Evolutionary Mechanisms

Biological Change:
A Proposed Addition to the Mechanisms of Evolution

It seems to be commonly accepted that Darwinian Evolution works well in explaining Micro Evolution. However, gradual evolution, through the mechanisms of occasional genetic mutation or genetic drift, and survival of the fittest, fails to explain well observed biological phenomenon. Particularly, the fact that advanced organisms are relatively stable for long periods of time and that they change radically over a very short period of time. This phenomenon is best characterized by the Great Extinction of about 250 million years ago and the latter extinction about 65 million years ago. Both events were accompanied by the birth of a large number of new organisms. Stephen Gould recognized this phenomenon and described it as “Punctuated Equilibrium”.

Conjecture: Viruses can become embedded in an organism’s genome and play a significant role in radical evolution.

If this conjecture is true, then we might make some progress in explaining Punctuated Equilibrium.

First, I would like to give a plausible reason for the stability of advanced organisms, and an explanation for the variable nature of viruses. Next, I would like to show that viruses can be naturally embedded in an organism’s genome and produce a sustainable subgroup. Finally, I would like to show that viruses can attack in sufficient quantity to produce a stable reproductive subgroup.

Why are advanced organisms relatively stable?

Cellular reproduction in advanced organisms is relatively stable because the Mis-Match protein, which is actually two proteins, searches for various mutations and replaces them with the original sequences in the genetic code. In addition, the immune system plays a significant role.

Why are viral organisms not stable?

Viral reproductions do not produce this mismatch protein which means that they can mutate at a much higher rate.

During periods of relative stability, viruses tend not to mutate very often. Their best strategy for survival is to serve as parasites, which means that they will do best when they do not destroy their hosts. However, during periods of ecological challenge viruses can mutate rapidly. Advanced organisms also have immunological defense systems which will attack viruses. Only during periods of great ecological change is it likely that mutated viruses will be able to overcome the immune systems defenses and also break down the mismatch protein.

We need to establish that there is some likelihood that viruses can in fact have their genetic code, or a generated intermittent code, embedded in the host in such a way that this modification can be reproduced in succeeding generations. We know that genetic engineering can already insert DNA fragments into viruses which will attack the germline of the host and that genome of the offspring will carry this embedded code, however we need to show that this insertion can happen naturally.

Consider the following illustrations:

There is a leukemia virus, MuLV, which has naturally become embedded in the genome of many strains of inbred mice**.

The genetic encoding for the egg attachment in mammalian
reproduction proceeds from a DNA sequence of a viral structure***.

In addition we know that gene therapy is accomplished by inserting genetically modified viruses in the germline of a host organism. While this does not demonstrate natural viral infection, the nature of the geometry of the sheaths needs to be compatible with the receptors in the germline for this to occur.

Can viruses attack in numbers sufficient to produce a sustainable reproducing sub group?

Some examples of large viral outbreaks include the Spanish Flu of 1918 in which 2 different viruses attacked and exchanged their protein sheaths*. This in turn played havoc with the immune systems response and the result was the death of about 10% of the worldwide population*. Another virus, which can be very dangerous to the host population, is the Hepatitis B virus, which is currently carried by about 20% of the World’s population*. The final virus sited is the Herpes Simplex A which is carried by about 90% of the population over 40 years of age*.

Assuming that the viruses can attack the germline and that the mutated offspring are provided with appropriate survival mechanisms, the subgroup should be large enough to sustain itself. It should be stressed that this will only happen during periods of great ecological change. Under these conditions, the non-mutated generating organisms will be at a point of collapse.

During periods of great ecological change, viruses can, in a short span of time, mutate, embedd themselves in the germline, and be passed to the genome of successive generations of the host organism. It should also be noted that viruses (with nucleotide counts ranging 2400 for Hepatitis B to 360,000 base pairs for the pox virus) could cause large scale genetic variation.

Assuming that viruses can embed themselves in the host genome should compel us to ask if embedded viruses have been found in mapping the Human Genome. The answer is yes. Approximately 8% of the Human Genome is remnants originated from retroviruses****. Additionally, we know that all but one of the mapped human endogenous retroviruses were implanted over 25 million years ago. I have found no references regarding embedded adenoviruses. It should be noted that only slightly over 1% of the Human Genome is used for encoding of genetic material.

The self recognized problems with this work are as follows:
There is no evidence that the viral attacks lead to new speciation i.e. while viral embedding does in fact happen, I have not found evidence that “Punctuated Equilibrium” is a causal result. Precisely, how does the mismatch protein get turned off or overcome by a large viral attack? There should be independent models showing long term biological stability with a final massive breakdown. (Is this somewhat analogous to buckling forces? Can we describe it with a mathematical model?) Why even bother discriminating about: which mutations are caused by what factors?

