HGRVs - Constructive general discussion - for exploring HGRV research

[Bob]

Everyone is very afraid of contamination at the moment. As these mouse viruses are popping up everywhere... And XMRV has become very controversial of course.

Yes, these viruses seem to be everywhere!

The main part of Hanson's study is negative anyway, but I thought she might publish her antibody results because she earlier seemed to be content that they could not be a result of any contamination.

I don't know if human cell lines can produce antibodies to MLVs, which could lead to contamination. That's something that I haven't thought of before.

 

[barbc56]

I have moved this post.

Barb C. :>)

 

[Bob]

The more I look, the more human retrovirus possibilities I find in past literature...

Now there's a "SSAV p28 cross-reactive protein found in some patients with leukemia" from the 1984 study that I've been looking at:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC391952/pdf/pnas00621-0247.pdf

'SSAV' seems to be the 'simian sarcoma-associated virus', which is very similar to the 'Gibbon Ape Leukemia Virus', GALV.

Of course, it could all still be contamination, but I didn't know that GALV-like viruses had been detected in leukemia patients.

Here the references from the paper, but I haven't looked at them yet:
35. Hehlmann, R., Schetters, H., Erfle, V. & Leib-Mosch, C. (1983) Cancer Res. 43, 392-399.
45. Derks, J. P. A., Hofmans, L., Bruning, H. W. & van Rood, J. J. (1982) Cancer Res. 42, 681-686.
46. Mellors, R. C. & Mellors, J. W. (1976) Proc. Nail. Acad. Sci. USA 73, 233-237.

ETA: In the first reference (no 35.) the SSAV cross-reactive protein seems to be a result of actual human DNA, not a viral infection:
http://www.sciencedirect.com/science/article/pii/0042682286902266
I haven't found the other references yet.

 

[currer]

Bob, Jamie Deckoff Jones discusses the possibility that retroviral contaminants (not necessarily complete or replication competent in themselves) can activate human endogenous retrovirus in our genome, that would otherwise remain latent.

Foreign DNA "contaminants" parenterally administered in vaccines could hypothetically provide enough variety of DNA to complement old inert viral remains in our genome and reactivate it.

I do not know whether an EXPERIMENT has ever been done to show this happening. Can anyone find one?
It is always referred to as an hypothesis.
Jamies website where this was discusses is being reconstructed atm.http://www.x-rx.net/index.html

The sequences in human DNA referred to are assumed to be the remnants of ancient endogenised infections as they are present in everyone's DNA. ( I assume)

There has been some interest in the theory that ancient retroviral infection of the mammalian germ-line could have enabled the development of the placenta. Marsupials do not have placentas (think kangaroo) The earliest date for the development of the placenta I can find on a quick search is the Jurassic!
Now this would be very ancient indeed!

 

[currer]

http://www.ncbi.nlm.nih.gov/pubmed/9619102

Placental endogenous retrovirus (ERV): structural, functional, and evolutionary significance.
Harris JR.
SourceInstitute of Zoology, University of Mainz, Germany. harris@uzomai.biologie.uni-mainz.de

Abstract
That endogenous retrovirus (ERV) is present within the placenta of humans and other mammals has been known for the past 25 years, but the significance of this observation is still not fully understood. Much molecular biological data have emerged in recent years to support the earlier electron microscopic data on the presence of placental ERV. The evidence for ERV in animal and human placental tissue is presented, then integrated with data on the presence of ERV in a range of other tissues, in particular teratocarcinoma cells. Placental invasiveness and maternal immunosuppression are then discussed in relation to metalloproteinase secretion, the immunosuppressive potential of retroviruses, and placental growth factors, while the evidence for a functional link between placental protooncogenes and trophoblast malignancy is reviewed. Finally, placental development, structure, and life span are discussed within an evolutionary context. The hypothesis that one or more ancient trophoblastic ERVs could have played a role in the evolution and divergence of all placental mammals is evaluated


One of the fascinations of retroviral research is the light is casts on evolutionary processes,. Because it is now being accepted that mutation does not occur "randomly" but could be much more to do with retroviral infection and modification of the genome. Hence the development of the placenta following retroviral infection.

