Endogenous retroviruses

[JohnR7]

Oh? You've tested the Bible's factual statements? Then tell me John, just what did you mean by these previous statements?
Gee, that doesn't sound like you tested the Bible John.

It is pretty clear here that you are a scoffer. So, it is a easy thing for me to run a search and look to see what the Bible says about scoffers:

Proverbs 22:10
Cast out the scoffer, and contention will leave;
Yes, strife and reproach will cease.

It looks like Solomon in the writting of Proverbs associates three things with a scoffer: contention, strife and reproach. Well, all three seem to apply here, so I would say once again the Bible has been tested and found to be true.

Yet, you do seem to have some interest in finding answers to your questions, so lets see what I can do to answer them.

That doesn't sound like you're even interested in testing the Bible.

I think that perhaps your the one that is not interested in "testing" the validity and the truthfulness of the Bible. I love the Bible and I love to study the Bible to learn more of what there is to learn from it. There is no end to what can be gained from a study of the word of God.

If anything, I think that if someone tested a factual statement from the Bible and the result "did not line up with the Bible," you would simply ignore the test.

I would not necessarily ignore the "test". I might check first to see if my understanding of what the Bible is saying is right or not. The Bible always remains steadfast, and consistantly true. If man's opinion does not lines up with the Bible, then the problem must be with his opinions. Even our own opinons we have to take them to the Bible to test them to see if they line up with the word of God or not.

Sounds good. Let's take a look at some of these promises.

This sounds like a purely psychological effect, John. Is God supposed to be some sort of supernatural Valium? From various descriptions, I had somehow expected something more material and less subjective. But more to the point, how can you be sure that this peace that you experience is the result of God and not merely your own self?

I do not like the word: "supernatural". But even if the effect was "purely psycyhological", at least you get the effect without taking drugs and having to deal with all the side effects that go along with drugs.

Now, your next question is very interesting. It is a key issue in the study of modern medicine today. It is pretty well known that in order for a patient to show improvement, they usually need to have some degree of confidence in the "cure". In some cases, if the "healer" shakes a baby rattle, sings a wierd song and does a dance, the sick person will improve and they may even get better. IF they have confidence that cure is going to work.

Now, you have three things to deal with here. First of all, in a lot of cases a illness is going to run it's course and the patient is going to get better anyways. So the doctor will give the patient a "cure" to help ease their mind and help speed along the recover process.

Second of all, we have the placebo effect, where as I mentioned, if the patient has confidence in the cure, this can help in the recover process. The opposite is also true. If the patient does not have confidence that they are going to get better, they may not.

Now, we come to your question and the heart of the matter. How do we go beyond what people can do on their own, and what can only be accomplished when God becomes a part of the healing process. Along with repentance and a change of heart of course. This is where we need to demonstrate healing that just does not take place in the natural. Two things that come to mind is where the patient has nerve damage in the ear that results in some degree of deafness. In most cases, nerves do not regenerate themselves. So this would require a reconstruction miracle for the person to show improvement. Another example would be Aids, esp in advanced stages. Where the patient is not able to work any longer and are on the edge of death. Again, in these cases I think it is pretty clear that a recovery is the work of God.

Now, as a Christian, I have spiritual discernment. That is the Holy Spirit of God shows me what God is doing in people lives at time. So, I can give a witness and a testimony to others in what I have seen God do.

For that matter, what is your explanation when a Christian does not find peace? Or what if a non-Christian finds peace. In your specific case, how was this test carried out?

Remember, we are not talking in general, we are talking about a specific promise from the Bible. Lets look at the scripture again:

Isaiah 26:3
You will keep him in perfect peace,
Whose mind is stayed on You,
Because he trusts in You.

The promise here is the perfect peace of God. Now the first thing we have to do is look at the "condition". What is our part in the deal. It is clear that our contribution is to keep our minds steadfast on God. We must put our trust in God. I have already talked about how powerful it is to trust in God. It is His desire for people to learn to trust Him. He wants us to know that He is trustworthy. So, if we do our part, then we can be sure that He will do His part to keep us in perfect peace. If we do not do our part, then we can not expect to claim the promise in our lives.

Again, this sounds like a purely psychological effect. Previous questions apply.