The first reference I could find on this conjecture was recorded in a lecture delivered at the University of Birmingham on May 12th 1967 as part of the Huxley Lecture Series entitled “Viruses and Evolution” by Sir Christopher Andrews M.D., L.L.D., F.R.C.P., F.R.S.

He states “There is reason to believe that in some instances the prophage and the bacterial genome are so fully integrated that no induction can occur: we then have no means of distinguishing between the prophage and the genetic material of the host. In discussing this at the Royal Society Leeuwenhock lecture (Andrews 1952) I suggested that perhaps the host genes admit a little brother to sit upon the chromosome bench inside them. Anderson (1966) has speculated along the same lines with regard to bacterial transfer factors. These genetic determinants perhaps become integrated into the chromosomes or they may remain cytoplasmic, but in either case “They become part of genome of the host cell”. Bacteriophages can also introduce new genetic material from one cell to another by means of the process called transduction. There seems every likelihood that such acquisitions of new genetic material for natural selection to play upon would offer opportunities for a speeding up of evolutionary change”.

References:

• Clinical Microbiology made ridiculously simple Edition 3 by Mark Gladwin and Bill Trattler.

**article entitled “Pattern of Expression of Ecotropic Murine Leukemia Virus in Gonads of Inoculated SWR/J Mice” which appeared in the May 1989 Journal of Virology, Jean-Jacques Panthier, Pierre Gounon, Hubert Condamine, and Francois Jacob

*** Reference Premed student. I have not independently verified.

****In an article published October 4, 2004 on the site retrovirology.com/content/1/1/32 entitled “Identification of endogenous retroviral reading frames in the human genome” published by Palle Villesen, Lars Aagaard,Carsten Wiuf, and Finn Skou Pedersen all of University of Aarhus located in Aahus Denmark published University of Aarhus. This is a very interesting site.

i dont know how i missed this essay,an oversight that would have probably never been corrected if you didnt mention it in the other thread. i must say its a pleasure to read a properly formed one in this section. now on to a few comments

as far as i know, neither the anti-mismatch or the imune system work at all against the reproduction of viruses in infected cells. the proteines will keep various random mutations at bay, usually ones with physical causes, such as chemicals or radiations. they will not really stop viruses from infecting a cell, or the cell from “executing” the viral code. the imune system will create anti-corps that will bind viruses, but once the virus is inside the cell, there is little the imune system will do (except lymphocites might eat the entire cell, but afaik this is very rare indeed). so the proteins dont work against viruses at all, and the imune system only works against them as long as they are outside a cell.

this leaves us with the question of why are complex organisms stable in spite of viral infections ? indeed there can not be, i think, a single example found of a warm blooded animal that didnt contain a single active viral body in it, and yet we have yet to observe a virally induced mutation of an individual in natural settings.

isnt this in fact begging the question ? do you define relative stability as that time when the viruses dont mutate ? or do you mean stability of the ecosystem of the likely hosts ? there are important examples, such as the avian pest transmitted to humans, or the sars epidemic, virtually any big epidemic is a case of a significant mutation, or at the very least change in the viral attack/anti viral defense equation that did not particularly follow a significant change in the ecosystem of the likely host. further, important changes such as hurricanes, catastrophic floods etseq never did, or at least not very often did produce significant surges of new viral strains (i conjecture if they were significant we should have seen them)

so, i dont think the position can be held if you mean ecosystem changes. this would need some clarification

this is a very doubtfull statement. hepatitis often destroys its host, and yet its not even remotely extinct. rabies destroys the host in an amazingly short interval and its not extinct. herpes does not significantly affect the host, and yet its best mechanism to survive comes from the fact that it is virtually indestructible chemically. so there might be some correlation between killing hosts and the virus’ chances to survive, but its obviously not the only factor, and i dont think it can be proven its the main factor.

viruses can mutate rapidly anytime, and in fact they do. i take it you mean a mutated strain is more likely to survive in condition of ecological stress for the host. however, its unclear how this would work. if a strain of an existing virus appears that is, say, not affected by one of the, say, three anticorp proteines the host normally uses to neutralize the mother strain, that strain will make it regardless if the population is growing or dwindling. arguably, a growing flourishing population will give it a chance to survive longer, and take over. consider three groups of gazelles are grazing in geographically separated areas. one group develops the mutated strain. if then the entire group gets wiped out by a volcano, or slowly dies from a shift in grazing land, the virus might die with them. on the other hand, if the three groups grow, their chances to make contact increase, and as such the virus chances increase too. on the other hand, if the change in waterfall patterns forces the gazelles together, to drink from the same one pond, the virus gets better chances, while the ecosystem is not particularly stressing for the gazelles (or not as stressing as it could be)

so im not very sure why you say it has to be bad conditions for the host in order for the mutated and valuable virus to survive. on the other hand, if the mutation is not valuable, its going to die out regardless.

