Immune system

Discussion in 'Fibromyalgia Main Forum' started by psychomama, Oct 11, 2006.

  1. psychomama

    psychomama New Member

    Does anyone think that people with CFS/fibro have kind of good immune systems? Just wondering because I very seldom get a cold or the flu and have both CFS and fibro. I don't every feel very well, but don't catch things easily from others.
  2. suz45

    suz45 New Member

    I was recently thinking about the same subject, my kids can bring home a bug and I usually dont' catch it. I used to work in a JHS/HS and never caught the bugs and colds from the kids there either.

    I have FMS/MPS or CMP whatever one wants to call it these days, yet my chiro who is also board eligible in Neurology thinks that these disorders involve both the CNS and immune system. I think though that each person is different. I think my CNS system is more invlved than my immune system as I do not have the level of fatigue that many with FM have. I think mine is more about my CNS receptors being more sensitive to pain... Go figure.


    good topic to think about and look at.


  3. happycanuk

    happycanuk New Member

    I don't know if it good or not, but I rarely get sick. Having said this, I probably will within the next week lol

    PITATOO Member

    I too have FMS and CFIDS and also MS. I have not had a flu or cold in over 10 years. I have gotten bacterial infections but not viruses. MS is definitely an auto-immune disease and I believe that FMS and CFIDS both are also. So our immune systems are over active and without a virus to attack it causes all these flu like symptoms. For many reasons I am afraid of getting a flu vacine. Bobby
  5. SteveInOZ

    SteveInOZ New Member

    There may be a different explanation, you may not get cold and flu symptoms because your immune system is not mounting a response to these viral infections.

    You still have the infection, and if you are lucky it dies out and you never know you had it in the first place.

  6. Michelle_NZ

    Michelle_NZ New Member

    One of the current theories about CFS is that the immune system is in overdrive. It kind of gets left in the "on" mode after the initital viral infection (75% of CFS cases come about after a viral illness).

    This in turn causes chemical changes in the brain and the muscles, and over time can lead to ongoing illness.

    I read somewhere (sorry, cant remember where now), that if you have CFS and you suddenly start getting colds it could mean that you are actually getting well again because your immune system is working more normally.

    But remember - these are all just theories, and the "medical profession" dont fully understand what causes CFS or why some people seem to recover while others continue to stay sick.

    Take care
  7. nerdieduckie

    nerdieduckie New Member

    My immune system is shot. I get pretty much everything (always have since I was about 13 or so) and I'm soooo glad I'm not around school right now.

    Interesting that some cfs/fm people possibly have immune systems that (over)fight stuff off, and others don't. I've read a lot of you didn't want flu shots, but I couldn't see myself NOT getting one. I figured the two days of being sick (which haven't happened this year) were worth not getting the flu for, and if I end up with the flu anyway, at least I know I tried :p

    I'm pretty sure I used to be healthy...once o_O
  8. TerryS

    TerryS Member

    I definitely have an overactive immune system in that I have all kinds of autoimmune issues going on.

    HOWEVER, I still seem to catch A LOT of viruses.

    That stinks!!!

  9. Slayadragon

    Slayadragon New Member

    This hypothesis is brilliant! I can't believe it's the first time I've heard it.

    Is there any evidence for this? It makes an awfully lot of sense to me.
  10. SteveInOZ

    SteveInOZ New Member

    I have Fibro and Chronic Lymphocytic Leukemia.

    It is a well known fact that people with very early stage CLL do not create antibodies to vaccinations even though they have a functioning immune system in other respects (eg normal immunoglobulin levels).

    It is thought this is related to a fault in dendritic cell functioning.

    In my case I do not mount an immune response to infections and have to rely on the humoral immune system. The complement system still works but T-Cell and B-Cell signalling is wonky. Hence no antibodies and no symptoms of colds and flu.
  11. psychomama

    psychomama New Member

    Can you explain what this is? I didn't really understand your explanation. Can you put it in simpler terms maybe?

  12. Beachtrekker1

    Beachtrekker1 New Member

    My own personal explanation is that everthing in my body is so whacko anyway. I don' think I can differentiate one thing from another! I could be sick and it all feels like the Fibro to me...
  13. SteveInOZ

    SteveInOZ New Member

    Complement is the most ancient form of immune system. Basically "complement" coats bacteria and viruses in "sludge" causing most of them to die.

    It also signals the other kinds of defence systems to kick in.

    Sorry I cannot explain it any better. :)

  14. murkinrg

    murkinrg New Member

    I'm the complete opposite.

    I'm always on the edge of getting a cold.This year I was only free of cold symptoms from about 1st May to late August
    The slightess bit if stress or a late night and it sends me down.It starts with bit of fatigue then the sore throat then 2 weeks of feeling groggy so the whole cycle takes 3 to 4 weeks then i'm ok but f its winter I'll never be to far from getting another one.

    I can't say I really suffer the other symptoms of CFS/Fibro just that my immune system is very delicate.

    I went to the GP in desperation this summer and had the full blood test thing and all came back normal.

