Ok, a question for slayadragon, Gerwyn, parvo, Natasa, anyone... Regarding mold and xmrv. I understand that some of the "groups" by employment category with greater percentages of CFS (and also in known outbreaks) are more likely to be exposed to pathogens-- (teachers, airplane pilots due to recirculating air moving airborne pathogens around and around, medical personnel). Overtraining athletes may be not any more likely to be exposed to pathogens, but may be more welcome hosts to those pathogens, due to a stressed if presumably healthy immune system. I also can see how some of these groups might be more likely to be in contact with mold. If a school or airplane-- or even a hospital-- has a mold problem, and the air is recirculated with poor ventilation as it is in many modern buildings, then people working there have many hours over many day/weeks/months/years of exposure to the mold or other airborne ickies. What I am not understanding-- apologies if it has already been explained somewhere-- is the proposed interplay between mold and xmrv. How do they interplay? Can the mold carry the xmrv? (OK, that sounds like a really, really, REALLY stupid question, since where on the mold would xmrv insert...) Can buildings with prior mousie problems (droppings, etc) pass xmrv in an airborne way, or through fleas, or other vectors? Or, would the mold toxins be one stressor on the immune system, xmrv another, such as the proposed case with multiple infections? I am trying to wrap my mind around this. It would help if I had a better science background, of that I am certain. But, I promise I will do my best to understand it, if explained. Thanks in advance, J. P.S. have worked in old, musty building with intermittent rodent visitations...
German study finds xmrv
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jewel,
I could be wrong, but I think there is no need to look for a SPECIFIC relationship between mold and XMRV. XMRV quite probably alters our ability to deal with substances that our bodies would normally reject easily. Mold is always offensive to the human body, but because of XMRV, reactions are exacerbated, immune system dysfunction inhibits proper elimination, and these things together are enough to explain mold sensitivities in CFS.
I could be wrong, but I think there is no need to look for a SPECIFIC relationship between mold and XMRV. XMRV quite probably alters our ability to deal with substances that our bodies would normally reject easily. Mold is always offensive to the human body, but because of XMRV, reactions are exacerbated, immune system dysfunction inhibits proper elimination, and these things together are enough to explain mold sensitivities in CFS.
slayadragon
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Yes, absolutely.
But there's also plenty of evidence in the literature that toxic mold has a variety of effects on the immune system, including specific problems reported in CFS.
That might explain why people exposed to more than their fair share of toxic mold (currently or previously) might be more likely to acquire the "causal" virus, to be unable to keep it in check, and/or to be especially compromised with regard to acquiring other opportunistic infections once it's in play.
As a result of Gerwyn's prodding, I'm putting together a literature review on this topic. I'll post it soon.
Best, Lisa
bullybeef
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I have also reread the groom study which does suggest XMRV is in the general population, even though they couldnt find it. In which actually contradicts their own study:
http://www.retrovirology.com/content/7/1/10 [in conclusions]
http://www.retrovirology.com/content/7/1/10 [in conclusions]
G
Gerwyn
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you cant use deductive logic based on subjective terminology to analyse scientific issues Eric.That is what the scientific method is for.hohn et al chose to look in stromal tissue and not epithelial tissue where the titres are much higher. They then neglected to amplify the viral titre prior to PCR.That made an apparently negative result inevitable.Hohn has clearly learnt from that experience!
G
Gerwyn
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XMRV is a RNA virus . They looked for viral DNA.It takes more than sloppy thinking to use a water control and other controls based on patients with highly expressed levels of endogenous retroviruses.That makes it impossible to tell if the tests worked and what the differences in the "CFS"
and controls are in terms of XMRV infection rates.That takes careful planning.The science study clearly stated reverse transcription DNA.NO retro virologist could mistake the two terms. Hypotheses are constructed on factual observation and are not beliefs.
oerganix
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I also think that airtravel may have had something to do with my illness. I was a travel agent in the late 70s, early '80s, and I would get sick every time I flew more than a short distance. My coworker said to me, you don't like to fly, do you?
That wasn't true; I loved to fly; in those days it was fun, pre-9/11 without all the 'security' we have to go through now. But around that time the Reagan administration deregulated the airline industry and they were allowed to recirculate cabin air many more times, with less exterior/fresh air added, to save money. I was also told by someone who worked for United that all international flights are 'fumigated' while the passengers are still in the cabin, but I don't know if that is true or not. I do know that I invariably got an upper respiratory infection every time I flew from then on.
