Suppose, just suppose for the sake of discussion, that true replication studies in well-defined cohorts confirm the Whittemore Peterson Institute's XMRV findings in ME/CFS. What does that actually tell us, where do we need to go from there, and what questions will need to be answered?
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Using the WPIs figure that 3.7% of healthy controls are XMRV positive, thats about 11,451,867 people in the <?xml:namespace prefix = st1 ns = "urn:schemas-microsoft-comffice:smarttags" /><st1:country-region w:st="on"><st1lace w:st="on">USA</st1lace></st1:country-region>. Its estimated that 1 to 4 million people in the <st1:country-region w:st="on"><st1lace w:st="on">USA</st1lace></st1:country-region> have ME/CFS. If you take the WPIs earlier figure of 67% infection in ME/CFS patients, that means that only between 6 23% of people who are XMRV positive are sick with ME/CFS. Even if you use their later figure of 98% infection in ME/CFS patients, thats still only 8 to 34% of XMRV infected people who have ME/CFS. [1]
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So at most, only about a third of people who test positive for XMRV are sick with ME/CFS. What is the difference between them and the healthy XMRV-positive people?
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Are the healthy people carrying around a ticking bomb, thats just waiting for the appropriate trigger to set it off? If so, what is the trigger? Or is the XMRV slowly doing its work on them so that they will all eventually become ill?
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Or is there something about the people with ME/CFS that makes them susceptible to the illness? Some genetic difference? Something different about the way their immune system acts? Some critical mass of allopathic load? Some lack of moral fiber?
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Or does it just depend on which cells happen to become infected?
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Are other viruses which ME/CFS sufferers are prone to, like Epstein-Barr, HHV-6, parvovirus, cytomegalovirus, etc, simply opportunistic infections taking advantage of a weakened immune system, or are they interacting with XMRV in some way to cause ME/CFS?
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Remember the Dubbo study, the prospective cohort study of post-viral fatigue? The only predictive factor for chronic post-viral fatigue they found was the severity of the initial illness. So what, if any, role does the severity of a co-morbid infection play in initiating ME/CFS? Does being infected with XMRV predispose you to more severe infections from other diseases, or does a severe illness effect the progression of XMRV infection?
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What, if any, role does gender play? Are there gender differences between healthy people who are XMRV-positive and ME/CFS patients? More women than men have ME/CFS, so are men who are XMRV-positive less likely to get ME/CFS?
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Are there gender differences between healthy people who are XMRV-positive and healthy people who are XMRV-negative? Are women more easily infected with XMRV? In those who are XMRV-positive, how does gender effect which cells are infected? We know only men have infected prostate cells!
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What accounts for the wide variation in symptoms in ME/CFS? In feline leukemia virus, another infectious gammaretrovirus, different strains produce different symptoms. Theres only one strain thats transmissible, but that type sometimes then morphs into other strains inside the cat's body. Is that true of XMRV?
And of course, the big T, transmission. How is XMRV transmitted and how contagious is it? This is a puzzle, because, although admittedly the epidemiological studies have been pretty pathetic, it appears the ME/CFS does not follow the risk patterns typical of a sexually transmitted disease, or of a blood-born pathogen. This may change once we have a standard XMRV test which will allow for better epidemiological studies, but so far theres no evidence that ME/CFS is more prevalent in people with a history of STDs, or intravenous drug users, hemophiliacs or those with a history of transfusion. There also dont appear to be the levels of infection among people living together that youd expect if it were transmissible by casual contact.
<o></o>
Again looking at feline leukemia virus for comparison, FeLV is not very contagious. Infection seems to be mainly from saliva, from mutual grooming and bites. The saliva and nasal secretions contain a lot of FeLV virus, but it usually takes prolonged close contact to infect. Cats can also transmit FeLV by sharing dishes (rarely) and litter boxes, and through mothers nursing kittens. FeLV doesnt survive long outside the cats body. It also appears that some cats can be infected without getting sick, but will become healthy carriers.
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Apparently some cats are able to mount an immune response to the initial infection, eliminate the virus from their bloodstream, and never progress to the diseased state. With about 70% of cats the virus is only in the bloodstream and shed in secretions for 1 16 weeks. A few cats with continue to shed virus even after its gone from their bloodstream. Sometimes the virus becomes latent in the bone marrow. About 30% of cats dont mount an adequate initial immune response and become permanently infected. Theyre the ones that go on to develop immunosuppression, lymphoma, leukemia, neuropathy, enteritis (GI problems), etc. Is FeLV a model for XMRV? Is it a better model than HIV?
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So many questions. Actually now that I think about it, since one thing we do know is that some people are infected with XMRV, Id like to know the answers to these questions even if the WPI study wasnt replicated. Some people are infected. What is it doing to them, and how is it spreading?
