Guest guest Posted June 4, 2006 Report Share Posted June 4, 2006 Hi, a. " pjeanneus " <pj7@...> wrote: > > The basis of the NCF speculation is DeMeirleir's work on RNaseL and > stat 1. Cort has written an outstanding summary of > DeMeirleir's book. You can find the section relating to the question > of stat 1 degradation and whether it is viral or bacterial at this > link: > http://www.phoenix-cfs.org/The%20SITE/CFSABAVII.htm ***This link has no mention or reference to STAT-1 so does nothing to answer the question. In fact, Cort's entire summary of DeMeirleir's book at the phoenix-cfs.org site is fairly thin on STAT-1 commentary. ***It is a summary, so perhaps that explains it. Nevertheless, the STAT-1 question I ask regarding its plausible depletion as a result of upstream ATP production problems in PWCs, before and more than what PIV-5 virus exposure might do, remains. davidhall2020wrote> > ***At first blush by my layman's reading of STAT-1 is it seems this > protein depends a lot on ATP to get made. If this is right, this > potentially creates a problem with NCF's hypothesis because it's > becoming fairly evident that PWCs are ATP production challenged to > start, given the glutathione status and methylation issues tying back > to genetics. > > > > > > > > ***STAT-1 depletion then seems to be more of a downstream terrain > issue and this virus of note possibly just adding insult to injury by > creating further depletion, but not properly characterized as THE > cause of it in PWCs. I'd like to here the NCF say more about they're > finding and aswage this concern that the gene variant/metabolic > predispostions may be the more relevant issue when it comes to STAT-1 > status. > > > > > > > > I just find it very strange that the > > > cfids community is so quiet about this announcement. > > > > > > > > *** > > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted June 4, 2006 Report Share Posted June 4, 2006 , Let me try to make my point again. 1. The NCF used DeMeirleir's research on Stat 1 and his patent information which is public domain knowledge, but did not give him any credit - no footnoted link to his studies. 2. The NCF funded research on a virus which may or may not have much to do with causing cfs. 3. DeMeirleir, who is arguably the foremost researcher along with Suhadolnik and Englebienne on this whole question, has not indicated that he feels a virus is the responsible infection for the downstream destruction of RNaseL or stat 1. Indeed, he gives at least equal responsibility to both viruses and bacteria. MY QUESTION ALL ALONG HAS BEEN WHY DOESN'T THE NCF LOCATED IN THE HEART OF LYME COUNTRY FUND RESEARCH INTO BACTERIAL INFECTIONS THAT COULD DAMAGE THE RNASEL PATHWAY? Please note that patients with borrelia often are also carrying mycoplasma mentioned by DeMeirleir as affecting RNaseL and stat 1. Cort doesn't go deeply into stat 1 since this was not covered in depth in DeMeirleir's book. DeMeirleir does mention repeatedly that the virus infections found in cfs may be opportunistic and that bacteria such as mycoplasma can alter the RNaseL pathway. Also, in DeMeirleir's treatment protocol he used both Ampligen and antibiotics alternating each 4 months at a time. I don't think he uses Ampligen at all anymore, probably because it causes further degradation of stat 1 - again this LOOKS LIKE a virus is not the cause according to DeMeirleir as Ampligen is used to treat viral infections. Hemespherix has started researching the use of Ampligen for AIDS after all. Here is another quote from Cort's summary just to make the point again. http://www.phoenix-cfs.org/The%20SITE/CFSABAVI.htm " Another possible factor in the apoptotic disregulation seen is the high number of opportunistic infections CFS patients have. Viruses, chlamydia and mycoplasma are all able to inhibit apoptosis. (We will see later that mycoplasmas also appear to be able to fragment RNase L. Opportunistic infections can also aggravate the pathogenic process in CFS by disrupting metabolic pathways and cytokine production. G-actin cleavage undoubtedly negatively effects antigen presentation and phagocytosis. " a Carnes > > ***This link has no mention or reference to STAT-1 so does nothing to answer the question. In fact, Cort's > entire summary of DeMeirleir's book at the phoenix-cfs.org site is fairly thin on STAT-1 commentary. > > > > ***It is a summary, so perhaps that explains it. Nevertheless, the STAT-1 question I ask regarding its plausible depletion as a result of upstream ATP production problems in PWCs, before and more than what PIV-5 virus exposure might do, remains. > > > > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted June 4, 2006 Report Share Posted June 4, 2006 a, 1. The NCF provided DeMeirleir's patent which is posted on their website so the reference is there. In particular, see: Methods for diagnosis and treatment of chronic immune diseases, US Patent # 200377674 2. From what I read into this, the NCF confirmed Dr. Robbins' finding. This is very important because the SER strain of PIV-5 is identified in both swine and humans. 