I remember reading something about this problem in a travel agent publication...flight attendants were complaining of more respiratory illnesses... where a doctor theorized that the lower pressure in the cabin and the cabin air being re-circulated without added fresh air was resulting in less oxygen available and that this would allow some types of bacteria and viruses a better environment, especially if they were breathed in, in a more concentrated 'soup' of other passengers' exhalations. Flight attendents tried to get fresh air circulation reinstated, but were turned down by the airlines.
This might be why hyperbaric oxygen treatments are helpful for some.
And the airlines have reconfigured their seating so that there are even more people packed into the same space, adding a higher probability of various bugs we haven't already got an immunity to being introduced into our lungs while we are vulnerable due to all of the above plus the added stress of travel under conditions whereby we are all treated as potential criminals.
(I found it especially stressful to be pulled out of line to have my bags and my person searched a second time. I asked the searcher, Has there been a rash of blue-eyed, red headed, 60 year-old disabled female terrorists that I haven't heard about? as she emptied my carry-on and swabbed it for explosives. No, it's a random selection, she said, don't take it personally. Right, an extra few minutes standing upright, feeling like I might faint, and having to pack my bags again...nothing personal about it.)
I got the 'killer flu' in the summer of 1982 and never fully recovered. Could be those flight-related respiratory infections lowered my immunity to the point this 'flu' was able to add XMRV or something else to the mix. Whatever that 'flu' was it had an effect unlike real flu, in that I had violent vomiting for 3 days, whereas regular flu does not involve vomiting. Having doctors, friends, lovers and family telling me it was all in my head (after all that's what the CDC and the newspapers said, so it must be true) encouraged me to push, push, push for another 6.5 years, until I could no longer get out of bed.
I went from 'health nut' to bedridden in 6.5 years, with no known risk factors involved; at age 39 my productive life was over. It's been downhill ever since, except for some improvement from Marshall's pulsed antibiotic protocol and more recently, LDN.
Now, when I plan to travel by air, I take antibiotics for a week before, and a few days after arriving; during the flight I meditate and rest as much as possible, with a cloth across my face, hoping it will act as a mask against airborne pathogens.
So, Martlett, maybe this is a possible scenario for you: You already had been exposed to XMRV from your friend prior to leaving UK. The long flight with less oxygen allowed it to begin to replicate. You continued to be physically stressed from travel. The higher altitude than you were used to in NM and CO may have meant you continued to get less oxygen, allowing your 'viral' illness to continue and escalate, even after you got down to Denver's lower altitude, which is still "the mile high city". Lowered immunity allowed the bacterial illness in your tonsils, etc. and advanced the virus or XMRV that was, by then, thriving to where your immune system could/can no longer combat it.
alex3619
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HI Parvo,
This is in reply for a private message from Parvofighter, with a question about whether or not researchers should be looking at transmission of other pathogens along with XMRV. I am posting it here because it might be relevant and because of technical difficulties with a private reply.
Thanks for the encouragement, I had already read your post but almost overlooked this message as it doesn't highlight well when I log in.
It is an open question as to whether they should be looking for copathogens, but that just means there is a real need for research in the area so that we can be sure. If the two strike hypothesis is valid, then treating xmrv should have a substantial impact on CFS, although for some the coinfections, toxins or other stressors will delay or prolong recovery. I also worry that the remodelling of the vascular system may be permanent ... but back to the blood. In some ways it doesn't matter. If XMRV is transmitted by blood, then any other infection or immune insult could trigger it, it doesn't have to come from the blood. Indeed, a latent infection that you had before XMRV could be reactivated and become the trigger. The really encouraging thing is the new treatment process that kiils most viruses in blood, including XMRV. This will greatly reduce risk from blood product contamination. However, they really need to know if xmrv is blood transmissable before they spend even more money on testing. This doesn't mean that patients shouldn't be tested, as many of the copathogens can be very virulent.
To me the issue is not if its transmissable (I cannot see any way it could not be transmitted - it is how lab animals are infected and how they culture the virus after all). The real issue is whether or not it is causal. If it isn't causing something nasty, it would be the very first virus of its type that doesn't, a complete anomaly. The only real issue that remains is determing exactly what it is doing, which will tell us how much of the problem is due to xmrv and how much is due to other factors such as copathogens and toxins.