If we have introduced large amounts of foreign DNA into humans inthe last 100 years we could be looking at some real changes to come!.

 

[currer]

The placenta develops in the woman from the fertilised and implanted egg, ie. this DNA is part of the foetus' - and not the maternal DNA.
So I do not know how much (if any) of this DNA could be found in a NON PREGNANT female!

However this is an interesting discussion so thanks to Bob for bringing it up.

If "XMRV" / HGRVs can be attributed to reactivated ERVs then an explanation can be developed to let modern medical technologies off the hook and reconstrue this debate as the "fault" of the sufferer and their faulty genes. This is going to be a popular argument.

 

[currer]

I don't know if human cell lines can produce antibodies to MLVs, which could lead to contamination. That's something that I haven't thought of before.

I dont think cell lines can produce antibodies. You need functioning B and T cells and a blood supply to do this and they would not be present in cell line tissue.

 

[Bob]

Thanks very much for the feedback currer...

Bob, Jamie Deckoff Jones discusses the possibility that retroviral contaminants (not necessarily complete or replication competent in themselves) can activate human endogenous retrovirus in our genome, that would otherwise remain latent.

Foreign DNA "contaminants" parenterally administered in vaccines could hypothetically provide enough variety of DNA to complement old inert viral remains in our genome and reactivate it.

I do not know whether an EXPERIMENT has ever been done to show this happening. Can anyone find one?
It is always referred to as an hypothesis.
Jamies website where this was discusses is being reconstructed atm.http://www.x-rx.net/index.html

Yes, I've read Jamie's blogs, and that's where I learnt about all of that.

Like you, I wasn't sure if Jamie's thoughts were based on experimental evidence or not, so it would be interesting to know if there was any research on this.

Reading the paper that i've been discussing, I was interested to learn that some of our own DNA is so similar to the retroviral DNA that we are interested in. I didn't know that there were such similarities. So that seems to add weight to Jamie's discussions.

The P30 protein, that was found in the human placentas, is the same protein that Judy was looking for in her hunt for MLVs (if I remember correctly, p30 was what she was detecting on the slide-gate slide.) And there is other human DNA, mentioned in one of the papers I've highlighted, that is very similar to GALV, a virus very similar to XMRV.

So it would seem that we have endogenous retroviral DNA that is very similar to MLV (etc) retroviral DNA.

The sequences in human DNA referred to are assumed to be the remnants of ancient endogenised infections as they are present in everyone's DNA. ( I assume)

Yes, that's right. I think that all ancient endogenous retroviral DNA is present in the entire human population.

 

[Bob]

There has been some interest in the theory that ancient retroviral infection of the mammalian germ-line could have enabled the development of the placenta. Marsupials do not have placentas (think kangaroo) The earliest date for the development of the placenta I can find on a quick search is the Jurassic!

One of the fascinations of retroviral research is the light is casts on evolutionary processes,. Because it is now being accepted that mutation does not occur "randomly" but could be much more to do with retroviral infection and modification of the genome. Hence the development of the placenta following retroviral infection.

Yes, it seems to be a widely accepted theory that our evolution was aided by retroviral infection over many millennia.
But I'm pretty certain that random mutations are still very much a part of evolutionary theory as well.

The placenta develops in the woman from the fertilised and implanted egg, ie. this DNA is part of the foetus' - and not the maternal DNA.
So I do not know how much (if any) of this DNA could be found in a NON PREGNANT female!

Well, the DNA of the foetus has to come only from the mother, or father, or both parents. But if it an endogenous human retrovirus that is being 'expressed' in the placenta, then it could be the case that it is only expressed in the placenta, and not in any other tissue in the body. Evolution could have been such that the endogenous retroviral DNA is normally switched off (not expressed) in the human body, but in the placenta the endogenous retroviral genes might not be switched off and so endogenous viral proteins and particles are expressed (this could be either an accident of evolution, or for evolutionary beneficial reasons).