Well, I think we covered all of that. I agree that we must show that by putting our faith in God, we need to show better results that what we would get by putting our faith in a person with a baby rattle that can sing funny songs and do strange dances. At times we will tell people to get all the help that man has to offer you. Do everything you know to do in order to get results. Then when all else fails, turn to God.

And just how does one know what God's plan is? Personages like Adolf Hitler, George W. Bush, and Mother Teresa thought they were carrying out God's orders. Were they? How can you distinguish someone who's genuinely carrying out God's plan from someone who is just saying that to someone who's simply mistaken? What happens when a Christian performs actions that are detrimental to society? What happens when a non-Christian performs actions that benefit society? In your case, how was this test carried out?

We need to be lead by the Holy Spirit of truth. We need to study the word of God to know what is of God and what is not of God. We really can know what God's plan is. He desires to redeem and to restore mankind. His offer is open to who so ever is willing to come, let them come to God and be healed and be made whole.

The desires of the heart, eh? Could you perhaps be more specific? Usual questions regarding Christians and non-Christians apply.

This is a good question. It only makes sense that God is wanting to give us what God is wanting us to have. Our heart needs to line up with the heart of God. Our desires need to line up with what He desires to give us and what He desires to do in our lives. This is all a result of purifying our hearts before God. Or allowing Him to do a work in our lives to purify us of all evil desire.

God wants to do good in our lives. He promises that He will not deny us of any good thing. He knows what we can handle and what is good for us, and he wants to pour out His blessing in our lives. Now, what maybe good for one person, may destroy another person. So, this is where we need to trust in God, to know that He knows what is best for us. Just as a child will trust in their parents to provide for them, to take care of them and to do good things for them.

The only one peddling anything is you, John.

Could be, but I am not on a commission. I will get my reward if you buy what I am "peddling" or if you do not "buy it". I am not asking you for any money. I give what I have for free, without cost. Actually, all I care about is that people do not give me a hard time when I make my presentation. If when I am done they say sorry, I am not interested, that is fine. As long as I have done my best to "peddle" my product, then what more can I do, other than to give my best and do my best to represent the one who sends me.

God is the one who will ultimately judge me, not man, so I do not seek tp please people, I seek to please God and I try to do His will.

 

[ed_m]

much as i hate to get involved in this.. i was referred to ERV on another thread, googled it and ended up back on here.
so i've read the whole shebang and tried my best to ignore the childish gleefull cries of 'yes... got them now!' and the usual personal slanging match that a few from either side always like to get themselves into.

just a couple of considered questions not that i truly beleive anyone here has the required phd in genetics to answer with authority! although it's possible i suppose.

Q1: Probability
relates i think to dexx's question on P.9.

Descriptions on the first page explains that some proportion of viral hijackings fail leaving their genetic material in the cell, out of all the cells in the body this must happen to one that is used for reproduction in order to be passed on to the next generation. assuming for now genetic drift explains why this non-advantageous genetic change propogates to the whole species.

In the pre-emptive creationist rebuttal of such an identical insertion by the same virus in two seperate species a big deal is made of the probability being minute.

A similar probability study does not seem to be presented for the original ERV process, what is the probability of a viral hijacking failing? what is the probability of a virus hitting the required cell to be used in reproduction?

As an example, if i get a suitable virus, what proportion of the cells in my body are succesfully hijacked? what proportion of the cells in my body would suffer a failed hijacking? what proportion of the cells in my body are used in reproduction (and hence capable of passing on the genetic material)?

Q2: Multiple Insertions

Given that
- We've said insertion points for the virus are essentially random (although this has been debated), or have many possibilities even if we consider there to be some hotspots.
- Genetic drift (if i follow correctly) is likely to propogate this non-advantageous genetic change throughout the population.
- The originating virus is likely to be passed around that progression of species repeatedly across a range of generations (?)

Do we see multiple insertions of the same ERV in the DNA?
Ideally could we see a species tree (or whatever it is!) whereby the ancester passes on a specific ERV, and one branch of that tree is hit by the same virus, which results in the same ERV in a different location?



I've tried to word and structure this clearly, but feel free to query anything that isnt clear.

Cheers guys & gals.