3. You better take a look VERY CLOSELY at DeMeirleir's group patent. Why? Because there IS a reference to viral attacks to STAT-1. The noted work was written by Dr. Alcami et. al. Go look, in the viral evasion paper, ONLY PIV-5 is listed as directly attacking STAT-1. DeMeirleir's group references Dr. Alcami's work! 4. As far as bacterial infections, lyme, etc....I suggest you go read Dr. Bell's paper on the epidemiology of the Lyndonville outbreak in adolescents. It can be found on the NCF's website. Bell along with the NYS Department of Health already tested for these sources, as mentioned in the paper, and they DIDN'T find supportive evidence for them. 5. I like to think that Bob Harrington is smiling about this news as he was a strong advocate for the NCF. Just my 2 cents worth, Beach > > , > Let me try to make my point again. > > 1. The NCF used DeMeirleir's research on Stat 1 and his patent > information which is public domain knowledge, but did not give him > any credit - no footnoted link to his studies. > > 2. The NCF funded research on a virus which may or may not have much > to do with causing cfs. > > 3. DeMeirleir, who is arguably the foremost researcher along with > Suhadolnik and Englebienne on this whole question, has not indicated > that he feels a virus is the responsible infection for the downstream > destruction of RNaseL or stat 1. Indeed, he gives at least equal > responsibility to both viruses and bacteria. MY QUESTION ALL ALONG > HAS BEEN WHY DOESN'T THE NCF LOCATED IN THE HEART OF LYME COUNTRY > FUND RESEARCH INTO BACTERIAL INFECTIONS THAT COULD DAMAGE THE RNASEL > PATHWAY? Please note that patients with borrelia often are also > carrying mycoplasma mentioned by DeMeirleir as affecting RNaseL and > stat 1. > > Cort doesn't go deeply into stat 1 since this was not covered > in depth in DeMeirleir's book. DeMeirleir does mention repeatedly > that the virus infections found in cfs may be opportunistic and that > bacteria such as mycoplasma can alter the RNaseL pathway. Also, in > DeMeirleir's treatment protocol he used both Ampligen and antibiotics > alternating each 4 months at a time. I don't think he uses Ampligen > at all anymore, probably because it causes further degradation of > stat 1 - again this LOOKS LIKE a virus is not the cause according to > DeMeirleir as Ampligen is used to treat viral infections. Hemespherix > has started researching the use of Ampligen for AIDS after all. > > Here is another quote from Cort's summary just to make the point > again. > > http://www.phoenix-cfs.org/The%20SITE/CFSABAVI.htm > > " Another possible factor in the apoptotic disregulation seen is the > high number of opportunistic infections CFS patients have. Viruses, > chlamydia and mycoplasma are all able to inhibit apoptosis. (We will > see later that mycoplasmas also appear to be able to fragment RNase > L. Opportunistic infections can also aggravate the pathogenic > process in CFS by disrupting metabolic pathways and cytokine > production. G-actin cleavage undoubtedly negatively effects antigen > presentation and phagocytosis. " > > a Carnes > > > > ***This link has no mention or reference to STAT-1 so does nothing > to answer the question. In fact, Cort's > > entire summary of DeMeirleir's book at the phoenix-cfs.org site is > fairly thin on STAT-1 commentary. > > > > > > > > ***It is a summary, so perhaps that explains it. Nevertheless, the > STAT-1 question I ask regarding its plausible depletion as a result > of upstream ATP production problems in PWCs, before and more than > what PIV-5 virus exposure might do, remains. > > > > > > > > > > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted June 4, 2006 Report Share Posted June 4, 2006 a, This is a quote directly from Dr. Bell's paper on the Lyndonville outbreak published in the medical journal Reviews of Infectious Diseases that's available for you to read from the NCF's website: " Extensive laboratory analyses were conducted, including serologic tests specific for Brucella abortus, Brucella suis, Brucella melitensis, and Brucella canis; iella burnetii; Cytomegalovirus; EBV; Toxoplasma gondii; Borrelia burgdorferi; HIV; Hepatitis B virus; Parvovirus B-19; and Francisella tularensis. " As you know, Borrelia burgdorferi is Lyme disease. The NCF probably WASN'T interested in this