    One thing I will say is that i've never been very good at coping with stress and as my wife is a life long depresion sufferer, i'm never far from stress.

  15. mollystwin

    mollystwin New Member

    I catch everything!! My sis also has CFIDS and we both have always been sickly as kids and adults. I am currently getting gamma globulin shots to help improve my immune system. There are many of us who suffer from Stealth infectsions both viral and bacterial.

    Maybe some of us have overactive immune and some underaactive?
  16. karinaxx

    karinaxx New Member

    so maybe this will help to answer the question about autoimmune or prone to infections.
    Dr.Meirleir subgroups ME/CFIDS patients, as you can read in his classification part or this Article.

    Dr. Kenny De Meirleir’s Breakthrough Research and Recommendations for CFS Testing & Treatment
    by Editor


    Kenny De Meirleir, MD, PhD, is a member of ProHealth’s Scientific Advisory Board
    As described in the following article, Dr. De Meirleir reports that his research indicates Chronic Fatigue Syndrome patients can be differentiated from healthy people with 99 percent accuracy based on a test for the presence of “low molecular weight” RNase L in the blood. He says the weight of LMW RNase L molecules found in the blood of CFS patients is less than half that of normal RNase L molecules. (And this holds true for individuals with several other illnesses, including Fibromyalgia.) Increased symptom severity correlates directly with increased levels of LMW RNase L.

    Additionally, though Dr. De Meirleir emphasizes that each patient’s profile is unique, he says his research indicates that CFS patients tend to fall into three groups with different test profiles and treatments. Based on the results of six tests, he reports he has been able to predict patients’ symptoms with 95 percent accuracy while the remaining 5 percent had overlap features. (See the footnotes for information about the workshop materials Dr. De Meirleir has developed for physicians and patients, and about his lab – located in Reno, Nevada – which offers diagnostic testing of samples from patients who may be candidates for a diagnosis of ME/CFS.)

    Highlights of Dr. Kenny De Meirleir’s Lecture on “Advances in ME/CFS Testing and Treatment,” presented in Calgary, Alberta, on April 2, 2006

    by Marjorie van de Sande


    Dr. De Meirleir is a world renowned researcher and is professor of Physiology and Internal Medicine at Free University of Brussels in Belgium. Dr. De Meirleir recently published his 600th peer-reviewed paper. He is co-editor of Chronic Fatigue Syndrome: A Biological Approach, co-editor of the Journal of Chronic Fatigue Syndrome, and reviewer for more than 10 other medical journals. Dr. De Meirleir was one of four international experts on the panel that developed the Canadian Consensus Document for ME/CFS. He assesses/treats 3,000 to 4,000 ME/CFS patients annually.

    Normal Response to Infectious Agents

    Numerous infectious agents can trigger ME/CFS. Infectious agents that invade cells release ribonucleic acid (RNA) or deoxyribonucleic acid (DNA) when they reproduce. Normally when a virus infects a cell, an enzyme called Ribonuclease L (RNase L) is activated and cuts the RNA of the infectious agent so it cannot replicate itself. The RNase L molecule also cuts the RNA of the infected cell, which triggers the cell’s death and removal. Then the RNase L molecule “switches off” and remains inactive so that it doesn’t damage healthy cells.

    Abnormal RNase L Molecule Found in ME/CFS Patients

    The normal weight of the RNase L molecule is 80 kilo Daltons (kDa). In ME/CFS patients, the RNase L molecule is being cut and weighs 37 kDa - less than half its normal weight. The low molecular weight (LMW) RNase L molecule can discriminate ME/CFS patients from healthy people, and illnesses such as Fibromyalgia, multiple sclerosis, cancer, AIDS and depression. The Centers for Disease Control and Prevention sent 100 blood samples to Dr. De Meirleir. Using the test for LMW RNase L, Dr. De Meirleir was able to identify which blood samples came from ME/CFS patients with 99 percent accuracy. These findings confirm an organic origin of ME/CFS and validate the diagnosis.

    Abnormal RNase L Molecule Causes Chronic Dysfunction of the Immune System

    The damaged RNase L molecule is not able to kill infectious agents and it keeps damaged cells alive. The body is unable to “switch off” these abnormal RNase L fragments, so they continue to cut the RNA of normal cells. The destructive RNase L fragment is six times more active than normal and consumes approximately 70 percent of the cells’ energy (ATP). RNase L fragments destroy normal protein synthesis, enzyme production, and other vital cellular functions. They inhibit respiratory muscles, and cause hyperventilation, metabolic alkalosis, sleep disturbances, and central fatigue. There is sodium retention, low magnesium levels, and dramatically low levels of potassium. Natural killer cells, which protect against viruses and intracellular infections, are also being damaged. Thus, the immune system is in a state of chronic dysfunction.