Best wishes, and appreciate your work,
Alex
This is in reply for a private message from Parvofighter, with a question about whether or not researchers should be looking at transmission of other pathogens along with XMRV. I am posting it here because it might be relevant and because of technical difficulties with a private reply.
Thanks for the encouragement, I had already read your post but almost overlooked this message as it doesn't highlight well when I log in.
It is an open question as to whether they should be looking for copathogens, but that just means there is a real need for research in the area so that we can be sure. If the two strike hypothesis is valid, then treating xmrv should have a substantial impact on CFS, although for some the coinfections, toxins or other stressors will delay or prolong recovery. I also worry that the remodelling of the vascular system may be permanent ... but back to the blood. In some ways it doesn't matter. If XMRV is transmitted by blood, then any other infection or immune insult could trigger it, it doesn't have to come from the blood. Indeed, a latent infection that you had before XMRV could be reactivated and become the trigger. The really encouraging thing is the new treatment process that kiils most viruses in blood, including XMRV. This will greatly reduce risk from blood product contamination. However, they really need to know if xmrv is blood transmissable before they spend even more money on testing. This doesn't mean that patients shouldn't be tested, as many of the copathogens can be very virulent.
To me the issue is not if its transmissable (I cannot see any way it could not be transmitted - it is how lab animals are infected and how they culture the virus after all). The real issue is whether or not it is causal. If it isn't causing something nasty, it would be the very first virus of its type that doesn't, a complete anomaly. The only real issue that remains is determing exactly what it is doing, which will tell us how much of the problem is due to xmrv and how much is due to other factors such as copathogens and toxins.
Best wishes, and appreciate your work,
Alex
cfs since 1998
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Yes it could. Just because 9% is more than than double the 3% healthy prevalence does not mean this can't be the explanation--that is why I determined the p-values for different scenarios. The difference between a hypothetical ~6% XMRV+ prevalence (double the healthy rate) on the transplant recipient group, and the 9.9% the study actually found, is not statistically significant. Meaning it is just as likely they could have found it at 6% on another random sample of transplant recipients. Also what Cookie Monster said, they could have received blood transfusions too. If all of them did, it would triple their risk, and the p-value would jump again to 0.89. Though, your idea that XMRV positives will be more likely to need a transplant is also an interesting one.
anciendaze
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We agree on a great deal here, and I don't want to lose sight of that agreement. I'm actually saying the positive controls seem to have been artificially created. They don't appear to have demonstrated that they could draw blood from people infected with XMRV, in any ordinary way, and detect it, before they launched into a big test of people alleged to have CFS, a subject they themselves call controversial.
The "charitable" view here is that they made a major blunder. Sitting in front of numerous doctors over the years has given me the important insight that they can't tell what is going on in my head. A corollary to this is that I can't tell what is going on in theirs. (Probably a good thing, too.)
I've seen Cort's report that Annette Whittemore said their test would have worked if they were looking for HIV, which is also a retrovirus, with single-strand RNA carrying genetic information. I believe she got this from someone who knows, but I could be wrong.
My main experience with scientists and facts comes from areas sometimes called "hard science", (not always with good reason.) The degree to which scientists will act like other people, based on belief rather than "cold, hard facts" could depress me, if I wanted to be depressed.
(In another time and place, which seems like a different life, I investigated accidents sufficiently bad to be linguistically depreciated as "incidents". What people who certainly have every reason to know better will do -- even when their own lives are at stake -- continues to astonish me. Exploding oil platforms do not.)
People involved in those studies did considerable work, and ended up with a result little stronger than my example of looking out the window and not seeing a black swan. At this point I have other questions: why did they rush into print, bypassing normal review processes? why publish a sententious editorial on the subject? This is the point where someone ought to bring in psychologists to investigate.
That could be entertaining.
G
Gerwyn
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HIV is a lentivirus XMRV is a gamma virus.They are liike chalk and cheese.Those controlls are the antithesis of the scientific method .I first year student would not have constructed controlls which made the effectiveness of the tests unverifiable.