Or, the proteins and viral particles found in the placenta could be an external exogenous retroviral infection (such as the ones we are interested in) which has an affinity for the tissue of the placenta. The paper does say that they have photographed a partial budding virus, after all, and they are only assuming that it is a result of endogenous DNA. (I think - i need to read it again to make sure about that - but i don't think they have evidence to prove it is an endogenous virus that is being expressed.) (We know far more about the human genome now than we did in 1984, so this paper is a bit out of date really.)

Or the viral particles could be just due to contamination! (Contamination from the dreaded cell lines etc.)

Like you say, currer, it's all really interesting (well, it is for some of us anyway!)

 

[Bob]

I dont think cell lines can produce antibodies. You need functioning B and T cells and a blood supply to do this and they would not be present in cell line tissue.

Yes, that's what I thought as well, but I didn't know enough about it to be certain that other cells couldn't produce any antibodies. I think you are probably right.

 

[bullybeef]

The more I look, the more human retrovirus possibilities I find in past literature...

I think you've seen this, Bob, but it must be relevant: http://forums.phoenixrising.me/showthread.php?15863-MLV-caused-leukaemia-in-kids!&goto=newpost

 

[Bob]

I think you've seen this, Bob, but it must be relevant: http://forums.phoenixrising.me/showthread.php?15863-MLV-caused-leukaemia-in-kids!&goto=newpost

Thanks BB... I've posted something in that thread.

 

[Bob]

http://www.ncbi.nlm.nih.gov/pubmed/9619102

Placental endogenous retrovirus (ERV): structural, functional, and evolutionary significance.
Harris JR.
SourceInstitute of Zoology, University of Mainz, Germany. harris@uzomai.biologie.uni-mainz.de

Abstract
That endogenous retrovirus (ERV) is present within the placenta of humans and other mammals has been known for the past 25 years, but the significance of this observation is still not fully understood. Much molecular biological data have emerged in recent years to support the earlier electron microscopic data on the presence of placental ERV. The evidence for ERV in animal and human placental tissue is presented, then integrated with data on the presence of ERV in a range of other tissues, in particular teratocarcinoma cells. Placental invasiveness and maternal immunosuppression are then discussed in relation to metalloproteinase secretion, the immunosuppressive potential of retroviruses, and placental growth factors, while the evidence for a functional link between placental protooncogenes and trophoblast malignancy is reviewed. Finally, placental development, structure, and life span are discussed within an evolutionary context. The hypothesis that one or more ancient trophoblastic ERVs could have played a role in the evolution and divergence of all placental mammals is evaluated


One of the fascinations of retroviral research is the light is casts on evolutionary processes,. Because it is now being accepted that mutation does not occur "randomly" but could be much more to do with retroviral infection and modification of the genome. Hence the development of the placenta following retroviral infection.

If we have introduced large amounts of foreign DNA into humans inthe last 100 years we could be looking at some real changes to come!.

Here's an article about viruses creating genes which have changed the course of evolution by enabling the placenta to be created:

Mammals Made By Viruses
http://blogs.discovermagazine.com/loom/2012/02/14/mammals-made-by-viruses/

 

[Bob]

Just in case there's any doubt about how XMRV has transformed the field of ME research for the better, this is from Cort's latest article:

Dr. Vernon believes the ME/CFS research field is turning a corner for several reasons. One the infrastructure needed to propel ME/CFS into a major research destination is being built at the CAA, the CFI and other groups. Two partly because of the attention XMRV brought, the research community is beginning to understand how large the opportunities to make a difference are s in this mostly undeveloped field. (Dr. Boneva at the CDC chose CFS for just this reason. At the Ottawa Conference she stated she could be one of thousands studying HIV or she might be the person to make a difference in CFS) The enormous needs of the ME/CFS community are another draw for the right type of researcher. Dr. Vernon noted that if you find something in this disorder you can help a lot of people.