actually i am pretty much convinced this is indeed possible, and has occured naturally

we agree that it can happen, but i still don follow why you insist on great ecological change. there was little ecological change going on in 1918, as far as i know. the bits of the genome that are being credited to viruses might have appeared in condition of ecological catastrophe or stability, as far as we can tell. so where does that requirement come from ?

and while we are not very sure what the overlap factor is, it might not be very large at all, the 8% would fit pretty well in the slack space left by the 1%. statistically, since the two should be independent, about the same 8% of viral influence should be found in significant human dna as it is found in overall dna. afaik its nowhere as important, which might suggest there are systems in place to keep the viral influence in the shadow of the slack dna.

actually i think i have read something about proof on the speciation due to viral infection conjecture, i will have to go check and get back. (reading down… never mind, you have them )

Ed3, there used to be a time when I could do molecular biology in my sleep, but I have since shifted my attention to biophysical matters and have forgotten most of it. For what it is worth, I think your thesis has a lot of potential but needs a further bit of work to fully realize that potential. Zenofeller’s comments are valid and I would advise you to incorporate them in your next version.

In general, I guess what Zeno did was to point out that there are quite a few implicit assumptions in your piece that you unconsciously seem to have adopted as “true” while a critical reader such as Zeno or myself will go “Wait a minute! Are you sure that’s accurate?”. Basically, I think you need much more references to the literature or other credible sources. Furthermore, the scope of your thesis is very large (it’s a profound topic) yet it is less than 1,300 words long. To do the topic justice, I guess, would take thrice that. Things you might need to address are (for example) the various kinds of mutation in relation to repair mechanisms, the role of ecological stress, the relationship between your conjecture and viral reproduction in general, your choice of hosts (it would seem you have chosen animals and humans, not plants or bacteria, as hosts) and (perhaps) the endosymbiotic hypothesis. You don’t have to spell all these subjects out, of course. Just present the elements most vital to your conjecture and back these elements up with a credible reference. These are the prerequisites for your conjecture - so everyone needs to be on the same level as you in order to fully embrace your theory.

Speaking strictly for myself: if I were to write a piece about this vast subject it would take me roughly 60 - 100 hrs to thoroughly collect and study the literature and make a rough sketch of the piece (outline, keywords, sequencing, etc) and a day or so to actually write it.

As an example of what I personally consider to be a really good piece, see this (the author tries to find evidence for creationism in current intron-related research; I disagree 100% with creationism, but that does not change the fact that this man knows how to write a good piece!).

Last but not least, I should say that it’s a great joy for me to see that people care enough about questions like these to invest time and effort in them!!! Way to go!!

Hi

I’m out of town on business for a few days, but will respond when I get back.

Thanks

Hi zeno:

I appreciate the time and effort you put into your response. I will go through it point by point.

Ed3 wrote:
"Biological Change:
Why are advanced organisms relatively stable?

Cellular reproduction in advanced organisms is relatively stable because the Mis-Match protein, which is actually two proteins, searches for various mutations and replaces them with the original sequences in the genetic code. In addition, the immune system plays a significant role".

as far as i know, neither the anti-mismatch or the imune system work at all against the reproduction of viruses in infected cells. the proteines will keep various random mutations at bay, usually ones with physical causes, such as chemicals or radiations. they will not really stop viruses from infecting a cell, or the cell from “executing” the viral code. the imune system will create anti-corps that will bind viruses, but once the virus is inside the cell, there is little the imune system will do (except lymphocites might eat the entire cell, but afaik this is very rare indeed). so the proteins dont work against viruses at all, and the imune system only works against them as long as they are outside a cell.

[b]I did not intend this paragraph to be addressing viruses specifically.

There are many different types of viruses. The viruses that I studied were generally the common pathogens and only the retroviruses e.g. HIV could actually embed themselves in the DNA. (These things are complex and maybe I should give more definitions)? The pathogens generally do not replicate in the DNA and therefore making any conclusions about the mismatch protein is probably premature. I only mentioned the immune system because it defends against a number of types of alien threats.[/b]

this leaves us with the question of why are complex organisms stable in spite of viral infections ? indeed there can not be, i think, a single example found of a warm blooded animal that didnt contain a single active viral body in it, and yet we have yet to observe a virally induced mutation of an individual in natural settings.

