again, right after your "Yep." I think (correct me if I am wrong) that you felt these articles really did answer the question being raised (or at least, a question being raised). It looks to me like you followed both article citations with a short synopsis of what was observed, and what you perceived as its relevance. In that case, you did not understand the question being raised. Nobody (I think) is disputing whether gene frequencies can vary with time, or whether those gene frequency variations can be partially predicted on the basis of perceived fitness functions. Your example of changes in virulence gene frequencies in powdery mildew is beating a dead horse. The article on cross-pollination of conventional crops by genetically modified crops has nothing to do with the naturalistic origin of genetic information. In fact, for that particular article, the origin of the genetic information, or at least that particular combination, is known to be intelligent design. That's what genetically modified means. The problem that needs solving, from a ME point of view, is to get enough information, fast enough, and sorted from all the genetic misinformation that would occur from random processes, to get from a "simple" cell to the variety of life we find today, in less than 4 billion years. You say that it can be done; we say (very highly) probably not. We say that evolution, meaning the grand biological materialist theory, is not on good mathematical ground. We offer some preliminary calculations, specifically in The Edge of Evolution. You come back with assertions, not calculations, and then challenge us with
Some of us do apply statistics to genomic processes, and we get nothing like Behe’s results. Some of the people who do this actually have degrees in the subject, and are professors in mathematics departments. Feel free to argue that they aren’t rigourous, or even rigorous. But back up your assertions by showing the faults in their analyses please.
But there is no outline of the statistics you use, or the results that you get, or even a link or reference, for the production of new information by stochastic processes, or how it allows apes to give rise to humans, or reptiles to turtles, or algae to spiders, or club moss to maples, or any major shifts. It is very hard to show the faults of a non-existent analysis. For large changes, what has been termed Megaevolution, the math is either absent, or in favor of Behe. Demonstrating microevolution, or even species formation, will not get you the grand theory unless you can show how the extra information can be expected to be obtained without intelligent input. What you need to show is mathematically, first, how much information you need (e.g., how much new information do humans, or whatever other group you wish to consider, have compared to the presumed ancestor), and second, what the probabilities are of crossing that gap with known stochastic processes combined with natural selection. Powdery mildew will not help with this question unless you can show that they can create new enzymes and/or structures on a routine basis. I haven't yet read your reference, but I doubt that it gives that kind of data, in which case it would be completely irrelevant to the question being raised. You now admit that the real reason you cited that article is to bolster an ad hominem argument:
Paul - I gave the Phytopathology reference to make the point, that you now acknowledge, that you don’t know the literature. I wanted to make that point so that it was clear that your claims about evolutionary theory not being predictive were based on ignorance.
In my major field, medicine, stacks of unread journals on a doctor's desk are a proverb. Most of us are lucky to read JAMA and the New England Journal of Medicine, plus perhaps a prominent specialty journal. That leaves a lot out, and we rely on various journal summarizers to alert us to the really important stuff (yes, there is stuff out there that is not really important). It is only on the really important stuff that we might do a full-court press on the literature. I have read enough biology and geology literature to observe the same phenomenon there. However, one can understand the major outlines of a given question without having exhaustively read the literature. Your claim that my "claims about evolutionary theory not being predictive were based on ignorance" is unfair, and smacks of "He's smarter than you, he studied biology." The reason it's unfair is not that I know everything, but that the specific points I made were accurate. Rather than challenge the points, you went after the person presenting them. That's classic ad hominem. And if you are not careful, your ad hominem argument will boomerang back on you. Your claim is that "Some of us do apply statistics to genomic processes, and we get nothing like Behe’s results." Well, then, what results do you get, and as the result of what statistics, and how do they differ from those of Behe? Or do you not really know, in which case your "claims" are "based on ignorance"?Paul Giem_{April 14, 2008
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Let’s take a specific, important example. Where, when, and how will HIV evolve? Will it become more tranmissable, less transmissable, or stay the same?