 

[Ondoher]

much as i hate to get involved in this.. i was referred to ERV on another thread, googled it and ended up back on here.
so i've read the whole shebang and tried my best to ignore the childish gleefull cries of 'yes... got them now!' and the usual personal slanging match that a few from either side always like to get themselves into.

just a couple of considered questions not that i truly beleive anyone here has the required phd in genetics to answer with authority! although it's possible i suppose.

Q1: Probability
relates i think to dexx's question on P.9.

Descriptions on the first page explains that some proportion of viral hijackings fail leaving their genetic material in the cell, out of all the cells in the body this must happen to one that is used for reproduction in order to be passed on to the next generation. assuming for now genetic drift explains why this non-advantageous genetic change propogates to the whole species.

In the pre-emptive creationist rebuttal of such an identical insertion by the same virus in two seperate species a big deal is made of the probability being minute.

A similar probability study does not seem to be presented for the original ERV process, what is the probability of a viral hijacking failing? what is the probability of a virus hitting the required cell to be used in reproduction?

As an example, if i get a suitable virus, what proportion of the cells in my body are succesfully hijacked? what proportion of the cells in my body would suffer a failed hijacking? what proportion of the cells in my body are used in reproduction (and hence capable of passing on the genetic material)?

I cannot answer this directly, however infection of a germ cell is obviously the only method to get a retrovirus to become a permanant part of our genome. According to Theobald, "In humans, endogenous retroviruses occupy about 1% of the genome, in total constituting ~30,000 different retroviruses embedded in each person's genomic DNA" http://www.talkorigins.org/faqs/comdesc/section4.html#retroviruses. That's a lot of such events.

Q2: Multiple Insertions

Given that
- We've said insertion points for the virus are essentially random (although this has been debated), or have many possibilities even if we consider there to be some hotspots.
- Genetic drift (if i follow correctly) is likely to propogate this non-advantageous genetic change throughout the population.
- The originating virus is likely to be passed around that progression of species repeatedly across a range of generations (?)

Do we see multiple insertions of the same ERV in the DNA?
Ideally could we see a species tree (or whatever it is!) whereby the ancester passes on a specific ERV, and one branch of that tree is hit by the same virus, which results in the same ERV in a different location?

As the insertions can be messy, it might be hard to pick out a "species" of retrovirus from the insertion to indentify them as "the same". However, what we do find is that we can build phyloegenies (evolutionary trees) from ERV data that match the phylogenies drawn from anatomical data: http://www.pnas.org/cgi/content/full/96/18/10254

I've tried to word and structure this clearly, but feel free to query anything that isnt clear.

Cheers guys & gals.

 

[Loudmouth]

Q1: Probability
relates i think to dexx's question on P.9.

Descriptions on the first page explains that some proportion of viral hijackings fail leaving their genetic material in the cell, out of all the cells in the body this must happen to one that is used for reproduction in order to be passed on to the next generation. assuming for now genetic drift explains why this non-advantageous genetic change propogates to the whole species.

Certain viral insertions may actually confer an advantage. One such insertion is thought to be important in placental evolution, for example.

In the pre-emptive creationist rebuttal of such an identical insertion by the same virus in two seperate species a big deal is made of the probability being minute.

A similar probability study does not seem to be presented for the original ERV process, what is the probability of a viral hijacking failing? what is the probability of a virus hitting the required cell to be used in reproduction?

The evidence for this comes in two different forms. First, infection of cells grown in petri dishes by retroviruses rarely creates these type of ineffective insertions. Second, if this type of ineffective insertion were common then we would expect to find large variations in retroviral content among humans. Simply, differences are rare and therefore it is thought that ERV production is a rare event.

As an example, if i get a suitable virus, what proportion of the cells in my body are succesfully hijacked? what proportion of the cells in my body would suffer a failed hijacking? what proportion of the cells in my body are used in reproduction (and hence capable of passing on the genetic material)?

I am not sure about the infection rate. But, as I said before, if the production of ERV sequences in germ cells was common then we would see large differences among humans. It is rare that humans differ in ERV insertions.