No control group containing people who all had illnesses with high levels of endogenous retroviral expression could have been constructed by accident.That needed specialist knowledge.Endogenous retroviruses activity impede the infectivity of an exogenous retrovirus.The chance of XMRV being present in those people were virtually nil. That took very careful planning and was no blunder.The whole point of adopting the scientific method is that it is impossible to act according to your belief because hypothesis testing is an active attempt to disprove said hypothesis and not attempt to gather information in support of it
eric_s
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Well, obviously my analysis has lead to the same conclusion like yours. Without having to get my hands dirty in a laboratory
. And i think you've just used deduction too.I'm just trying to make sense of some pieces of news, not trying to conduct a study in a natural science. I don't claim that my conclusions are facts.
rebecca1995
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Martlet
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I used to love to fly until a particularly scary occasion, since when I see the world TERMINAL and have to slug back a Xanax.
This is what I was wondering. I know we speculated every which way, when XMRV was first linked to CFS/ME but I was and still am fairly sure that sexual transmission is not the issue, particularly since I was one of a cluster, some of whom knew each other but others did not. But if XMRV is in respiratory secretions but it takes a series of other immune-lowering events for it to pass by our normal immune response, I think that would go a long way towards answering quite a few puzzles. So many of us were either virgins or monogamous when we got sick. So many of us had some precipitating illnesses/stressors. So many of us had that "killer flu" you aptly named even while no-one around us was sick. Although some of us had a more gradual onset, I think most of us can identify some precipitating factors, can we not?
I guess I am sitting here with fingers crossed (you try typing that way
) just hoping that they eventually discover that it is transmitted as are respiratory infections, because we all remember the immense suffering of AIDS victims, not just from the illness but from the stigma, suspicion and finger-pointing.
slayadragon
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Immune Lowering Events
This is what Erik was suggesting in his recollection of what happened during the Incline Village epidemic (quoted in my post "Airline, School, Medical Workers" above).
His observation was that people living or working in Sick Buildings were more likely to get the "Killer Flu" and much more likely to remain sick permanently as a result of it than those who were not in those moldy environments.
Of course, there could be other especially predisposing "stressors" as well.
I wonder what specifically those might be, apart from the normal "I was working too hard" stuff.
Best, Lisa
This is what Erik was suggesting in his recollection of what happened during the Incline Village epidemic (quoted in my post "Airline, School, Medical Workers" above).
His observation was that people living or working in Sick Buildings were more likely to get the "Killer Flu" and much more likely to remain sick permanently as a result of it than those who were not in those moldy environments.
Of course, there could be other especially predisposing "stressors" as well.
I wonder what specifically those might be, apart from the normal "I was working too hard" stuff.
Best, Lisa
Forbin
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I sometimes wonder if XMRV could, in some instances, be food borne. The hepatitis A virus can be food borne and has, on several occasions, been transmitted by infected workers in the food industry.
Also point sources of food are another thing that people probably share more in institutional or closed environments like hospitals, nursing homes, airplanes, convents, ski resorts, remote Icelandic towns, Air Force bases, cross country tour buses, island communities, Army bases, and schools.
Just a thought.
Also point sources of food are another thing that people probably share more in institutional or closed environments like hospitals, nursing homes, airplanes, convents, ski resorts, remote Icelandic towns, Air Force bases, cross country tour buses, island communities, Army bases, and schools.
Just a thought.
RustyJ
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Why hasn't this latest study been taken up by the mainstream media, particularly when the 3 negative studies got so much attention? Hasn't it been published. Too small? Frustrating.
ixchelkali
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Perhaps it is obvious to everybody but me, but it seems there actully 2 events we need to discuss and without making a distinction the conversation gets more confusing. The first is exposure to XMRV and the second is actually contracting the virus.
We must somehow be more susceptible to contracting the virus once we are exposed. This would seem to be a faulty layer in the immune system that precedes any damage done by XMRV. Genetics is one reasonable hypothesis.
As a result I can't see XMRV being the entire cause of what ails us, but that is not to say XMRV doesn't do most of the damage. We just don't know.
Fire away smart people!
Maybe 3 events: 1) exposure, 2) infection with the virus, 3) getting sick. It's possible that the virus could work in the body a long time before one becomes symptomatic. Remember, even without anti-retroviral therapy, some people were HIV positive for years without coming down with an AIDSyndrome disease (like Karposi's sarcoma, Pneumocystis carinii pneumonia, etc).