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[1]<o></o>
<st1:country-region w:st="on"><st1lace w:st="on">US</st1lace></st1:country-region> population 309,509,942 x 3.7% =<o></o>
11,451,867<o></o>
<o></o>
if PW ME/CFS - 4,000,000<o></o>
x 98% = 3,920,000 = 34% of healthy XMRV+<o></o>
x 67% = 2,680,000 = 23% of healthy XMRV+<o></o>
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if PW ME/CFS - 1000000<o></o>
x 98% = 980,000 = 8% of healthy XMRV+<o></o>
x 67% = 670,000 = 6% of healthy XMRV+
<?xml:namespace prefix = o ns = "urn:schemas-microsoft-com
fficeffice" /><o></o>Using the WPIs figure that 3.7% of healthy controls are XMRV positive, thats about 11,451,867 people in the <?xml:namespace prefix = st1 ns = "urn:schemas-microsoft-com
ffice:smarttags" /><st1:country-region w:st="on"><st1lace w:st="on">USA</st1lace></st1:country-region>. Its estimated that 1 to 4 million people in the <st1:country-region w:st="on"><st1lace w:st="on">USA</st1lace></st1:country-region> have ME/CFS. If you take the WPIs earlier figure of 67% infection in ME/CFS patients, that means that only between 6 23% of people who are XMRV positive are sick with ME/CFS. Even if you use their later figure of 98% infection in ME/CFS patients, thats still only 8 to 34% of XMRV infected people who have ME/CFS. [1]<o
></o>So at most, only about a third of people who test positive for XMRV are sick with ME/CFS. What is the difference between them and the healthy XMRV-positive people?
<o
></o>Are the healthy people carrying around a ticking bomb, thats just waiting for the appropriate trigger to set it off? If so, what is the trigger? Or is the XMRV slowly doing its work on them so that they will all eventually become ill?
<o
></o>Or is there something about the people with ME/CFS that makes them susceptible to the illness? Some genetic difference? Something different about the way their immune system acts? Some critical mass of allopathic load? Some lack of moral fiber?
<o
></o>Or does it just depend on which cells happen to become infected?
<o
></o>Are other viruses which ME/CFS sufferers are prone to, like Epstein-Barr, HHV-6, parvovirus, cytomegalovirus, etc, simply opportunistic infections taking advantage of a weakened immune system, or are they interacting with XMRV in some way to cause ME/CFS?
<o
></o>Remember the Dubbo study, the prospective cohort study of post-viral fatigue? The only predictive factor for chronic post-viral fatigue they found was the severity of the initial illness. So what, if any, role does the severity of a co-morbid infection play in initiating ME/CFS? Does being infected with XMRV predispose you to more severe infections from other diseases, or does a severe illness effect the progression of XMRV infection?
<o
></o>What, if any, role does gender play? Are there gender differences between healthy people who are XMRV-positive and ME/CFS patients? More women than men have ME/CFS, so are men who are XMRV-positive less likely to get ME/CFS?
<o
></o>Are there gender differences between healthy people who are XMRV-positive and healthy people who are XMRV-negative? Are women more easily infected with XMRV? In those who are XMRV-positive, how does gender effect which cells are infected? We know only men have infected prostate cells!
<o
></o>What accounts for the wide variation in symptoms in ME/CFS? In feline leukemia virus, another infectious gammaretrovirus, different strains produce different symptoms. Theres only one strain thats transmissible, but that type sometimes then morphs into other strains inside the cat's body. Is that true of XMRV?
And of course, the big T, transmission. How is XMRV transmitted and how contagious is it? This is a puzzle, because, although admittedly the epidemiological studies have been pretty pathetic, it appears the ME/CFS does not follow the risk patterns typical of a sexually transmitted disease, or of a blood-born pathogen. This may change once we have a standard XMRV test which will allow for better epidemiological studies, but so far theres no evidence that ME/CFS is more prevalent in people with a history of STDs, or intravenous drug users, hemophiliacs or those with a history of transfusion. There also dont appear to be the levels of infection among people living together that youd expect if it were transmissible by casual contact.
<o
></o>Again looking at feline leukemia virus for comparison, FeLV is not very contagious. Infection seems to be mainly from saliva, from mutual grooming and bites. The saliva and nasal secretions contain a lot of FeLV virus, but it usually takes prolonged close contact to infect. Cats can also transmit FeLV by sharing dishes (rarely) and litter boxes, and through mothers nursing kittens. FeLV doesnt survive long outside the cats body. It also appears that some cats can be infected without getting sick, but will become healthy carriers.
<o
></o>Apparently some cats are able to mount an immune response to the initial infection, eliminate the virus from their bloodstream, and never progress to the diseased state. With about 70% of cats the virus is only in the bloodstream and shed in secretions for 1 16 weeks. A few cats with continue to shed virus even after its gone from their bloodstream. Sometimes the virus becomes latent in the bone marrow. About 30% of cats dont mount an adequate initial immune response and become permanently infected. Theyre the ones that go on to develop immunosuppression, lymphoma, leukemia, neuropathy, enteritis (GI problems), etc. Is FeLV a model for XMRV? Is it a better model than HIV?
<o
></o>So many questions. Actually now that I think about it, since one thing we do know is that some people are infected with XMRV, Id like to know the answers to these questions even if the WPI study wasnt replicated. Some people are infected. What is it doing to them, and how is it spreading?
<o
></o><o
></o><o
></o>[1]<o
></o><st1:country-region w:st="on"><st1
lace w:st="on">US</st1lace></st1:country-region> population 309,509,942 x 3.7% =<o></o>11,451,867<o
></o><o
></o>if PW ME/CFS - 4,000,000<o
></o>x 98% = 3,920,000 = 34% of healthy XMRV+<o
></o>x 67% = 2,680,000 = 23% of healthy XMRV+<o
></o><o
></o>if PW ME/CFS - 1000000<o
></o>x 98% = 980,000 = 8% of healthy XMRV+<o
></o>x 67% = 670,000 = 6% of healthy XMRV+