Q2: Multiple Insertions

Given that
- We've said insertion points for the virus are essentially random (although this has been debated), or have many possibilities even if we consider there to be some hotspots.
- Genetic drift (if i follow correctly) is likely to propogate this non-advantageous genetic change throughout the population.
- The originating virus is likely to be passed around that progression of species repeatedly across a range of generations (?)

Do we see multiple insertions of the same ERV in the DNA?
Ideally could we see a species tree (or whatever it is!) whereby the ancester passes on a specific ERV, and one branch of that tree is hit by the same virus, which results in the same ERV in a different location?

That is exactly what Ondoher's post shows. There are ERV's in the chimp genome that are not in the human genome. This is an important point, so I will try and clarify. For evolution to be true, and therefore common ancestory, if humans and chimps share an ERV insertion then gorilla's must also share that same ERV insertion. If chimps and gorillas share an ERV insertion humans DO NOT have to have that ERV since chimps and gorillas share a more recent common ancestor. Just to continue, if orangutans and chimps share a common ERV, then humans must also have that ERV. These are predictions made by the theory of common ancestory and the theory of evolution, and in every test of those predictions the theories pass. There is no requirement for a creator to adhere to this pattern, but there is a requirement for common ancestory to follow this pattern. Therefore common ancestory is a better model.

Also, if you do a search for "ERV" at www.pubmed.com you will get references to the primary literature and research in this field. There are several families of ERV's, such as ERV-K, ERV-H, ERV-W. They are characterized by their genes and LTR's. There are several insertions of each family in our genomes and they are spread over all of our chromosomes. A recent paper looked at the insertion pattern of three retroviruses: HIV, ASLV, and MLV (paper here). This study mapped the insertion of these retroviruses in the DNA of the host cells. From this table you can see that the viruses inserted in different places for each separate infection (over 3,000 insertions were tested). The HIV sites are blue, the MLV sites in lavender, and the ASLV sites in green. The paper did find hotspots for each viruse. However, there are thousands of hot spots for each virus and thousands of bases within each hotspot. Therefore, the data supports the interpretation that the same insertion at the same nucleotide in two different species would be very improbable.

I've tried to word and structure this clearly, but feel free to query anything that isnt clear.

Cheers guys & gals.

Same here. If you need clarification on anything let us know.

 

[ed_m]

Simply, differences are rare and therefore it is thought that ERV production is a rare event.

so sticking to Q1 for now, to become embedded in the genetics of a species a virus has to fail to infect a cell (rare occurence), that cell has to be one out of billions in the body (for want of a better term) used for reproduction (one in hundreds of thousands?), and that sperm/egg has to be the one of many that results in a viable offspring (one in hundreds?), and the resulting offspring has to stick about long enough to reproduce (reasonable odds? 50:50?).

the combination of odds strikes me as likely to get to less than the one in 11000 considered unlikely enough to be negligible in the independant insertions deconstruction.

 

[kingreaper]

That is exactly what Ondoher's post shows. There are ERV's in the chimp genome that are not in the human genome. This is an important point, so I will try and clarify. For evolution to be true, and therefore common ancestory, if humans and chimps share an ERV insertion then gorilla's must also share that same ERV insertion. If chimps and gorillas share an ERV insertion humans DO NOT have to have that ERV since chimps and gorillas share a more recent common ancestor.

I'm pretty sure its chimps and humans that are closer together than chimps and gorillas (otherwise chimps and gorillas would be equally distant from us, and chimps are alwayss mentioned as our closest relatives)

Correct me if I'm wrong

 

[Loudmouth]

I'm pretty sure its chimps and humans that are closer together than chimps and gorillas (otherwise chimps and gorillas would be equally distant from us, and chimps are alwayss mentioned as our closest relatives)

Correct me if I'm wrong

Doh, you got me on that one. I always seem to forget that humans and chimps share a more recent ancestor than gorillas and chimps. Good catch.

 

[Loudmouth]

so sticking to Q1 for now, to become embedded in the genetics of a species a virus has to fail to infect a cell (rare occurence), that cell has to be one out of billions in the body (for want of a better term) used for reproduction (one in hundreds of thousands?), and that sperm/egg has to be the one of many that results in a viable offspring (one in hundreds?), and the resulting offspring has to stick about long enough to reproduce (reasonable odds? 50:50?).

the combination of odds strikes me as likely to get to less than the one in 11000 considered unlikely enough to be negligible in the independant insertions deconstruction.