I know someone who is doing genetic engineering, and during my discussions on this topic she mentioned that the geometry of the viral sheath and the receptors on the cells under attack are critically important. This is why certain viruses tend to only attack certain types of cells. For this reason I tried particularly hard to show that viruses could in theory attack the germ line. I believe that I read this same thing in the book Clinical Microbiology made ridiculously simple Edition 3 by Mark Gladwin and Bill Trattler.

Quote:
"Why are viral organisms not stable?

Viral reproductions do not produce this mismatch protein which means that they can mutate at a much higher rate.

During periods of relative stability, viruses tend not to mutate very often".

isnt this in fact begging the question ? do you define relative stability as that time when the viruses dont mutate ? or do you mean stability of the ecosystem of the likely hosts ? there are important examples, such as the avian pest transmitted to humans, or the sars epidemic, virtually any big epidemic is a case of a significant mutation, or at the very least change in the viral attack/anti viral defense equation that did not particularly follow a significant change in the ecosystem of the likely host. further, important changes such as hurricanes, catastrophic floods etseq never did, or at least not very often did produce significant surges of new viral strains (i conjecture if they were significant we should have seen them)

so, i dont think the position can be held if you mean ecosystem changes. this would need some clarification

[b]By ecosystems I meant the regional area where a viral group emerges. Such as the appropriate area in Africa for AIDS and the appropriate area in China for Sars.

In general I might have been overly swayed by Christopher Andrews’ view of viruses as parasites. I will need additional review.

In addition I did assume that if conditions did not change then there would be no need for the viruses to change and in fact that they would at least remain relatively stable. That assumption is not necessarily true.[/b]

Quote:
“Their best strategy for survival is to serve as parasites, which means that they will do best when they do not destroy their hosts”.

this is a very doubtfull statement. hepatitis often destroys its host, and yet its not even remotely extinct. rabies destroys the host in an amazingly short interval and its not extinct. herpes does not significantly affect the host, and yet its best mechanism to survive comes from the fact that it is virtually indestructible chemically. so there might be some correlation between killing hosts and the virus’ chances to survive, but its obviously not the only factor, and i dont think it can be proven its the main factor.

See above. Though I am not sure you are correct statistically. If Hepatitis B is found in 20% of the world’s population, it surely does not kill 20% of the people. Similarly, though I can’t hazard a guess, I assume that rabies is carried by a significant percentage of animals in the wild. With this in mind and if the kill/carrier ratio is small it might be possible to think of these systems as stable.
(I am starting to accept the Andrews’ view of viruses as parasites again).

Quote:
“However, during periods of ecological challenge viruses can mutate rapidly. Advanced organisms also have immunological defense systems which will attack viruses. Only during periods of great ecological change is it likely that mutated viruses will be able to overcome the immune systems defenses and also break down the mismatch protein”.

viruses can mutate rapidly anytime, and in fact they do. i take it you mean a mutated strain is more likely to survive in condition of ecological stress for the host. however, its unclear how this would work. if a strain of an existing virus appears that is, say, not affected by one of the, say, three anticorp proteines the host normally uses to neutralize the mother strain, that strain will make it regardless if the population is growing or dwindling. arguably, a growing flourishing population will give it a chance to survive longer, and take over. consider three groups of gazelles are grazing in geographically separated areas. one group develops the mutated strain. if then the entire group gets wiped out by a volcano, or slowly dies from a shift in grazing land, the virus might die with them. on the other hand, if the three groups grow, their chances to make contact increase, and as such the virus chances increase too. on the other hand, if the change in waterfall patterns forces the gazelles together, to drink from the same one pond, the virus gets better chances, while the ecosystem is not particularly stressing for the gazelles (or not as stressing as it could be)

so im not very sure why you say it has to be bad conditions for the host in order for the mutated and valuable virus to survive. on the other hand, if the mutation is not valuable, its going to die out regardless.

I assumed that the environmental stress was on the virus, and that the virus had to change sufficiently to overcome the immunological defense system. In addition, and I think that this is very important (and that I did not stress it enough), the geometry of the viral sheaths and/or the receptors needs to mutate because the virus NEEDS to attack the germ line. Finally, the minuscule percentage of viruses that could ultimately be embedded in the DNA of the germ line must be able to withstand the mismatch protein(s). Of course the host system would likely be strained as well.

Quote:
We need to establish that there is some likelihood that viruses can in fact have their genetic code, or a generated intermittent code, embedded in the host in such a way that this modification can be reproduced in succeeding generations. We know that genetic engineering can already insert DNA fragments into viruses which will attack the germline of the host and that genome of the offspring will carry this embedded code, however we need to show that this insertion can happen naturally.

actually i am pretty much convinced this is indeed possible, and has occured naturally

This was not clear to me and I spent a lot of time working on it. The leukemia
virus in mice was the only example that I could come up with where the virus was transmitted to the offspring’s genome. In all other examples that I looked at, the viruses were attached to specific cell types that were not transmitted to the offspring’s genome. I think the Danish work also supports my position because it is both extremely rare but it does in fact happen.