BECAUSE the epidemiology of the outbreak showed that IT WASN'T INVOLVED! It was tested but wasn't found to be involved in the outbreak and therefore WASN'T causitive. By the way, a quick check in the National Library of Medicine turned up NO publications on Lyme/Borrelia and either RNaseL or STAT-1. If Borrelia influenced either RNaseL or STAT-1 in a major way, don't you think that it would have been previously published. As it stands, there's nothing published to date on this! I suggest if you have any questions regarding this epidemiologic study, write or call Dr. Bell. He's in the Lyndonville phone directory! Beach > > , > Let me try to make my point again. > > 1. The NCF used DeMeirleir's research on Stat 1 and his patent > information which is public domain knowledge, but did not give him > any credit - no footnoted link to his studies. > > 2. The NCF funded research on a virus which may or may not have much > to do with causing cfs. > > 3. DeMeirleir, who is arguably the foremost researcher along with > Suhadolnik and Englebienne on this whole question, has not indicated > that he feels a virus is the responsible infection for the downstream > destruction of RNaseL or stat 1. Indeed, he gives at least equal > responsibility to both viruses and bacteria. MY QUESTION ALL ALONG > HAS BEEN WHY DOESN'T THE NCF LOCATED IN THE HEART OF LYME COUNTRY > FUND RESEARCH INTO BACTERIAL INFECTIONS THAT COULD DAMAGE THE RNASEL > PATHWAY? Please note that patients with borrelia often are also > carrying mycoplasma mentioned by DeMeirleir as affecting RNaseL and > stat 1. > > Cort doesn't go deeply into stat 1 since this was not covered > in depth in DeMeirleir's book. DeMeirleir does mention repeatedly > that the virus infections found in cfs may be opportunistic and that > bacteria such as mycoplasma can alter the RNaseL pathway. Also, in > DeMeirleir's treatment protocol he used both Ampligen and antibiotics > alternating each 4 months at a time. I don't think he uses Ampligen > at all anymore, probably because it causes further degradation of > stat 1 - again this LOOKS LIKE a virus is not the cause according to > DeMeirleir as Ampligen is used to treat viral infections. Hemespherix > has started researching the use of Ampligen for AIDS after all. > > Here is another quote from Cort's summary just to make the point > again. > > http://www.phoenix-cfs.org/The%20SITE/CFSABAVI.htm > > " Another possible factor in the apoptotic disregulation seen is the > high number of opportunistic infections CFS patients have. Viruses, > chlamydia and mycoplasma are all able to inhibit apoptosis. (We will > see later that mycoplasmas also appear to be able to fragment RNase > L. Opportunistic infections can also aggravate the pathogenic > process in CFS by disrupting metabolic pathways and cytokine > production. G-actin cleavage undoubtedly negatively effects antigen > presentation and phagocytosis. " > > a Carnes > > > > ***This link has no mention or reference to STAT-1 so does nothing > to answer the question. In fact, Cort's > > entire summary of DeMeirleir's book at the phoenix-cfs.org site is > fairly thin on STAT-1 commentary. > > > > > > > > ***It is a summary, so perhaps that explains it. Nevertheless, the > STAT-1 question I ask regarding its plausible depletion as a result > of upstream ATP production problems in PWCs, before and more than > what PIV-5 virus exposure might do, remains. > > > > > > > > > > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted June 4, 2006 Report Share Posted June 4, 2006 Hi, a. " pjeanneus " <pj7@...> wrote: > > , > Let me try to make my point again. > > 1. The NCF used DeMeirleir's research on Stat 1 and his patent > information which is public domain knowledge, but did not give him > any credit - no footnoted link to his studies. ***Yes. I see this they didn't do this. > 2. The NCF funded research on a virus which may or may not have much > to do with causing cfs. ***Yes. I agree with your conclusion here. The announcement of this one viral finding in PWCs doesn't seem to answer key questions that would make it a well developed hypothesis of cause, which would gather much stronger interest if it did. 3. DeMeirleir, who is arguably the foremost researcher along with Suhadolnik and Englebienne on this whole question, has not indicated that he feels a virus is the responsible infection for the downstream destruction of RNaseL or stat 1. Indeed, he gives at least equal responsibility to both viruses and bacteria. MY QUESTION ALL ALONG HAS BEEN WHY DOESN'T THE NCF LOCATED IN THE HEART OF LYME COUNTRY FUND RESEARCH INTO BACTERIAL INFECTIONS THAT COULD DAMAGE THE RNASEL PATHWAY? Please note that patients with borrelia often