It makes sense that new ERV insertions happen rarely since we do not see them occuring with any frequency in the human population. The odds are slim for an ERV even becoming part of the genome, much less the same one occuring in two separate individuals in the same exact nucleotide position in the genome. Do you agree that it is very improbable that two people would share the same ERV in the same nucleotide position from two separate viral infections?

 

[h2whoa]

not that i truly beleive anyone here has the required phd in genetics to answer with authority! although it's possible i suppose

Know thy enemy. Know thy enemy.

I am currently working for my PhD. So I do have a BSc in Genetics from the University of Liverpool and am currently working for a research group in order to get my PhD.

h2

 

[ed_m]

Do you agree that it is very improbable that two people would share the same ERV in the same nucleotide position from two separate viral infections?

well no i don't agree because i don't have time to fully understand the complexities of ERV and hotspots. best ask h2whoa but i suspect we know the answer there

The odds are slim for an ERV even becoming part of the genome, much less the same one occuring in two separate individuals in the same exact nucleotide position in the genome.

well thats exactly my question. the odds for one case are presented but not for the other.
so far no one has made an attempt to critique the odds i put in my Q1 example (which were off the top of my head).

 

[h2whoa]

Well you are right that the odds against the retrovirus (RV) inserting into the germline are low compared to them inserting into somatic cells (that is to say cells that comprise most your body). There are a lot of RVs out there and it is because of this realtively low chance of infecting a germline cell that the whole genome is not swamped with ERVs.

Don't forget as well, and this is really the vital main point, that viruses have very specific points of action. They can only successfully infect certain target cells (on the whole). Therefore, to become an ERV, the RV has to be a virus that specifically targets the germline cells for infection. This targeted infection removes the factor of random infection of the germline.

I hope I've explained that reasonably well

h2

 

[Karl - Liberal Backslider]

I'm not sure Ed_m is comparing odds for the same things. It seems that his 1:11000 probabilility is that of a ERV occurring in a given individual in a way it can be passed on; the original 1:11000 was the probability of two individuals getting the same ERV in the same position independently, given extremely generous parameters.

Given the size of populations, an event with a probability of 1:11000 is going to happen quite a lot. This is where the second observation comes in; the way in which those ERV patterns match the patterns predicted by already established evolutionary phylogeny. For this to have happened by chance, the 1:11000 chance of two individuals randomly getting the same ERV has to have happened every time there was an insertion, to just the right individuals to mimic the evolutionary phylogenic tree.

That's a whole lot of improbability. Eddie the shipboard computer? Are you there?

 

[Jet Black]

That is exactly what Ondoher's post shows. There are ERV's in the chimp genome that are not in the human genome. This is an important point, so I will try and clarify. For evolution to be true, and therefore common ancestory, if humans and chimps share an ERV insertion then gorilla's must also share that same ERV insertion. If chimps and gorillas share an ERV insertion humans DO NOT have to have that ERV since chimps and gorillas share a more recent common ancestor.

Just want to correct you here. if your final statement was correct, the rest would be correct too, however it isn't. Humans and chimps share a more recent common ancestor. So if we find a human and a gorilla with an ERV, then we will find chimps have them too, but an ERV shared between a human and a chimp will not nescessarily be shared by gorillas. but if only humans have an ERV and chimps don't then gorillas won't either.

 

[ed_m]

I'm not sure Ed_m is comparing odds for the same things.

please read the question again. forget i mentioned 1:11000 (which was me rounding up btw). although you seem to say in one case this would be good odds whilst in the other it's so small as to be negligible.

what i'm after is the probability of a virus becoming part of the genome for the species, that depends on:

odds of failed insertion
odds of failed insertion in germline cell (whatever that is)... i.e. proportion of RV's that target those cells (thanks h2whoa)
odds of the germline cell going on to become a viable next generation
odds of that next generation animal living long enough to reproduce.