    Testing for ME/CFS

    Dr. De Meirleir is co-founder of REDLABS (, which recently opened a lab in Nevada. This lab offers diagnostic and treatment tests for ME/CFS patients. Although each patient’s profile is unique, patients tend to fall into three groups with different causes and treatments. Based on the results of six tests, Dr. De Meirleir was able to predict patients’ symptoms with 95 percent accuracy while the remaining 5 percent had overlap features. Symptom severity rises in correlation to the rise in the level of LMW RNase L.

    Group Profiles

    Group 1: (15 to 20 percent)

    This group has high levels of LMW RNase L and elastase, low levels of protein kinase (PKR) and uric acid, and low to normal levels of nitric oxide. Spinal taps indicate elevated levels of lymphocytes and proteins in the spinal fluid, and there is increased pressure upon opening the lumbar puncture.

    These patients have a chronic low-grade viral infection and inflammatory reaction in the brain. Many micro-organisms are associated with this profile. Heavy metals, pesticides, and other triggers may also be involved. Approximately 20 percent of this group has low-grade Herpes Virus 6A (HHV6A) encephalitis.

    The prominent feature is neurocognitive problems such as confusion and impaired concentration and memory. Fatigue originates in the brain. Pain is not prominent. Patients exhibit symptoms that have some similarities to multiple sclerosis (MS).

    Group 2: (10 to 15 percent)

    These patients have very high levels of LMW RNase L and elastase, high protein kinase activity, severely low natural killer cell activity, and very low serum uric acid levels.

    This group of severely ill patients has bacterial infections originating from animals such as pets, rodents, ticks, etc. These patients have severe bowel problems. The gut is an important part of the immune system because 70 percent of immune cells are in the digestive tract. When a patient has leaky gut syndrome, the gut has become permeable and foreign proteins enter the blood and tissues and inflammation results. Dr. De Meirleir tests for 12 pathogenic gut bacteria.

    Group 3: (60 to 70 percent)

    The majority of ME/CFS patients are in this group. This profile is basically similar to Group 2, but not as severe. Generalized pain originating from dysfunction in the pain processing areas of the brain and CNS is a prominent feature. These patients have gastrointestinal infections, and bacteria are in the blood.

    Some Other Areas of Investigation


    Part of the immune system is activated and part is suppressed, leaving the patient vulnerable to opportunistic infections. Patients may have one or a number of infections. Serum Immunobilan tests are done to identify which ones are active. Suspect microorganisms include viruses, bacteria, and mycoplasma. A chlamydia pneumonia infection is often found in patients with chronic sinus infections. Approximately 8 to 10 percent of ME/CFS patients have infections of animal origin such as Rickettsiae, Coxiella, Bartonella, and Borrelia. Many of these infections come from pets. A small percentage come from ticks.

    Heavy Metals

    Exposure comes from many sources including food, insulation, air, etc. ME/CFS patients have increased sensitivity to chemicals, environmental pollutants, and heavy metals, particularly mercury and nickel. Toxins can trigger an inflammatory response.

    One of the RNase L fragments has a structure that is almost identical to a protein involved in the removal of heavy metals and toxic chemical from cells. When this protein is blocked by the RNase L fragments, the cells become more sensitive to mercury. Now a tiny amount of mercury that would normally kill 10 percent of the cells can kill 50 to 100 percent of the cells.


    Fungi such as Aspergillus Niger and Candida can contribute to ME/CFS symptoms. Candida is a yeast fungal infection that changes sugars to aldehydes, a toxic form of alcohol.

    Digestive Tract

    Gastrointestinal problems are a serious concern in ME/CFS patients: 70 percent of the body’s immune cells are found in the gastrointestinal tract. These immune cells prevent bacteria and foreign protein from entering the blood stream. When the gut becomes permeable and foreign protein enters the blood stream, elastase is produced. Elastase is the enzyme that is responsible for cutting the RNase L molecule into fragments. Elastase breaks down elastin, which gives elasticity to collagen. As a result, there is pain and a loss of elasticity in ligaments and tendons.

    Peripheral Resistance to Thyroid Hormone

    Most patients have normal results for common thyroid tests. However, ME/CFS patients have a much higher level of a protein that is 98 percent identical to T3, which is the active form of thyroid. Because this foreign protein can bind to T3 receptors, T3 cannot find receptors and is therefore ineffective in its role of activating cellular metabolism.

    Treatment Summary

    Some psychiatrists advocate that no tests or lab work be done on ME/CFS patients because testing will reinforce delusions of physical illness. Given the wealth of confirmed biochemical abnormalities, such a rationale is ludicrous. Dr. De Meirleir stressed that tests must be done in order to determine the origin of the problem. Then treatment can be prescribed to eliminate the cause. A “clean-up” of all the consequences of the problem must also be undertaken. Therapies and the order of treatments vary according to the patient’s unique test profile. Treatment includes:

    Restoring immune competence
    Removing microorganisms
    Restoring hormonal balance
    Restoring intestinal flora
    Decreasing prostaglandins and protein kinase activity
    Removing heavy metals and toxic chemicals.
    This summary of Dr. De Meirleir’s lecture, written by Majorie van de Sande, B Ed, Grad Dip Ed, was reproduced with permission from Quest, the newsletter of Canada’s National ME/FM Action Network. Ms. van de Sande is the Action Network’s Advisor and Webmaster, Conference Planning Committee.

