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XMRV Study No. 4

Discussion in 'XMRV Research and Replication Studies' started by Orla, Feb 25, 2010.

  1. Gerwyn

    Gerwyn Guest

    There are a number of things that can cause glutathione depletion. This is how gammaretroviruses are transmitted

    XMRV is known to be inserted in the genome so vertical transmission no problem.

    Gammaretroviruses are not transmitted like lentilviruses a virology textbook will reveal that.

    Are you saying that gammaretroviruses cant be transmitted.

    My comment was also specific for that herv mutation you would expect it to be activated by endogenous hhv-6 expression but not i repeat by exogenous infection.And that association cannot be demonstrated experimentally in MS
  2. kurt

    kurt Senior Member

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    Well, I do not have access to a virology textbook, so have searched a little online for more info on gammaretrovirus transmission, but what I have read suggests that gammas are just as hard to transmit as lentils. In fact here is a quote from an interesting paper that also discusses a mouse immunity mechanism to X MuLV:

    In my opinion this challenges the idea that XMRV has anything beyond a blood-borne infection vector. And I believe that may contradict the XMRV hypothesis for CFS...

    Regarding vertical transmission my point is that this requires an initial infection and in those unusual family lines with modern CFS and not ancestral CFS, with current records that can go back well over 150 years. So that pretty much rules out blood-borne AND vertical transmission unless you place initial infection back before the early 19th century.

    I was not trying to say CFS = MS, only that another illness with some commonalities to CFS has known HERV involvement. Yes, they may have different HERV details although I did read one paper somewhere that implicated HHV6+HERV for MS, maybe that was a Huber paper.
  3. Gerwyn

    Gerwyn Guest

    Kurt if viruses dont pass through the blood at some stage there would be no antibodies.Beleve it or not there is a connection between the mouth mucus membrane and the bloodstreamEven droplet bourne viruses get in there at some stage

    Are you seriously saying that HIV is hard to transmit

    Are you seriously basing your case re vertical transfer on a tiny unrepresentative religious population .How many people are there in America?

    Your original point was that exogenous nonretroviruses invoked a herv response this is not so

    As you can see the mulv virus concentrates in the lymphoid tissue so what idiot would look for it in whole blood samples

    If you can avoid vertical transfer with an integrated virus then you would be re writing the books

    I think that you originally said that XMRV could not be transmitted via blood and you didnt think it could be transmitted at all
  4. kurt

    kurt Senior Member

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    Yes, HIV is hard to transmit, it is blood-borne transmission typically, otherwise we would probably all be infected by now, but we are not.

    And of course, in some cases blood-borne may transmit through kissing, although that has been debated as an open sore or wound is required of the recipient of the infection, so still mostly blood-borne.

    Statements being made about XMRV being sexually transmitted do not work in many groups in the US, yes I think enough to be representative, but that does not really matter if I can prove anything, many people know this themselves from their own history and family background. So this is my own observation from knowing about some of these cases. I don't know research into this, so it is anecdotal. But basically, you have to get the virus into the family somehow before vertical is possible.

    Also, people with CFS who have had multiple partners generally find those prior partners did not get CFS from them, although there are a few exceptions. This is based on what many people have said over years online.

    Yes, HHV6 can invoke HERV activation, I don't know if that is new HHV6 only or re-activated infection. See:

    http://www.ncbi.nlm.nih.gov/sites/entrez/19505843

    The vertical transfer point is referring to XMRV, which is exogenous, not integrated HERV.

    I never said XMRV could not be transmitted by blood, only that if it is found in such small concentrations that many labs can not even find it with RT-PCR, then how is it even transmitted? The issue there is concentration, to transmit even in blood there must be enough viral copies to survive initial immune onslaught.

    The only transmission vector that makes sense to me for XMRV, given the epidemiology of CFS, would be through an insect that takes multiple blood meals. There actually was one HIV study in Africa that showed HIV would survive for a few days in a certain species of Tick. But that is a bit of a stretch to explain outbreaks. And again, with ultra-low concentrations in the blood, could an insect even transmit the virus?
  5. ggingues

    ggingues $10 gift code at iHerb GAS343 of $40

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    A better explanation is that whatever gives you CFS is there before you get mono, and that your cytokine response (from day 1) will reflect this. This isn't just a theoretical argument for me, but based on my own experience. As soon as I got mono/ebv, whatever it is that causes CFS was activated. I knew something was wrong from day 1. Not only that but I suspect the agent was there before mono/ebv since I was getting minor symptoms such as poor stress tolerance & unrefreshing sleep. I wasn't "sick" before EBV, but I wasn't fully "healthy" either.

    I caught mono and never recuperated either. but I thought I was healthy before, probably could have gotten more sleep but I ate pretty healthy. Perhaps to much stress and exercise? I was just curious as to why you say you were not fully "healthy" either?
  6. kurt

    kurt Senior Member

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    The WPI virachip study showed multiple concurrent activated herpes infections. So this is pure speculation, but maybe you already had some other chronic herpes, after all there are 7-8 different herpes viruses and I believe WPI found 3-4 of those activated on some cases. Also, if one of those was HHV6 (Roseola), then maybe that activated HERV K18, which IS a retrovirus but endogenous form, and that creates massive cytokine response, due to superantigen (sAG).