 

[Jet Black]

please read the question again. forget i mentioned 1:11000 (which was me rounding up btw). although you seem to say in one case this would be good odds whilst in the other it's so small as to be negligible.

what i'm after is the probability of a virus becoming part of the genome for the species, that depends on:

odds of failed insertion

not sure how to calculate that one

odds of failed insertion in germline cell (whatever that is)... i.e. proportion of RV's that target those cells (thanks h2whoa)

well this is easier, it is the first number multiplied by the fraction of total cells infected, assuming the virus can affect any cell in the body.

odds of the germline cell going on to become a viable next generation

say only one sperm, then the odds are one in however many sperm the male produces.

odds of that next generation animal living long enough to reproduce.

assuming the ERV is neutral in its phenotypical effects, you also need the odds of that ERV coming to be present in all members (or a given percentage) of the population, and also the mutations in that ERV which crippled the virus being the same in each of multiple suggested infections. There are also alot of other odds missing, such as the organism having an infection at the same time as they are breeding and so on. you are going to get a really small number anyway.

 

[h2whoa]

germline cell (whatever that is)

Most concise way of defining it is:

"In biology and genetics, the germline of a mature or developing individual organism is the subset of cells which either are capable of being passed to an offspring--such as the sex cells--or belong to the lineage from which these cells directly descend, such as the gametocyte and the stem cells from which the gametocytes derive. Mutations or other genetic changes arising in the germline are liable to be passed to offspring, while those arising in non-germline somatic cells are not."

Copied from Wikipedia (http://en.wikipedia.org/wiki/Germline).

That's a fairly good definition.

h2

 

[h2whoa]

say only one sperm, then the odds are one in however many sperm the male produces.

Have to correct you there Jet. If the germline cells that divide to produce the sperm are infected then, depending on the nature of the RV insertion, at least 50% of the sperm will carry the RV. If the RV is inserted more than once into the germline cell's DNA, then potentially 100% of the sperm would carry the RV.

h2

 

[Jet Black]

Have to correct you there Jet. If the germline cells that divide to produce the sperm are infected then, depending on the nature of the RV insertion, at least 50% of the sperm will carry the RV. If the RV is inserted more than once into the germline cell's DNA, then potentially 100% of the sperm would carry the RV.

h2

you are talking all of the germline cells though. This would be fine for an organism that contained the ERV in every cell of it's body, but if you are doing that, then you should be considering genetic drift. I am talking about the initial infection, which would only occur in one or two of the germ cells (spermatagonium or oocyte).

 

[h2whoa]

you are talking all of the germline cells though. This would be fine for an organism that contained the ERV in every cell of it's body, but if you are doing that, then you should be considering genetic drift. I am talking about the initial infection, which would only occur in one or two of the germ cells (spermatagonium or oocyte).

No I still disagree. The initial infection could happily take place in the cells from which the sperm and the oocyte are derived. If this were the case then my scenario stands and it still describes initial infection leading to huge infection in sperm or oocytes.

h2

 

[Karl - Liberal Backslider]

please read the question again. forget i mentioned 1:11000 (which was me rounding up btw). although you seem to say in one case this would be good odds whilst in the other it's so small as to be negligible.

what i'm after is the probability of a virus becoming part of the genome for the species, that depends on:

odds of failed insertion
odds of failed insertion in germline cell (whatever that is)... i.e. proportion of RV's that target those cells (thanks h2whoa)
odds of the germline cell going on to become a viable next generation
odds of that next generation animal living long enough to reproduce.

Well yes. The thing is, whether 1:11000 or any other probability is a good one depends on the number of trials.

If you have a million trials, then it's very good odds. Indeed, it will probably happen about a hundred times.

So any given ERV has millions of goes at getting into the germline. So it is going to happen from time to time. If it happens (and why calculate the odds of something happening that we know happens anyway - the ERVs are there), then if common descent is true, the insertions will almost always (probably vanishingly close to always) follow the same pattern as other evolutionary phylogenies. And this is what we see.

Compare this with the scenario where all the correspondances here are by chance. The 1:11000 chance has to be multiplied by the number of shared ERVs, if they didn't arise by common descent. Suddenly, we are not comparing a raw 1:11000 with 1:11000 - we are comparing a virtual certainty with an extremely low probability. And this extremely low probability - that all the ERVs could by chance mimic common ancestry - has only one trial - there is only one set of ERVs whose pattern we are considering.