    Dr. De Meirleir describes various treatment therapies in a full-day physicians’ workshop, which is available as a set of four DVDs and a CD. For information about how to order these materials, and a patient workshop in DVD format, visit the National ME/FM Action Network site, at

    For information on the diagnostic testing supplies and services available via Dr. De Meirleir’s lab – REDLABS USA, in Reno, Nevada – visit This site also offers a free downloadable PowerPoint presentation for physicians on the interpretation of test results.

    Note: The information provided here is not intended to diagnose, treat, cure, mitigate, or prevent any disease.

    Stay Healthy this Cold Season
    Healthy NK cells defend your body

    Stop Fatigue in 8 Weeks!
    Improve cell activity to boost energy

    Guaifenesin FA
    Tested by Dr. St. Amand, FDA approved.

    Top Energy Nutrient CoQ10
    Pure pharmaceutical grade
    All strengths available

    Increase Energy 33% Clinical research shows increased cell permeability.

    Physician Favorite
    for promoting healthy NK cell function.

  17. karinaxx

    karinaxx New Member

    connects this all, so here part two. this is long, but worth reading for those who are new to the ME/CFIDS topic.
    have fun
    Part One - Unmasked Research:

    STAT1-alpha and p53 Deficiencies are Found in Patients with
    Chronic Fatigue Syndrome;
    The National CFIDS Foundation Responds by Funding Several
    New Research Initiatives

    Investigative Report by Alan Cocchetto, Medical Director
    National CFIDS Foundation, Inc.
    Copyright © 2003 Written Permission Required for Reprinting or Distributing

    Through its own extensive six month medical investigation, the National CFIDS Foundation (NCF) uncovered research that will have widespread ramifications among the CFS patient community, their physicians, as well as CFS researchers worldwide establishing CFS as a serious and perhaps fatal illness. Because of these implications, the NCF has responded to this major discovery by dynamically funding new medical research by several noted scientists.
    Briefly stated, the NCF has uncovered a key scientific discovery, previously made by prominent CFS researchers, that has yet to see the 'light of day.' The critical component: STAT1. The STAT1 protein is crucial for proper immune function and regulation. Without it, cells are unresponsive to interferons leaving the body defenseless against viral and bacterial infections. In fact, human STAT1 deficiency is lethal. In this report, the NCF identified CFS researchers that previously found STAT1 to be absent in CFS patient blood.

    "The NCF began its investigation by thoroughly reviewing work that had been previously published by Kenny DeMeirleir, MD, PhD and his colleague's group in Belgium" stated Gail Kansky, President of the NCF. "Then one discovery lead to another and our own investigation just skyrocketed" said Kansky. "As the CFS patient community is aware, Dr. DeMeirleir is a highly visible CFS researcher, both in the U.S. and abroad. He is a medical editor for the Journal of Chronic Fatigue Syndrome, is on the board of the American Association for Chronic Fatigue Syndrome (AACFS), and is actively involved with R.E.D. Laboratories which has worked to further the studies of Dr. Robert Suhadolnik, from Temple University, whose research group made the initial RNase L discoveries in CFS patients" stated Kansky. "I strongly feel that the NCF's investigational and medical research efforts will greatly add to those efforts that we have previously undertaken to unravel the mysteries of CFS. This should lead to much greater understanding of the disease process" said Kansky. Furthermore, she stated that "Our funded medical research is aimed to solidify and scientifically expand this important work so that desperately needed and appropriate patient treatments will follow. The NCF's efforts will continue to illuminate the darkness that has overshadowed this very serious illness."

    The NCF first began its investigation with a published book titled Chronic Fatigue Syndrome: A Biological Approach edited by Dr. Patrick Englebienne and Dr. Kenny DeMeirleir [1]. Published in 2002, examination of the chapters, by NCF staffers, revealed that Dr. DeMeirleir and his collegues carefully and methodically probed various signal transduction pathways in patients with CFS via examination of their peripheral blood mononuclear cells (PBMC's or monocytes). These authors stated that "the importance of STAT1 in mediating the action of both type I and II IFNs (interferons) is no longer questioned, as a lack of its expression is consistently associated with IFN resistance. The apparent dysregulation in types I and II IFN pathways in chronic fatigue syndrome led us to investigate the expression of STAT1 in PBMCs. We classified the samples according to the ratio of 37- over 80- kDa RNase L which is representative of the proteolytic activity of the PBMC samples. As shown in Figure 5.9, STAT1 is fully degraded in positive samples, suggesting that it may also be a substrate of the proteases responsible for RNase L cleavage. A degradation of STAT1 in those cells might well constitute the missing link explaining unresponsiveness to IFNs" (interferons) [2].