It's always evolving, even within the host. So the "where" and "when" is "everywhere the virus is replicating within its host". The how is trickier. That depends on how its environment changes - i.e. how human behaviour changes, and what sort of drugs are developed. One thing I would predict is that any drug we find that cures AIDS will be overcome by the virus. Now, I'll hedge my bets and say this isn't certain, not least because we don't have a drug yet, so we don't know how it will act. I am pleased with Dave's ID prediction: evolution operates.Bob O'H_{April 13, 2008
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Richard 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? In that case they aren't needed. I don't make presumptions that are unnecessary. There's no need for a designer who can wave a magic wand to manipulate matter when I've just given you an adequate material mechanism that requires nothing more than a custom designed virus and ability to broadcast it. Humans already have the capacity to do this which is why we take bio-warfare as a deadly serious subject. DaveScot_{April 12, 2008
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Richard re; how much time to evolve fish into Fermi Somewhere beyond the age of the universe yet still short of an infinite amount of time. How much time does the pure chance theory of evolution predict it would take? What are YOUR boundaries?DaveScot_{April 12, 2008
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What makes that an ID prediction? Design will curtail the transmission of HIV. To my mind an ID prediction could be something like “Every time a cure is almost found some mysterious force steps in and moves the virus one step ahead. Then you don't understand ID. The actions of a "mysterious force" can never, almost by definition, be predicted. But if some force is preventing an AIDS vaccine via unknown means then HIV will not be made less transmissible the way I predict. OTOH, if this force somehow communicates to us that if you don't do this or this or this you will not be likely to transmit or acquire HIV, and if all follow the directives of this force and the transmission of HIV is greatly curtailed I guess you can say that's an ID prediction too. Of course, conversely, if the directives are rejected with greater frequency then you would expect the transmissibility to increase in accordance with the prediction set by your "mysterious force" theorem.tribune7_{April 12, 2008
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Richard There was some excitement earlier here when it was noted that a cure for malaria (a drug that requires evolition past the protein binding site limit) was potentially around the corner due to the work in that book. Who exactly got excited about it? Not me, that's for sure.DaveScot_{April 12, 2008
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So basically you’re saying that virulence will decrease unless it increases.
I'm saying that if I was going to have a bet of my own money that's where I'd put it. However, due to the somewhat special circumstances surrounding Hiv (mutiple strains merging in a single person then going back out again) a side bet might not be a bad idea. And no, I'm not saying virulence will decrease unless it increases, I'm saying that our best predictions come from other similar situations and those situations usually show a decrease in virulance. And perhaps we even co-exist with viri over time. Otherwise how do you get things like this?
Buried within the genetic blueprint of every human is a snippet of DNA that resembles a gene sequence from the human immunodeficiency virus (HIV). Humans have been carrying this unwanted genetic baggage around for more than 30 million years, according to researchers from the Howard Hughes Medical Institute (HHMI) at Duke University.
http://www.hhmi.org/news/cullen.html If a virus on average got worse the more it spread why are we all still here?RichardFry_{April 12, 2008
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I’ll recommend that you read Behe’s “Edge of Evolution” to know what ID predicts in this case.
There was some excitement earlier here when it was noted that a cure for malaria (a drug that requires evolition past the protein binding site limit) was potentially around the corner due to the work in that book. Has anything come of that of pratical benefit yet and is there some site tracking progress in that regard?RichardFry_{April 12, 2008
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It is unlikely that the virulence of HIV will increase and likely will decrease So basically you're saying that virulence will decrease unless it increases. Perfect answer. Thanks. Below is my answer from a year ago when an anonymous biologist asked ME that question. He was amazed I got it correct and accused me of somehow cheating because no knuckle dragging IDiot could possibly understand evolution that well:
You asked about virulenece and I answered. There is no answer. Extreme virulence usually becomes more mild because if it kills its host before it can be transmitted the more virulent form gets selected out. But if tranmission is really easy like then you get stuff like the Spanish Flu in WWI which became more virulent or bird flu on crowded poultry farms. Or take staph infections in hospitals. Those are becoming more virulent as antibiotic usage selects for stronger strains and crowding and open wounds aids in transmission. There is no right answer for your question, at least not the way you put it.