are also carrying mycoplasma mentioned by DeMeirleir as affecting RNaseL and stat 1. ***I think you have a valid complaint or at least something the NCF should address as to why they may think lyme is not a valid lead to rule out or in for those diagnosed with CFS. This is similar to my question concerning STAT-1, which may be explained by the upstream poor ATP production commonly found in PWCS and not much if anything to do with any type of infection to start. Dr DeMeirleir's book couldn't address this given it was written several years ago and is out dated enough that he didn't know there would be a much larger body of data to support this connection this to CFS now. Cort doesn't go deeply into stat 1 since this was not covered in depth in DeMeirleir's book. DeMeirleir does mention repeatedly that the virus infections found in cfs may be opportunistic and that bacteria such as mycoplasma can alter the RNaseL pathway. Also, in DeMeirleir's treatment protocol he used both Ampligen and antibiotics alternating each 4 months at a time. I don't think he uses Ampligen at all anymore, probably because it causes further degradation of stat 1 - again this LOOKS LIKE a virus is not the cause according to DeMeirleir as Ampligen is used to treat viral infections. Hemespherix has started researching the use of Ampligen for AIDS after all. ***I'm not surprised he gave-up on ampligen for treating PWCs. I wasn't aware of the issue of it degrading STAT-1, but I do know from personal experience and research that it doesn't really work for CFS, excepting a rare few cases temporarily. Here is another quote from Cort's summary just to make the point > again. > > http://www.phoenix-cfs.org/The%20SITE/CFSABAVI.htm > > " Another possible factor in the apoptotic disregulation seen is the > high number of opportunistic infections CFS patients have. Viruses,chlamydia and mycoplasma are all able to inhibit apoptosis. (We will see later that mycoplasmas also appear to be able to fragment RNase > L. Opportunistic infections can also aggravate the pathogenic > process in CFS by disrupting metabolic pathways and cytokine > production. G-actin cleavage undoubtedly negatively effects antigen > presentation and phagocytosis. " > > a Carnes ***Thanks for clarifying your point(s). davidhall2020wrote>> Nevertheless, the > STAT-1 question I ask regarding its plausible depletion as a result > of upstream ATP production problems in PWCs, before and more than > what PIV-5 virus exposure might do, remains. > > > > > > > > > > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted June 4, 2006 Report Share Posted June 4, 2006 Beach, running tests on blood is not the same as testing lymph node biopsies. I sat in the room when Dr. Bell spoke with quiet rage over the total ignoring of those kids' biopsies. I also asked at the CDC about the use of those biopsies. I was told in front of many people in the meeting room that " they were probably in a refrigerator somewhere and that they should be tested someday. " This was 1998, years after Bell sent them to Atlanta. We all know the tests for borrelia are almost totally useless. I AM ASKING AGAIN WHY THE NCF HAS NOT FUNDED ANY VALID RESEARCH ON THE POSSIBILITY THAT A TICK BORNE PATHOGEN UNDERLIES A HUGE PERCENTAGE OF CFS AND FMS? All I want is to look at the real possibility that there may not be one virus causing cfs, there may be several bacteria. I don't think that is too much to ask. a Carnes > > > > , > > Let me try to make my point again. > > > > 1. The NCF used DeMeirleir's research on Stat 1 and his patent > > information which is public domain knowledge, but did not give him > > any credit - no footnoted link to his studies. > > > > 2. The NCF funded research on a virus which may or may not have much > > to do with causing cfs. > > > > 3. DeMeirleir, who is arguably the foremost researcher along with > > Suhadolnik and Englebienne on this whole question, has not indicated > > that he feels a virus is the responsible infection for the downstream > > destruction of RNaseL or stat 1. Indeed, he gives at least equal > > responsibility to both viruses and bacteria. MY QUESTION ALL ALONG > > HAS BEEN WHY DOESN'T THE NCF LOCATED IN THE HEART OF LYME COUNTRY > > FUND RESEARCH INTO BACTERIAL INFECTIONS THAT COULD DAMAGE THE RNASEL > > PATHWAY? Please note that patients with borrelia often are also > > carrying mycoplasma mentioned by DeMeirleir as affecting RNaseL and > > stat 1. > > > > Cort doesn't go deeply into stat 1 since this was not covered > > in depth in DeMeirleir's book. DeMeirleir does mention repeatedly > > that the virus infections found in cfs may be opportunistic and that > > bacteria such as mycoplasma can alter the