I am very excited about 2012, 2013, 2014 I think significant progress will be made to improve the way research is being done and that will reap benefits for everyone. Suzanne Vernon.

http://forums.phoenixrising.me/cont...-Movement-Seeks-to-Bolster-CFS-Research-Field

 

[Bob]

Ha! Three years later and I finally work out how to interpret Blast results properly!

No one ever told me that I need to click on the link underneath 'Max Score", in the list of results, in order to understand the results! I've always just looked at the figure under "Max Ident" in the list of results, and thought that this showed the overall similarity. I wondered why it never made much sense!

Lucky that I've never quoted my Blast results very much!

 

[Bob]

Oh, it seems that I might have been wrong about the Lipkin & CFI pathogen study, in relation to XMRV...
In an old Amy Dockser Marcus blog (the info might be out of date), it says that he won't be looking for XMRV or all known and unknown pathogens, but just a selection of pathogens previously associated with ME. I don't know if that's a misunderstanding, or if the study really is that limited. I had thought (did I assume it?) that they would be looking for all pathogens - known or unknown.

Amy Dockser Marcus' Blog:
http://blogs.wsj.com/health/2011/09/15/applying-venture-philanthropy-to-chronic-fatigue-syndrome/
(It's not a new article)

 

[Bob]

I haven't found out the correct details re the pathogen study yet, in relation to testing for all pathogens, but it's not surprising that I might have got it wrong, based on this sort of ambiguous info, quoted below, which doesn't exactly correspond with the rest of the article it was taken from.

It gives the appearance that they are looking for unlimited pathogens, but doesn't actually state that's what they are doing, so I still don't know what the actual situation is:

"Unlike microarray chips that have a finite number of known pathogens for testing, deep sequencing allows researchers to find not only an unlimited number of varying strains of known pathogens, but novel pathogens as well. Testing will most likely be done at a sequencing center pooling the resources of several large centers as the equipment is very expensive and personnel have to be specially trained, according to Dr. Hornig."

http://trialx.com/curetalk/2011/11/...equencing-and-proteomics-to-hunt-cfs-viruses/

 

[RustyJ]

I haven't found out the correct details re the pathogen study yet, in relation to testing for all pathogens, but it's not surprising that I might have got it wrong, based on this sort of ambiguous info, quoted below, which doesn't exactly correspond with the rest of the article it was taken from.

It gives the appearance that they are looking for unlimited pathogens, but doesn't actually state that's what they are doing, so I still don't know what the actual situation is:

"Unlike microarray chips that have a finite number of known pathogens for testing, deep sequencing allows researchers to find not only an unlimited number of varying strains of known pathogens, but novel pathogens as well. Testing will most likely be done at a sequencing center pooling the resources of several large centers as the equipment is very expensive and personnel have to be specially trained, according to Dr. Hornig."

http://trialx.com/curetalk/2011/11/...equencing-and-proteomics-to-hunt-cfs-viruses/

Bob, from memory, you are correct. Lipkin is not looking for XMRV. In fact it appears in both of the studies he is involved in he has carefully avoided looking for it. My guess is they will find hundreds of active viruses in patients, but nothing that will stand out (this of course is already known). They may even find a few new ones, but these will not be in sufficient numbers of patients to be called the cause of me/cfs. I wouldn't at all be surprised if the principal beneficiary is EBV research.

Once you get more than a few active viruses, you need to look for a trigger.

 

[Firestormm]

Lipkin is not looking for XMRV. In fact it appears in both of the studies he is involved in he has carefully avoided looking for it.

Eh?

 

[Bob]

Lipkin is not looking for XMRV. In fact it appears in both of the studies he is involved in he has carefully avoided looking for it.

Eh?

I think Rusty is referring to reports that Lipkin is not using NGS in the XMRV study.