DaveScot_{April 12, 2008
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Where we disagree is whether or not RM+NS can turn a fish into Fermi in 500 million years.
Is it just a matter of degree then? What about 500 billion years? 500 trillion billion? Or can this "barrier" never be breached by RM+NS not matter how much time is available, in your opinon Davescot?RichardFry_{April 12, 2008
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When he fails to answer the question to your satisfaction, will you be offering the ID predictions? I'll recommend that you read Behe's "Edge of Evolution" to know what ID predicts in this case. What it predicts is this level of variation from what's already there is well within the domain of random variation and natural selection. We don't deny RM+NS is able to cause change and adaptation. We just disagree on the constraints. We both agree RM+NS turning a fish into Fermi in 500 years is so close to impossible it's not worth further consideration. Where we disagree is whether or not RM+NS can turn a fish into Fermi in 500 million years.DaveScot_{April 12, 2008
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But how about this for an ID prediction w/regard to HIV — it will be become better understood, means will be developed to curtail its transmission, hence it will be less transmissible.
What makes that an ID prediction? It seems to be that it's all equally applicable to "evilutions" interpretation. To my mind an ID prediction could be something like "Every time a cure is almost found some mysterious force steps in and moves the virus one step ahead. A cure is never found, and one cannot be evolved either as the virus changes and adapts somehow, almost as if there was an intelligence controlling it that wanted it to persist"RichardFry_{April 12, 2008
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Here's my go. Over the course of thousands of years the fraction of the human population resistant to HIV/AIDS will increase. It is unlikely that the virulence of HIV will increase and likely will decrease in accordance with similar situations. However, due to the fact that HIV can evolve much faster then the humans it infects it's unlikely that we will ever evolve resistance in 100% of the population and so intervention in the form of technology will be required.RichardFry_{April 12, 2008
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When he fails to answer the question to your satisfaction, will you be offering the ID predictions? Leo -- if he should fail to offer, to your satisfaction, an ID prediction will you at least concede that ID and Darwinism are scientific equals? But how about this for an ID prediction w/regard to HIV -- it will be become better understood, means will be developed to curtail its transmission, hence it will be less transmissible.tribune7_{April 12, 2008
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Bob Ok, give me some predictions that evolution makes about the future. Let's take a specific, important example. Where, when, and how will HIV evolve? Will it become more tranmissable, less transmissable, or stay the same?DaveScot_{April 12, 2008
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Bob So Oxford is saying one thing and doing another (i.e. quoting the spelling rules in the English language then not following them in its dictionary). I guess that's par for the course for things with Oxford's name on it. Richard Dawkins is another fine example.DaveScot_{April 12, 2008
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And you compare the plastic predictions of evolution on a grand scale with the plastic predictions of single atoms by statistical mechanics?
Yep. Here's another article you might like to look at: Kuparinen, A., Schurr, F., Tackenberg, O., O'Hara R.B. (2007). Air-mediated pollen flow from genetically modified to conventional crops -risk assessment with a mechanistic model. Ecological Applications 17: 431-440. Link In which my student showed that we can't even predict the movement of a single particle (in this case a pollen grain) with any sort of precision. We can't even predict the average movement of an ensemble of grains. She used methods from statistical mechanics to do this, so yes I can make this comparison. Paul - I gave the Phytopathology reference to make the point, that you now acknowledge, that you don't know the literature. I wanted to make that point so that it was clear that your claims about evolutionary theory not being predictive were based on ignorance.Bob O'H_{April 11, 2008
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Oh hold on. Check the date on your OED. Oxford’s current position is that it’s a misspelling.