    In this figure from the book, with RNase L ratios (37 kDa/80 kDa) greater than 0.25, native STAT1-alpha is lost but some cleavage (breakdown) products are shown until the RNase L ratio hits approximately 2.0. After that, there is the complete absence of both STAT1-alpha and the cleavage product! Explaining further, STAT is notation for Signal Transducers and Activators of Transcription. STAT's are a family of transcription factors that play central roles in the responses of cells to cytokines, molecules that control every aspect of the immune system [3]. STAT1 has two forms, alpha and beta. Dr. DeMeirleir's group tested STAT1-alpha, a native 91 kDa protein, in patients with CFS and correlated it with the RNase L ratios. STAT1-alpha is intimately involved in the response of cells to type I (alpha and beta) and type II (gamma) interferons. Most important is the fact that a STAT1-alpha deficiency is associated with fatal infections by both viruses and bacteria [3,4,5,6,7,8]. Furthermore, in animals, STAT1-alpha deficiency is associated with impaired responses to interferons, increased susceptibility to tumors, as well as impaired growth control. STAT1-alpha also plays a critically important role in antigen presentation.

    The NCF staff then wondered if Dr. DeMeirleir and his colleagues realized the importance, as well as the significance, of their discovery and when might they have first identified it? To answer this question, we uncovered a patent filed in April 1999 titled "Methods and compositions for use in characterizing multiple sclerosis disease activity in a subject." [9] In this patent, Dr. DeMeirleir and his colleagues at R.E.D. Laboratories determined the amount of 37 kDa and 80 kDa RNase L proteins and utilized RNase L ratios to characterize multiple sclerosis disease activity. This patent was filed after one filed by inventor Dr. Robert Suhadolnik, in April 1999, titled "Chronic fatigue syndrome diagnosis" in which the diagnosis of CFS was made through the detection and determination of both the 37 kDa and 80 kDa RNase L proteins [10]. Examination of both these patents indicated that, in both CFS and MS, these same RNase L proteins can be used to assist in diagnosis as well as for determining disease activity. Multiple sclerosis patients have previously been found to have alterations in STAT1-alpha [11]. Furthermore, in CFS, this is vitally important due to the correlations that were found between the RNase L ratios and STAT1-alpha.

    This is further stated in two additional patent applications by Dr. DeMeirleir's colleagues. One of these applications directly discusses the specific role of STAT1-alpha in CFS patients [12,13]. Quoting these patent applications directly: "STAT1 plays an important role in growth arrest, in promoting apoptosis and is implicated as a tumor suppressor. STAT1 null cells are resistant to apoptotic induction by TNF-alpha....STAT1 deficient mice exhibit a severe defect in IFN-dependent immune responses against viruses and microbial pathogens....If STAT1 is disabled or otherwise inactive in the cells of the immune system, treatment with interferon or interferon inducer will not be effective in promoting and establishing the interferon-inducible antiviral and antiproliferative pathways." Furthermore these applications state "the results demonstrate that the presence and amount of STAT1 protein fragmentation directly correlates with the presence and amount of low molecular weight RNase L fragments in PBMC samples. These data indicate that native STAT1 protein is fragmented at an earlier point in the disease cycle than RNase L, and that by the time native RNase L is demonstrably attacked by proteases (ratio > 2.0), that native STAT1 protein has entirely disappeared due to proteolysis, leaving the cells unable to respond to interferons and/or interferon inducers."

    It became obvious to NCF staffers that Dr. DeMeirleir and his colleagues had made a vitally important discovery but had only published part of the information in the book and the remainder in patents or patent applications that we were aware of. Was there other information to be found?

    A quick check of the R.E.D. Laboratories website [14] indicated that "The company's scientists have discovered a number of other cellular proteins that play important roles in the initiation, progression, and pathogenesis of immune dysfunction. The most important revelation to date has been the discovery of one protein, which is used as a serum-based assay for the detection of chronic immune disease. Such a serum-based marker has been developed as a screening test for the blood supply to reduce the number of transfusion-related infections with persistent (and covert) viral infections."

    It became obvious to the NCF staffers, that both the book and the patent information told a significant story regarding the critical importance of STAT1-alpha in CFS patient blood. One thing is certain, blood doesn't lie! Likewise, the true implications, pathological and perhaps life threatening for patients as well as financial potentially for R.E.D. Laboratories, regarding transfusion-related infections in the blood supply by "covert infections", were enormous and certainly worthy of worldwide attention!

    Probing further, the NCF discovered vitally important testimony given directly by Dr. Kenny DeMeirleir before the Flemish Parliament of Belgium in a hearing on March 5, 2001 [15]. In his testimony given before Flemish Parliament, Dr. DeMeirleir stated "Caspases and calpain are induced by cellular stress, which leads to apoptosis. In an intracellular disorder, calcium influx is increased. Calcium will further activate calpain, so that some caspases are inhibited and therefore block apoptosis. One of the cellular proteins that are split by these enzymes is STAT1, the carrier of the interferon-gamma signal in the immune cells, which leads to the Th1-to-Th2 shift. Unfortunately, the Chronic Fatigue Syndrome is often called psychosomatic. This is, however, more indicative of medicine's inability to deal with it. We now understand the nature of the disorder. In its early phase, apoptosis increases. In a subsequent evolution, apoptosis is blocked and the interferon signal disappears due to the destruction of the protein which transports the intracellular interferon signal to the nucleus (where apoptosis is initiated). This leads to more and more infections. This process goes on at all levels (in the central nervous system, the muscle cells, the white blood cells, and so on). Some patients suffering from the Chronic Fatigue Syndrome develop epilepsy. We find that most patients have a light form of epilepsy. This leads to sleep disturbances and a situation where the fatigue increases since one does not recover anymore."