Quote:
"Can viruses attack in numbers sufficient to produce a sustainable reproducing sub group?

Some examples of large viral outbreaks include the Spanish Flu of 1918 in which 2 different viruses attacked and exchanged their protein sheaths*. This in turn played havoc with the immune systems response and the result was the death of about 10% of the worldwide population*. Another virus, which can be very dangerous to the host population, is the Hepatitis B virus, which is currently carried by about 20% of the World’s population*. The final virus sited is the Herpes Simplex A which is carried by about 90% of the population over 40 years of age*.

Assuming that the viruses can attack the germline and that the mutated offspring are provided with appropriate survival mechanisms, the subgroup should be large enough to sustain itself. It should be stressed that this will only happen during periods of great ecological change. Under these conditions, the non-mutated generating organisms will be at a point of collapse."

we agree that it can happen, but i still don follow why you insist on great ecological change. there was little ecological change going on in 1918, as far as i know. the bits of the genome that are being credited to viruses might have appeared in condition of ecological catastrophe or stability, as far as we can tell. so where does that requirement come from ?

[b]I think that the most critical thing that I have failed to communicate is that the viral change has to be sufficient to overcome the immunology of the species that is modified, and the viral sheath geometry must be changed to match the germ line of the species that is modified. Finally the viral attack, once embedded in the germ line DNA, must defend against the mismatch protein(s)

The most desirable traits that I could hope for are:
that this type of genomic embedding is a very rare occurrence (I want a system with a long term stability), and I also need a relatively massive attack so that the offspring can have a sufficiently large population to sustain itself. [/b]

Quote:
“Assuming that viruses can embed themselves in the host genome should compel us to ask if embedded viruses have been found in mapping the Human Genome. The answer is yes. Approximately 8% of the Human Genome is remnants originated from retroviruses****. Additionally, we know that all but one of the mapped human endogenous retroviruses were implanted over 25 million years ago. I have found no references regarding embedded adenoviruses. It should be noted that only slightly over 1% of the Human Genome is used for encoding of genetic material.”

and while we are not very sure what the overlap factor is, it might not be very large at all, the 8% would fit pretty well in the slack space left by the 1%. statistically, since the two should be independent, about the same 8% of viral influence should be found in significant human dna as it is found in overall dna. afaik its nowhere as important, which might suggest there are systems in place to keep the viral influence in the shadow of the slack dna.

I should have stressed the viral open reading frames. The work by the Danes, that I referenced, goes into some detail on this matter. I should make a better effort to understand and communicate it’s implications. I will only say that it does not appear to be insignificant.

It’s gonna be a long time before we play go, if I do all the work ToWander wants me to do.

Thanks again Ed

Hi ToWander:

Thanks for your response.

From zeno’s comments, I think that it is obvious that I need to do a better job of explaining the nature of viruses in the first place, giving some fundamental definitions which would aid people in reading this material, and most importantly, concisely stating all of the hurdles that a virus would have to overcome in order to actually be embedded in an offspring genome.

I am, however, having reservations about writing a formal paper on the subject. The most obvious problem is that the Danish people are younger, brighter, better educated, better equipped, and looking for the same things as I.

I started working on this concept about a year and a half ago. I believed that it was a fundamental thing, it should add to the Theory of Evolution and as such at least in part answer who are we? and where do we come from? The more evidence I gathered the more convinced I became that the conjecture was true as well as the secondary assumptions that I made. Finding the Danish research which was published just last October really seemed to finalize and verify my efforts. For these reasons, I am willing to do the work you suggested, but is there any reason to think there will be any weight given to it by others (I have no qualifications what so ever), or that it will offer any significant advantage over the Danish work?

[contented edited by ILP]

Hi abgrund:

Thanks for filling in that information. By the way, what is IIRC?

I think that most people simply consider viruses as agents of disease. In fact that is essentially what I thought until I got into this subject. It wasn’t until I read Christopher Andrew’s view on this matter that I realized that viruses could be viewed as parasites. It was actually kind of eye opening.

You must have done a lot of reading to get to this point, and I want to thank you for that.

[contented edited by ILP]

ed, in feyman’s words, science listens to a bright lad with an idea just as attentively as to the old professors. should you find the time and inclination, you can safely complete your paper, and i am sure it will not be overlooked.

I thought I might give a status update.