That was yesterday - I checked the online edition. It's not in my shorter OED (which is older, but I don't think the language has changed that quickly).Bob O'H_{April 11, 2008
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Bob O'H, "on Behe’s results, I was thinking of his big result in Edge of Evolution, that malaria couldn’t evolve. That’s gone around the houses enough times that it’s clear he blundered in understanding some of the figures he used." What did he blunder on? We are of the impression that none of the reviewers ever touched him or his conclusions except for a trivial thing here or there. Maybe you could set both Behe and us straight.jerry_{April 11, 2008
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Bob, (88) You write,
The second half of Paul’s response is not surprising. Look at how statistical mechanics predicts the location and velocity of an individual atom. It says the atom is over here, except when it isn’t.
I expected bettter from you, Bob. The examples I used in (86) for evolution (meaning materialistic evolution)were the behaviors of entire groups, large statistical ensembles, if you will; the ancestors of various Cambrian assemblages of organisms, the presence or absence of large quantities of "Junk DNA" in the genomes of large groups of species, the convergence or lack thereof of different ways of organizing entire phyla into a tree of common ancestry. And you compare the plastic predictions of evolution on a grand scale with the plastic predictions of single atoms by statistical mechanics? I recognize my finiteness. You can always pull articles off of the shelf, and the probability that I have read them will be near zero, especially if they come from journals like Phytopathology which are not in any of my specialties. But if I were to cite a source to you with which I had reason to believe you were unfamiliar, I would give a brief summary of the source and why it was relevant to the question at hand. Perhaps you could do the same. As I recall the discussion centered around whether the (stochastic) math more closely supported an edge of evolution that was closer to Behe's or to one that would allow a complete materialistic evolution of all life from an original living cell. Then if it looks interesting enough, I can run the reference down and we can discuss it. In the absence of that, I would consider this literature bluffing, and believe that it was not worth my time to chase down the details. (Everyone has an edge to evolution. I have yet to run into even a strict creationist that would say that randomness has absolutely no place in the variation of living organisms. On the other hand, I have yet to run into a mechanistic evolutionist that would say that within one generation, cockroaches can be randomly obtained from an algal culture. As the old joke goes, we're now haggling about the price. That means that quantity is important.}Paul Giem_{April 11, 2008
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BobOH I suggest you go correct the wiki page on misspellings. http://en.wikipedia.org/wiki/Wikipedia:Lists_of_common_misspellings/R The talk section history is that "rigourous" was in there in the beginning, a Brit complained so it was removed from the list, and then someone quoted the spelling rule that applies, and it was added back to the list of misspelled words. Be a hero for your country and correct this outrage! Here's the editor who last reverted it due to the rule: http://en.wikipedia.org/wiki/User:CmdrObot/archive4#spelling Oh hold on. Check the date on your OED. Oxford's current position is that it's a misspelling. http://www.askoxford.com/betterwriting/spelling/
Rule: When adding certain endings, such as -ous and -ist, to words that end in -our (in this case, humour), change -our to -or before adding the ending: humorous; humorist.
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Ooh, Dave. I decided to reach for the ultimate sanction - the OED. So I did. It says this:
Also 5 ryger-, rygour-, rygor-; 5 regor-, rigur-, 5-6 riger-, 6 rygur-, 6-7 rigourous; 5 -is, 5-6 -us; 5 -use, 5-6 -ouse. 1. Characterized by rigour; rigidly severe or unbending; austere, harsh, stern; extremely strict: a. Of laws, procedure, etc.