    "Given the true significance of this work and its implication in a functionally oppressive disease that desperately struggles for proper recognition, validation, and affirmation at all levels of medical science, the NCF's Board of Directors unanimously voted to immediately fund several important research grant projects to be carried out by noted researchers" said Kansky.

    The NCF first contacted a well-known research group, who has asked to remain anonymous at this time, and arranged to send grant funding to them via our NCF Research Grant Program. "We are very excited by this since this group will be the first to begin studying "STAT1-alpha in Chronic Fatigue Syndrome Patients" stated Kansky. Lead scientists for this research group commented that this was an enormous step forward towards understanding the disease process in these patients.

    Next, the NCF arranged another research project, also funded by our Research Grant Program. The NCF sent grant money to Dr. Konstance Knox and Dr. Donald Carrigan, both from the Institute for Viral Pathogenesis, for "A Study for the Potential Role of STAT1 in the Pathogenesis of Chronic Fatigue Syndrome." "This grant is aimed at significantly expanding our knowledge about the specifics of STAT1 and its role in CFS from a pathological standpoint" stated Kansky. "Futhermore, since we are expecting both teams (first group and Knox/Carrigan) to complete their work with research physicians in the months ahead, we are anticipating significant medical breakthroughs as the direct result of these grants. The NCF has expedited this work because our patients are seriously ill and we anticipate that these efforts will certainly confirm this" said Kansky.

    The NCF staff also contacted two world renown experts on the STAT1 protein: Dr. Joan Durbin from Columbus Children's Research Institute and Dr. David Levy from New York University School of Medicine. Both Dr. Durbin and Dr. Levy have published extensively on STAT1 and are responsible for the development of the animal model for STAT1-alpha deficiencies. In NCF interviews with both of them and from their numerous published medical journal articles, it is clear that the complete loss of the native STAT1 protein constitutes a serious illness that may ultimately be fatal unless this protein defect can be corrected.

    Ironically, this is where the NCF is truly hopeful. In one of the patent applications [13], Dr. DeMeirleir's colleagues determined that the "STAT1 protein is degraded when a cell extract from a healthy control (i.e., 'negative extract'; RNase L ratio < 0.2, STAT1 protein containing) is incubated with a cell extract from a patient (RNase L ratio = 3.0; STAT1 protein negative). This degradation is inhibited in the presence of proteasomal inhibitor (MG132) but not in the presence of the other protease inhibitors tested. Thus the degradation of STAT1 protein is a specific cellular process that involves proteasome and does not involve the apoptotic enzymes caspase-3 or calpain."

    What this implies is that Dr. DeMeirleir's colleagues had already found a very specific inhibitor, MG132, for STAT1-alpha degradation in CFS patient blood in-vitro! In our own research, the NCF found that MG132 functions as both a specific inhibitor of the ubiquitin-proteasome pathway [16] as well as a specific beta-secretase inhibitor [17]. Both of these pathways are intimately involved with amyloid formation. Amyloidogenesis is a general phenomenon of protein misfolding. Protein misfolding and the formation of abnormal protein fibrils appear to play a central role in a variety of neurodegenerative diseases including Alzheimer's disease, Parkinson's disease, Huntington's disease, etc. This is why the expression of the Huntington's protein in CFS patients, by the CDC using gene expression analysis, is intriguing [18]. These are all scientific clues to a bigger picture for this disease.