The most important finding so far is actually in the Danish Research which I referenced with a link.

Certain embedded viruses have been shown to produce the protein Syncytin, which “mediates cell-cell fusion during human placenta formation”.

This means that placental mammals, scientifically Eutherian Mammals, could not develop as we know them without the embedding of a virus in our DNA.

You might think about that the next time you contemplate your navel!

Things that have gone wrong:

We do not know for certain that the viruses come through the germ line. They could have always been part of the soup that makes up our cell structure. (I have found three references all of whom believe that the viruses have entered through the germ line, and one of which referenced yet another as a source for this conjecture, but I am not convinced that I can overcome this logical problem).

I have done some research on mammals and found that they are DNA dated from about 95 million years ago to 105 million years ago (2). While this appears to fit my theory that significant ecological change should be occurring - the continent of Gondwanaland was breaking apart at that time - the explosion of mammals does not take place until about 65 million years ago, after the dinosaurs became extinct.

Also my topic seems to be all the rage on the Virology site for about the last 4 years. Not to mention that the pre-med student got it right. This means that it is being taught at the undergraduate level.

Proposed Outline

[code]I) State Thesis
********An additional Evolutionary Mechanism should include viral embedding
********in an organism’s genome.
II) Background
********A) The problem of stasis - Punctuated Equilibrium
***************1) What are the probable causes of vertebrate stability.
***************(Is this the right group - is the mismatch protein
***************generated for all vertebrates)?
***************2) Discribe the Immunological System in some
***************detail.
***************3) Discribe the mismatch protein in some
***************detail
***************4) Show how subgroups can be too small to
***************sustain themselves. Give examples.
************************a) There is some evidence that
************************complex organisms require a larger ************************sucessor population to survive.
************************Explore
************************b) Side note on 3. Population
************************Biology specifies the Logistics
**********************function Nnext = AN(1-N) to describe ************************population growth. This is a classic ************************chaotic recursion problem.
***************5) Others?
********B) The General Nature of Viruses
***************1) Examples:
************************a) RNA - I thought this would fail
************************because of Uracil (Not found in DNA)
************************b) DNA - I thought that this was
************************the best canidate
************************c) Retroviruses. - At first I thought this
************************would fail for the same reason as a
***************2) How Retro viruses work - contrast with
***************RNA and DNA viruses
***************3) How Retro Viruses can become embedded in a
***************cell’s DNA generally
***************4) View of Viruses as Parasites (even
***************though viruses change frequently, will this
***************psychologically allow the reader to accept
***************that viruses do not go through radical changes
***************all the time)? Should I just skip? Note -
***************there are a number of references and I think
***************this is the standard view at this time.
********C) How do viruses actually attack a cell structure.
***************1) Describe sheaths
***************2) Describe the nature of the receptors on
***************the cell wall
***************3) Give examples of how viruses attack
***************specific types of cells.
III) Restate Thesis
********A) State Thesis - An additional Evolutionary
********Mechanism should include viral embedding in an
********organism’s genome. (Why? Because the time
********frames are significantly different). I should try to
********emphasize this
***************1) Show how Viruses can overcome the
***************Immunological response - Easy
***************2) Explain why it is critical that the virus
***************should become embedded in the germ line DNA.
***************3) Show that it is possible that a virus can
***************naturally enter the germ line. (This may be
***************difficult but I think that I can make a
***************plausible argument)
***************4) Show that it is possible for the virus to
***************be embedded in DNA of a germ line host where
***************the mismatch protein does not replace the
***************embedding .
***************5) Show that it is plausible that viruses
***************can attack in sufficient numbers so that a
***************sustainable offspring might support itself.
***************(Also Easy)
***************6) Give the Results of the Danish Study.
***************Then admit that at present it is not possible
***************to determine if the retrovirus came from the
***************germ line or if it was mixed from the viral
***************retroposons (Unless I can find compeling
***************contary information)
********B) Show consequences
***************1) HERV K group comes in around the time of
***************the radiation of the great apes?
***************2) Specific Examples of change.
***************3) Expected results & unexpected results.
********C) Talk about unresolved matters in the “Junk DNA”
********D) Check out the timing for the older HERV groups.
********Could they actually have occurred at the times of the
********Great extinction (250 Million years ago) and/or the
********extinction of 65 Million years ago?