I agree that it's not the usual form (and less usual than I had thought!), but it's there. Jerry - on Behe's results, I was thinking of his big result in Edge of Evolution, that malaria couldn't evolve. That's gone around the houses enough times that it's clear he blundered in understanding some of the figures he used.Bob O'H_{April 11, 2008
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Any word in the english language
I am not a native speaker but shouldn't it be English?sparc_{April 11, 2008
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BobOH I hate to have to educate you on British spelling rules but I feel compelled. In this case the spelling rule is not unique to British spelling. Any word in the english language follows this rule: If the word ends in "-our" (like honour and rigour) you must drop the u out of "our" when adding either the suffix "-ous" or "-ary". Honour becomes honorary and rigour become rigorous. I don't make the rules so don't shoot the messenger.DaveScot_{April 11, 2008
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Bob O'H, you said "Some of us do apply statistics to genomic processes, and we get nothing like Behe’s results." What Behe results are you referring to. I assume you mean that researchers are getting complex changes that Behe said he has never seen. Do you have any references? It would be interesting to see what they get if it understandable to us lay people. The real proof of Behe's ideas and these researchers that are using models would be in the actual genomes. Are there any analysis of genomes that back up those who are using statistical models to predict changes in genomes? Everytime I see something it is always micro evolution or trivial changes. You mention breeding. Does anything ever get beyond micro evolution with breeding experiments?jerry_{April 11, 2008
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Dave - whilst you may wish to do things with rigor, those of us on this side of the Atlantic prefer our own rigour. And we invented the language. :-) Paul's response about statistical mechanics really makes my point - it is a stochastic theory, but yet it is used to make predictions (albeit not at the level of an individual atom). Hence, the argument that a stochastic process isn't predictable doesn't hold water. The second half of Paul's response is not surprising. Look at how statistical mechanics predicts the location and velocity of an individual atom. It says the atom is over here, except when it isn't. Of course, Paul is also ignorant of the literature like this: Hovmøller, M.S.; Munk, L.; Østergård, H., Observed and predicted changes in virulence gene frequencies at 11 loci in a local barley powdery mildew population. Phytopathology (1993) 83 , 253-260. Wherein they actually do predict evolutionary changes (albeit over a short timescale). The animal breeding literature also provides cases where they also have to make evolutionary predictions (i.e. of the quality of individual animals). The models for this spring from Fisher's model in 1918, and are also pretty rigourous: indeed fitting the models was the motivation for the development of REML, which is a really hoopy technique for dealing with complex statistical models. Some of us do apply statistics to genomic processes, and we get nothing like Behe's results. Some of the people who do this actually have degrees in the subject, and are professors in mathematics departments. Feel free to argue that they aren't rigourous, or even rigorous. But back up your assertions by showing the faults in their analyses please.Bob O'H_{April 11, 2008
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Bob OH It's rigorous not rigourous. Paul Giem's response to you is essentially how I would have responded so I won't repeat it.DaveScot_{April 11, 2008
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Bob, (84) What's this about statistical mechanics? Statistical mechanics isn't rigorous because it's not predictable? What are the first and second laws of thermodynamics all about? Can we not engineer various heat pumps and engines precisely because statistical mechanics is predictable? On the other hand, the theory of evolution predicts the presence of large amounts of "Junk DNA", except when it doesn't. It predicts the existence of multiple intermediate forms leading up to the Cambrian fauna (and birds, and edicaran fauna, and so on) except when it doesn't. It predicts the congruence of molecular and anatomic cladograms, except when it doesn't. It is totally plastic, nowhere near like statistical mechanics. If one does apply statistics to genomic processes, one gets predictions that are somewhat similar to those of Behe in The Edge of Evolution. But I doubt that this is the mechanical rigor you have in mind.Paul Giem_{April 11, 2008
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Teh problem with ToE is that it is ultimately based on an unpredictable mechanism. If you can’t predict you can’t be rigorous.
The claim was that ToE wasn't mathematically rigourous. There's several areas of mathematics devoted to unpredictable (i.e. stochastic) problems. Probability theory, stochastic processes, mathematical statistics etc. These are all as rigourous as any mathematics. As for mechanisms not being predictable, and hence not possible to be treated rigourously, that means that statistical mechanics isn't rigourous either.Bob O'H_{April 10, 2008
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I will not comment further Allen Macneill's story about the two-three nucleotides "issue". Paul Giem has already said the essential things. I just would like to remark that, if we abandon any connection with the need of a causally credible explanation, imagination and creativity can bring us anywhere. And that is not intended, in any way, to be unkind to Allen, but only as a due methodological defense of a minimum of scientific approach.gpuccio_{April 10, 2008
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