RNaseL pathway. Also, in > > DeMeirleir's treatment protocol he used both Ampligen and antibiotics > > alternating each 4 months at a time. I don't think he uses Ampligen > > at all anymore, probably because it causes further degradation of > > stat 1 - again this LOOKS LIKE a virus is not the cause according to > > DeMeirleir as Ampligen is used to treat viral infections. Hemespherix > > has started researching the use of Ampligen for AIDS after all. > > > > Here is another quote from Cort's summary just to make the point > > again. > > > > http://www.phoenix-cfs.org/The%20SITE/CFSABAVI.htm > > > > " Another possible factor in the apoptotic disregulation seen is the > > high number of opportunistic infections CFS patients have. Viruses, > > chlamydia and mycoplasma are all able to inhibit apoptosis. (We will > > see later that mycoplasmas also appear to be able to fragment RNase > > L. Opportunistic infections can also aggravate the pathogenic > > process in CFS by disrupting metabolic pathways and cytokine > > production. G-actin cleavage undoubtedly negatively effects antigen > > presentation and phagocytosis. " > > > > a Carnes > > > > > > ***This link has no mention or reference to STAT-1 so does nothing > > to answer the question. In fact, Cort's > > > entire summary of DeMeirleir's book at the phoenix-cfs.org site is > > fairly thin on STAT-1 commentary. > > > > > > > > > > > > ***It is a summary, so perhaps that explains it. Nevertheless, the > > STAT-1 question I ask regarding its plausible depletion as a result > > of upstream ATP production problems in PWCs, before and more than > > what PIV-5 virus exposure might do, remains. > > > > > > > > > > > > > > > > > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted June 4, 2006 Report Share Posted June 4, 2006 Bless your heart, , you made my day. I must be communicating a bit better. a > > Hi, a. > > > > " pjeanneus " <pj7@> wrote: > > > > , > > Let me try to make my point again. > > > > 1. The NCF used DeMeirleir's research on Stat 1 and his patent > > information which is public domain knowledge, but did not give him > > any credit - no footnoted link to his studies. > > > > ***Yes. I see this they didn't do this. > > > > > 2. The NCF funded research on a virus which may or may not have much > > to do with causing cfs. > > > > > ***Yes. I agree with your conclusion here. The announcement of this one viral finding in PWCs doesn't seem to answer key questions that would make it a well developed hypothesis of cause, which would gather much stronger interest if it did. > > > > 3. DeMeirleir, who is arguably the foremost researcher along with > Suhadolnik and Englebienne on this whole question, has not indicated > that he feels a virus is the responsible infection for the downstream destruction of RNaseL or stat 1. Indeed, he gives at least equal responsibility to both viruses and bacteria. MY QUESTION ALL ALONG > HAS BEEN WHY DOESN'T THE NCF LOCATED IN THE HEART OF LYME COUNTRY > FUND RESEARCH INTO BACTERIAL INFECTIONS THAT COULD DAMAGE THE RNASEL > PATHWAY? Please note that patients with borrelia often are also carrying mycoplasma mentioned by DeMeirleir as affecting RNaseL and stat 1. > > > > > ***I think you have a valid complaint or at least something the NCF should address as to why they may think lyme is not a valid lead to rule out or in for those diagnosed with CFS. This is similar to my question concerning STAT-1, which may be explained by the > upstream poor ATP production commonly found in PWCS and not much if anything to do with any type of infection to start. Dr DeMeirleir's book couldn't address this given it was written several years ago and is out dated enough that he didn't know there would be a much larger body of data to support this connection this to CFS now. > > > > Cort doesn't go deeply into stat 1 since this was not covered > in depth in DeMeirleir's book. DeMeirleir does mention repeatedly > that the virus infections found in cfs may be opportunistic and that > bacteria such as mycoplasma can alter the RNaseL pathway. Also, in > DeMeirleir's treatment protocol he used both Ampligen and antibiotics > alternating each 4 months at a time. I don't think he uses Ampligen > at all anymore, probably because it causes further degradation of > stat 1 - again this LOOKS LIKE a virus is not the cause according to > DeMeirleir as Ampligen is used to treat viral infections. Hemespherix > has started researching the use of Ampligen for AIDS after all. > > > > ***I'm not surprised he gave-up on ampligen for treating PWCs. I wasn't aware of the issue of it degrading STAT-1, but I do know from personal experience and research that it doesn't really work for CFS, excepting