IV) Close. How do you close this thing?[/code]

Things to research:

********I) Environmental Stasis
********II) Virus sheaths and cell receptors
********III) Show how the viral embedding changed the human species
********IV) Research timing of other viral infections
********V) Give additional detail on how viruses might enter the germ line.
********VI) Others?
Facts General:
********Minimum of 26 embedded HERV groups could be over 100. (1)
********There are seven genera of retroviridae. (1)
********Viruses are presumed to have entered via the germ line, but it is possible that
********they evolved from pre-existing genomic elements such as LRT
********retrotransposons. (1)
********“Conservation of an open reading frame during primate evolution clearly
********suggests some biological function.” (1) - I need to know more about this!!!
********the presence of enhancers and hormone-responsive elements in the LTR
********structure of existing HERVs may up- or down- regulate the transcription of
********flanking cellular genes. (1)
********HERV-H, HERV-W, and HERV-R still retain at least a single open reading frame
********(1)

Facts showing specific change:
********“HERV loci have been shown to alter gene expression by providing alternative
********transcription initiation, new splice sites or premature polyadenylation
********sites.” (1)
********“animal studies have demonstrated that ERV proteins may in fact serve a
********useful role for the host either by preventing new retroviral infection or by
********adopting a physiological role.” (1)
********“Syncytin, an Env-derived protien that mediates cell-cell fusion during
********human placenta formation provides a striking example.” (1)
********“Env proteins may also inhibit cell entry of related exogenous retroviruses that
********use a common surface receptor, and a Gag-derived protein restricts incoming
********retroviruses in mice.” (1)
********“In the literature, expression of HERVs has frequently been linked with human
********disease including various cancers and a number of autoimmune disorders.
********While causal links between disease and HERV activity have yet to be
********established, it is clear from animal models that expression of endogenous
********retroviral proteins can affect cell proliferation and invokes or modulate
********immune responses.” (1)

The following are the known active viral genes (fewer than I had guessed):

Gene Chromosome Position of locus
HERV H-like Env X 70307525-70316940 (+1)
EnvF(c)1 X 95868842-95875915 (+1)
HERV-W Env X 105067535-105070015 (-1)
HERV-K Env (type 1) 1 75266332-75270814 (+1)
HERV-K Env (type 1) 1 157878336-157885675 (+1)
EnvH3 2 155926784-155933168 (+1)
HERV-K Env (type 1) 2 130813720-130815944 (-1)
EnvH1 2 166767087-166774769 (-1)
EnvR(b) 3 16781208-16788508 (+1)
HERV-K Env (type 1) 3 114064939-114072223 (-1)
EnvH2 3 167860265-167867997 (-1)
HERV-K-like Env 5 34507318-34513254 (-1)
EnvFRD 6 11211667-11219905 (-1) Syncytin 2
EnvK4 6 78422690-78431275 (-1)
EnvK2 7 4367317-4383401 (-1)
EnvR 7 63862984-63871411 (-1)
EnvW 7 91710047-91718755 (-1) Syncytin (1)
EnvF(c)2 7 152498159-152502575 (-1)
EnvK6 8 7342682-7353583 (-1)
HERV-K Env 11 101104479-101112064 (+1)
HERV-K-like Env 12 104204746-104209814 (+1)
EnvK1 12 57008431-57016689 (-1)
ZFERV-like Env 14 91072914-91085655 (-1)
HERV-K Env (type 1) 16 35312483-35314318 (+1)
EnvT 19 20334642-20343232 (+1)
HERV-W/FRD-like Env 19 58210000-58211244 (+1)
HERV-W/FRD-like Env 19 58244133-58246051 (+1)
EnvK3 19 32821287-32829201 (-1)

The following are the known locations of the viral embeddings:

********Chromesomne # 1****2****3****4****5****6****7****8 ********HERV #*******654**534**581**641**446**496**342**396 ********Chromesomne # 9****10***11***12***13***14***15 ********HERV #*******258***304**379**393**239**205**581 ********Chromesomne # 16***17***18***19***20***21***22 ********HERV #*******101***98***167**259**76***85***55 ********Chromesomne # X ****Y ********HERV #*******629***359
(1) The article published October 4, 2004 on the site retrovirology.com/content/1/1/32 entitled “Identification of endogenous retroviral reading frames in the human genome” published by Palle Villesen, Lars Aagaard,Carsten Wiuf, and Finn Skou Pedersen all of University of Aarhus located in Aahus published University of Aarhus. This is a very interesting site.

(2) The article published in Journal of Heredity 2001:92: 212-219 by E. Eizirik, W.J. Murphy, and S.J. O’Brien.

Hi to everyone:

I ran across this link christianforums.com/t96639-e … tml&page=8 Dated March 27, 2004 while doing some research on my Evolutionary Mechanisms conjecture. I found it by searching for HERV-L with the exact word genome. I was struck by the poignancy of the conversation of these obviously bright and informed posters. You might notice that it predates my original post.