    Because of our previous efforts with the ciguatera epitope and its effects on neuroblastoma cells as well as other specific unannounced scientific findings related to this epitope, the NCF has also provided new research grant funding to Dr. Yoshitsugi Hokama, from the University of Hawaii, for the "Development of an Immunological Assay for Assessment of Amyloids in Chronic Fatigue Syndrome." "Dr. Hokama's previous research dovetailed nicely into the scientific work we are describing here" said Kansky. "In fact, the NCF believes there is a relationship between the ciguatera epitope, protein misfolding, and amyloid formation. Amyloids directly alter sodium channels and that is part of the significance of the ciguatera epitope finding as it relates to our previous CFS patient studies. This is something that we had known prior to the initial funding of Dr. Hokama's work but this previous work had to be scientifically verified and expanded upon first before we pressed on further" stated Kansky. The NCF is also aware that a relationship already exists between amyloid formation and STAT1-alpha. Amyloids can potentially bind the STAT1-alpha protein and take it out of commission. This mechanism is very important. Dr. DeMeirleir and his colleague's discovery on STAT1-alpha and RNase L cleavage is central to our working hypothesis but the NCF believes that we have found other missing pieces, regarding the infectious agent as well as other disease mechanisms, that are absent from their work. What is exciting is that our NCF staff has already identified very specific PCR binding sequences for STAT1-alpha in the infectious agent that we believe is directly responsible for this disease. This implies that once infection begins, STAT1-alpha becomes one of the first critical immune system proteins to get "chewed up" as a result of being a direct target of the infectious agent thereby greatly damaging the immune system! This would be in agreement with Dr. De Meirleir's findings where STAT1-alpha binding occurs before the degradation of the native RNase L protein. "Furthermore, in full agreement with Dr. Elaine DeFreitas' previous work, the NCF believes this infectious agent is of non-human origin" stated Kansky. "We are meeting the dragon head-on and we hope that our funded research will help crack the code, once and for all, for this disease. The NCF continues to break important new ground in the understanding of the disease mechanisms while going scientifically where no other CFS organization has ever been before! This appears to be our forte and it reflects our true passion and full committment to the CFS patient community. As a result, we are much further ahead in the discovery process than most patients and researchers realize" said Kansky.

    In addition, Dr. DeMeirleir's colleagues also made another significant discovery critical to the health and welfare of patients with CFS [19,20]. Excerpts from the book and the patent application state "Fig. 1 represents a densitometric scan of a Western blot detecting p53 protein and p53 protein fragments from PBMC extracts from CFS patients....The above results demonstrate that the presence and amount of p53 protein fragmentation directly correlates with the presence and amount of low molecular weight RNase L fragments in PBMC samples. These data indicate that native p53 protein is fragmented at a later point in the disease cycle than RNase L protein. The loss of functional p53 protein in PBMCs render these cells unable to respond to normal growth inhibitory stimuli and provide the means whereby unregulated cell growth occurs, ultimately giving rise to hematopoietic tumors."

    Furthermore, their explanation in this application states: "Another important protein that regulates the induction of apoptosis is p53. The p53 protein is normally activated in response to genetic damage within the cell and its activation is accompanied by self-stabilization, allowing it to accumulate to high levels and cause cell cycle arrest and induce apoptosis. In addition, the p53 protein has a critical role in protecting the cell from malignant development; mutations in the p53 gene (and protein) are the most frequently detected genetic event in cancer.

    Mutations in p53 may occur at the genetic level (i.e. DNA sequence alterations that change the amino acid structure of the protein), or its function may be altered by alterations in the numerous proteins with which p53 interacts. p53 may also be altered by the action of certain proteases, resulting in cleavage, preventing the formation of active tetramers of the protein. If p53 is cleaved and/or otherwise disabled in the cells of the immune system, these cells would be blocked from entering the apoptotic pathway if infected with a virus or other microorganism. In addition, persistent inactivation of the p53 protein may lead to increased incidence of cancer (Levine et. al., J. Chronic Fatigue Syndrome 7: 29-38, 2000). Activation of the 2-5A synthetase / RNase L antiviral pathway has been demonstrated to induce apoptosis, while induction of the same pathway in cells expressing mutant forms of p53 was demonstrated to suppress the apoptotic pathway. The inactivation of p53, RNase L, and other proteins within the cells of the immune system most certainly leads to a dysfunctional immune system, unable to respond to challenge by microorganisms and/or the presence of pre-malignant cells. Indeed the immune system itself may be in a pre-malignant state."

    In a review of the literature on STAT1-alpha and p53, we found an article [21] on STAT1 deficient mice that states "when the STAT1 deficiency was placed on a p53 null background there were increased rates of tumor formation and an increase in the non-lymphoid tumor types." This helps to explain the importance of these two proteins that are essential to appropriate immune responses since STAT1 and interferon are central to antitumor effects [22]. In fact, this study suggests that NK (Natural Killer) cells from STAT1 deficient mice may have a reduced capacity to eliminate tumor cells in-vivo.

    Part one article review at a glance:

    Dr. DeMeirleir and colleagues scientific finding:

    STAT1-alpha deficiency in CFS patients
    p53 deficiency in CFS patients
    Scientific interpretation:

    Loss of STAT1-alpha constitutes a serious illness that may ultimately be fatal because the cells are unresponsive to interferon leaving them unable to adequately defend against infections.
    Loss of p53 constitutes a pre-malignant state because surveillance against DNA mutations, protein alterations, and unregulated cell growth/division are left unguarded.
    Loss of these proteins assists in immune deficiency and dysregulation.

    [Ed. Note: The references for this article have been combined with the article, "Total Exposure."]