    I don't know who you are talking to here, but FWIW my case was similar to what you describe, I had the rash characteristic of HHV6 activation about 6 years prior to getting CFS, and during those years also noticed my energy levels were slowly going down. I was a swimmer and each year could swim fewer and fewer laps until at the end I could barely manage one lap (I had been swimming a quarter and sometimes half mile daily for years previous). And that was the last year before CFS, which hit after another bad flu-like illness that I am guessing might have activated another herpes (and activated mono, or an enterovirus? hard to say). About a year into the CFS I tried to swim again, I had to switch to a tiny spa pool, the laps were about 10 meters, and I could hardly manage more than one or two laps! Now it is over 10 years later and I can not swim at all. What a contrast.
  7. natasa778

    natasa778 Senior Member

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    There are indications that it is (easily) transmitted through saliva. We'll have to wait and see for something on paper...
  8. Gerwyn

    Gerwyn Guest

    Transmission route and ease of transmission are not the same thing

    That is precisely my point labs cant detect such a low titre virus with PCR

    The trim protein early warning system which provokes the immune response only activates upon cellular entry

    XMRV was originally found integrated into the human genome and behaves like an endo as far as vertical trasmission is concerned

    I read the paper you would expect HHV_6 leaviingl latency to activate a herv response.hervs act as regulatory pseudogenes

    Actively pumpind HHV-6 into a cell line for 72 hours is not exactly ecologically valid is it

    !It is about as far away from in vivo infective conditions as you can get

    Exogenous HHV-6 does not activate intrinsic retrovirus specific herv expression--the infalpha levels generated by that artificial savage response would

    You dont find xmrv in the blood much because like other gammas it spreads via cell cell transfer within lymphoid tissue like MuLv from which it is seperated by a tiny base alteration inthe env gene.

    The trouble with surveys is that people interpret the results on the basis of their theoretical preconceptions and past experience.They can also produce results as a result of demand characteristics social schema and stereotypicity.Generating meaningful surveys is quite a science in itself.Interpreting the results demands absolute neutrality only approximated by triangulation

    Anecdotal evidence and the interpretation of personal experience tends to be frowned on
  9. natasa778

    natasa778 Senior Member

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    LOL see my post above, you probably won't have to.

    If XMRV shown linked to autism, it will explain why many special needs school teachers later have affected children of their own (no data but I know a few, and sadly those tend to be very severely affected - it could be something to do with when the infection happens, vertical versus horizontal, also probably repeated exposures during pregnancy etc...). I also believe it could be shed and present in stool (as with HIV), but that should not be a problem in developed countries with good hygiene standards

    Btw Annette Whittemore used to be a special needs teacher working with autistic kids http://www.wpinstitute.org/about/about_execboard.html
  10. kurt

    kurt Senior Member

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    Is there a study showing this? I can think of several alternate explanations if that is true in more than a few anecdotes. For one thing, autism has exploded, so there will be many people who end up having autistic children with with no warning. Also, some people who become interested in special needs children may be have exposure to high functioning traits (like Asperger's) in their own background, helping create that interest. So even if that is a small group, having a slightly higher than normal rate of autistic children may have other explanations.

    On the other hand, there certainly might be infectious elements, but they must be transmissible in a casual classroom setting. And there might be multiple viral co-infections involved in autism. Anyway my point is that this is possible but not a conclusive observation.
  11. natasa778

    natasa778 Senior Member

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  12. natasa778

    natasa778 Senior Member

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  13. garcia

    garcia Aristocrat Extraordinaire

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  14. kurt

    kurt Senior Member

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    natasa,
    That is really strong evidence for some readily transmissible factor, certainly not a blood borne infection. More like CFS clusters than AIDS epidemiology. Makes one wonder if there are some highly virulent strains of some common viruses. I believe that is the case with HHV6, what some call 'superbugs', or perhaps some others.
  15. kurt

    kurt Senior Member

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    Just realized I never responded to this. The two UK studies did look at whole blood, but they then looked at the WBCs and that is about 33% PBMC. So while this was a less rigorous design than the WPI and Dutch studies, only by a factor of three. Therefore ALL of the four studies so far have looked at lymphocites from PBMC, just at different concentrations. There are other issues and also some things are unclear about WPI's testing process and cohort, but just wanted to mention that using whole blood by itself is not a disqualification, it just lowers the resolution.
  16. Gerwyn

    Gerwyn Guest

    Initial concentration is the key of course that this why they should have used peripheral blood., a third of very little is still very little . Activation to get provirus in the fist place. would also have been handy!


    There is a lot more info re cohort details in WPI method than the britsh studies as to how the patients were finally selected for inclusion from the initial cohorts.

    At least the WPI didnt use patients whose symptoms had an entirely psychological origin
  17. bakercape

    bakercape Senior Member

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    I was

    working at a school for autistic children as a teacher when my wife and I had our 2 children. Both of them are on the autism spectrum. They are high functioning. One PDD-NOS the other Aspergers.

    I had had CFS for 10 years prior to having my children and had been working at the school for autistic children as a teacher for 2 years prior to having our kids. I had heard through the grapevine while working at the school that one of the children had tested positive for a stealth virus.

    This got around word of mouth through the teachers. The Administration gave us no info on the stealth virus.
  18. ukxmrv

    ukxmrv Senior Member

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    I noticed that Dr Martin (who used to be involved in CFS Stealth virus work years) had been working with the autistic community and diagnosing the same virus. I think that his CFS lab was closed down. There used to be a yahoo group but I think that this closed as well.

    With the increased interest in the Elaine DF virus I had a look on the internet for Dr Martin as I remember his virus at the same time.

    I wonder if this is the same "stealth" virus as before.
  19. Countrygirl

    Countrygirl Senior Member

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  20. bakercape

    bakercape Senior Member

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    I have thought this too. Look at HIV. Once it is knocked down or kept to a low level indivuals like Magic Johnson are not sick. Why if XMRV is at such a low , hard to detect level would it cause a disabling illness such as CFS? I was really excited about XMRV explaining CFS when the science paper came out but the more I think about it the more it seems to have a lot of holes.

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