I also need to correct an error I made in assuming that Syncytium was required for the development of placentas. The protein Syncytium is not present in some rodents.*

The best dating that I have run across for Syncytium, the HERV-W env gene’s expressed protein, is about 45 million years ago.. An older viral embedding dated at about 60 million years was found in an HERV-W-LTR though the open reading frames have mutated and are no longer active. The oldest known still genetically active gene encoding for Syncytium (technically termed Syncytium 2) is derived from the viral family HERV-FRD*. I have been unable to find a specified date for the embedding of this virus.

The oldest specific dating for a viral insertion into our genome is simply stated to be approximately 70 million years. The particular virus family is denoted as HERV-H**. I would like to find much older dates in order to better support my conjecture.

With regard to current events, the HERV-K viruses are the most recent embeddings. These viruses have embedded themselves in our genome repeatedly over a long period of time. The initial embedding is dated to about 45 million years ago****. Another embedding took place about 5 million years ago , “both before and after the evolutionary separation of humans and chimpanzees.” **** The most recent embedding is HERV-K113 which is found exclusively in humans and is dated to less than 200,000 years ago. This viral embedding is found in about 19% of the population. “…it is rare in Caucasians, it is more abundant in African, Asian, and Polynesian populations.” ****

Relative to the methodology of entry, I continue to find that virtually everyone thinks that the initial embedding of a given HERV family comes as a viral infection to the host, and then enters the hosts germ line. However, there is some interesting work showing that, after this first infection, there may be some reinfections that are internal to the host.*****

As a final comment, for now, I have not been noting all the possible negative influences. There are many diseases which have been statistically linked to “provirus partials” and the interest in this matter is quite high. In fact it is obvious to me that the relatively plentiful data on HERV’s exists because there are institutions with big bucks wanting all the information they can get on this matter.

• In an article entitled Expression and Functions of Human Endogenous Retroviruses in the Placenta: An Update accepted January 5, 2004 by A Muir, A Lever, and A Moffett,

** Journal of Virology (1999). Citing Steinhuber et al form (1995), Anderssen et al (1997), and Medstrand & Mager (1998).

***National Academy of Sciences publication entitled “Retroelements and the human genome: New perspectives on an old relation” by Norbert Bannert and Reinhard Kurth. Dated October 5, 2004

****National Academy of Sciences publication entitled “Therapeutic Vaccines: Realities of Today and Hopes for Tomorrow” by Norbert Bannert and Reinhard Kurth. Dated October 5, 2004

*****Molecular Biology and Evolution. Article entitled “High Copy Number in Human Endogenous Retrovirus Families is Associated with Copying Mechanisms in Addition to Reinfection” by Robert Belshaw, Aris Katzourakis, Jan Paces, Austin Burt, and Michael Tristem. Originally Published Online January 19, 2005.

******(2) The article published in Journal of Heredity 2001:92: 212-219 by E. Eizirik, W.J. Murphy, and S.J. O’Brien.

Nice essay Ed3, you’ve done a hell of a lot more reading than me.

Hi Tab,

I was surprised to see that you actually went back and read my essay. Not so easy to find, and fairly lengthy to read. I am truly honored.

Of all the posts that I have made on ILP, this is my favorite. How many times in our lives do we get a chance to advance a significant theory about our origins? Don’t get me wrong, I think that it is unlikely that I was the first to propose this mechanism, but I do think I might have aided some others in understanding these things. (There are still about 30 views per week, virtually all of them from various search engines, I assume).

My only regret is that I lacked the literary skills to do it justice. Funny how we all have our strengths and weaknesses.

Thanks Ed

I’m surprised Tabula Rasa didn’t think your essay was too long.
Perhaps it was just right; borderline between being too verbose and interesting enough to maintain his attention sufficiently before the baby distracted him or a fly buzzed by braking his concentration.
Maybe it was short enough for him to justify the time required to get through it and the cost to his ego, for wanting to.
Maybe your reasoning was unfamiliar enough to him or exotic enough, to not insult him for not thinking of it first.

Why study viruses when human beings provide ample behaviors requiring analysis?

Hey, sorry to bust in and off topic, but I was glancing through and am I the only one creeped out by the posts with,‘‘edited by ILP’’ and ‘‘deleted by management’’ on them?

I am sure that the person was offensive or something serious like that, but I just got a little Stazi-Alarm in my head.

Hope I don’t get snatched or something, no offense meant to the…‘‘management’’…

Hi Satyr,

I have a hard time keeping up with my current commitments and interests.

Hi TertiaryMindset.!,

Abgrund made those comments and deletions himself in response to a management enforcement on an unrelated matter in a different post on a different forum.

Hi to All,

I am just posting in order to keep this post close to my post on the Twin Paradox.

Thanks Ed