a rare few cases temporarily. > > > > Here is another quote from Cort's summary just to make the point > > again. > > > > http://www.phoenix-cfs.org/The%20SITE/CFSABAVI.htm > > > > " Another possible factor in the apoptotic disregulation seen is the > > high number of opportunistic infections CFS patients have. Viruses,chlamydia and mycoplasma are all able to inhibit apoptosis. (We will see later that mycoplasmas also appear to be able to fragment RNase > > L. Opportunistic infections can also aggravate the pathogenic > > process in CFS by disrupting metabolic pathways and cytokine > > production. G-actin cleavage undoubtedly negatively effects antigen > > presentation and phagocytosis. " > > > > a Carnes > > > > ***Thanks for clarifying your point(s). > > > > > > > > davidhall2020wrote>> > > > Nevertheless, the > > STAT-1 question I ask regarding its plausible depletion as a result > > of upstream ATP production problems in PWCs, before and more than > > what PIV-5 virus exposure might do, remains. > > > > > > > > > > > > > > > > > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted June 4, 2006 Report Share Posted June 4, 2006 a, Why not ask the CFIDS Association to do this....after all, they bring in $2,000,000 per year..... This would be a drop in the bucket to them. As for the NCF, they have spent $ 350,000 thus far on their research. The CFIDS Association has spent ten times that thus far. It's economies of scale! Beach > > > > > > , > > > Let me try to make my point again. > > > > > > 1. The NCF used DeMeirleir's research on Stat 1 and his patent > > > information which is public domain knowledge, but did not give > him > > > any credit - no footnoted link to his studies. > > > > > > 2. The NCF funded research on a virus which may or may not have > much > > > to do with causing cfs. > > > > > > 3. DeMeirleir, who is arguably the foremost researcher along with > > > Suhadolnik and Englebienne on this whole question, has not > indicated > > > that he feels a virus is the responsible infection for the > downstream > > > destruction of RNaseL or stat 1. Indeed, he gives at least equal > > > responsibility to both viruses and bacteria. MY QUESTION ALL > ALONG > > > HAS BEEN WHY DOESN'T THE NCF LOCATED IN THE HEART OF LYME COUNTRY > > > FUND RESEARCH INTO BACTERIAL INFECTIONS THAT COULD DAMAGE THE > RNASEL > > > PATHWAY? Please note that patients with borrelia often are also > > > carrying mycoplasma mentioned by DeMeirleir as affecting RNaseL > and > > > stat 1. > > > > > > Cort doesn't go deeply into stat 1 since this was not > covered > > > in depth in DeMeirleir's book. DeMeirleir does mention repeatedly > > > that the virus infections found in cfs may be opportunistic and > that > > > bacteria such as mycoplasma can alter the RNaseL pathway. Also, > in > > > DeMeirleir's treatment protocol he used both Ampligen and > antibiotics > > > alternating each 4 months at a time. I don't think he uses > Ampligen > > > at all anymore, probably because it causes further degradation of > > > stat 1 - again this LOOKS LIKE a virus is not the cause according > to > > > DeMeirleir as Ampligen is used to treat viral infections. > Hemespherix > > > has started researching the use of Ampligen for AIDS after all. > > > > > > Here is another quote from Cort's summary just to make the point > > > again. > > > > > > http://www.phoenix-cfs.org/The%20SITE/CFSABAVI.htm > > > > > > " Another possible factor in the apoptotic disregulation seen is > the > > > high number of opportunistic infections CFS patients have. > Viruses, > > > chlamydia and mycoplasma are all able to inhibit apoptosis. (We > will > > > see later that mycoplasmas also appear to be able to fragment > RNase > > > L. Opportunistic infections can also aggravate the pathogenic > > > process in CFS by disrupting metabolic pathways and cytokine > > > production. G-actin cleavage undoubtedly negatively effects > antigen > > > presentation and phagocytosis. " > > > > > > a Carnes > > > > > > > > ***This link has no mention or reference to STAT-1 so does > nothing > > > to answer the question. In fact, Cort's > > > > entire summary of DeMeirleir's book at the phoenix-cfs.org site > is > > > fairly thin on STAT-1 commentary. > > > > > > > > > > > > > > > > ***It is a summary, so perhaps that explains it. Nevertheless, > the > > > STAT-1 question I ask regarding its plausible depletion as a > result > > > of upstream ATP production problems in PWCs, before and more than > > > what PIV-5 virus exposure might do, remains. > > > > > > > > > > > > > > > > > > > > > > > > > > Quote Link to comment Share on other sites More sharing options...
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