    The National CFIDS Foundation * 103 Aletha Rd, Needham Ma 02492 * (781) 449-3535 Fax (781) 449-8606
  18. karinaxx

    karinaxx New Member

    this is the newest dot, which connects the research done before.
    now , we are all not sure that this is realy the final cause!
    But after reading since one and half year nearly every research article , paper, report and reports from members here on the board and many other websites from all over the world , this seems to connect every thing.
    the implications are huge; meaning that we all have viral infections, funguls inf. and stealth pathogens which cause different symptoms and a wide range of complications.
    more you can read by Dr.G.Nicholson, Dr.Cheney and well , i have so many sites stored, but this will have to go once on another post. Just want to give some starting point here.
    love karina

    “Previously Undetected” Virus Implicated In Developmentof Chronic Fatigue Syndrome and other Conditions
    by Editor


    Note: This article includes our follow-up suggestions regarding its implications for Chronic Fatigue Syndrome patients.

    Medical science may be just a few research steps away from cracking the secret of Chronic Fatigue Syndrome (CFS), according to news from the National CFIDS Foundation (NCF). Bottom line, states NCF’s Medical Committee: “Parainfluenza Virus-5 plays what the Foundation sees as a predominant and primary role in the development of CFS.”

    This is news that the NCF believes can “change the very nature of this disease.” CFS has been an unexplained ailment, characterized by chronic debilitating fatigue and a combination of flulike symptoms.

    Virus in the Cross-Hairs

    Independent research and detective work funded by the nonprofit NCF has confirmed evidence of a “previously undetected” viral infection in patients with CFS. The research “dovetails” with work by virologists at the private biotechnology research firm Cryptic Afflictions, LLC. It also builds on years of NCF sleuthing for clues in the work of dozens of scientists around the globe, both published and held proprietary.

    The NCF defines the CFS culprit as a strain of the recently named Parainfluenza Virus-5 (PIV-5); formerly called Simian Virus-5, or SV5, owing to its initial isolation in monkey tissue. It is an RNA virus, or “rubulavirus” in the category of viruses known to be associated with diseases such as mumps, encephalitis, and meningitis. And, as an RNA virus, it might be a mutating “chameleon.” At least a dozen strains of mumps virus have been identified, for example.

    It is further defined as a "zoonotic" virus - one that in mutating can be transmitted between animals and people. And, at least as found in an initial CFS patient test performed by NCF-funded researchers, it exactly matches the “SER” strain of PIV-5 virus isolated in diseased swine by German researchers in 1994.

    The Research-Detective Story So Far

    NCF-funded scientists identified a new viral “footprint” in the blood of Chronic Fatigue Syndrome patients, in the form of a deficiency of the Stat-1 protein, which “plays a vital role in immunity.” The researchers then created a “short list” of viruses known to “directly attack and degrade the Stat-1 protein” as part of a viral strategy for evading the host’s immune response. PIV-5 was on that list.

    Meanwhile, they learned that Steven Robbins, MD, a virologist and CEO of Cryptic Afflictions, LLC, had tested blood samples from 56 CFS patients, and cerebrospinal fluid samples from 11 CFS patients, for antibodies specific to an RNA virus he calls “Cryptovirus.” Dr. Robbins found that the vast majority (96 percent) of his CFS blood samples and 91 percent of the CFS spinal fluid samples tested positively for “Cryptovirus-specific” antibodies.

    The NCF also learned that a recent medical journal article suggests Cryptovirus “is most similar to PIV-5” – and that Cryptic Afflictions has “extensive U.S. and international patents pending and owns the intellectual property rights” for Cryptovirus, according to a report from its parent company, Century Pacific Financial Corp.

    Dr. Robbins also found that the Cryptovirus could “cause virtually identical disease in experimentally-infected animals,” according to Century Pacific. Further, he found that “nucleotide sequence data indicate that the virus is pandemic and represents a single virus ‘species’ more akin to measles virus than hypervariable viruses like HIV.”

    In addition to the Cryptovirus’s association with Chronic Fatigue Syndrome, Cryptic Afflictions reports it is also believed implicated in other neurological disorders, including multiple sclerosis and idiopathic (unexplained) epilepsy. For example, the company reports it found Cryptovirus antibodies “in the cerebrospinal fluid and blood of over 90 percent of patients tested with multiple sclerosis.”

    Next Steps for CFS Research?

    At a minimum, Century Pacific says Cryptic Afflictions is now pursuing tests of brain lesions in multiple sclerosis patients, and next plans to ask the FDA for approval of the diagnostic tests. Their testing plans for CFS seem to be unstated.

    The National CFIDS Foundation, meanwhile, reports it is working to get this information out to “medical and health groups that may be interested in further research,” and says it is “interested in funding those researchers who have expertise in the area.”

    The NCF is an all-volunteer patient organization with no paid employees, and is funded solely by individual donations for the primary purpose of funding CFS research.

    To review the NCF press release on this discovery, as well as a highly detailed, sourced report on the National CFIDS Foundation Medical Committee’s detective work, titled “Parainfluenza Virus-5: A new paradigm and a serious host challenge,” visit the Foundation’s site at

    What does this mean for you?

    1. Clearly, this and further research that may establish Chronic Fatigue Syndrome as a pathogen-triggered disease would lend medical validity to the condition.

    2. Further, increasing knowledge regarding this virus or viruses may lead to preventive measures such as vaccines and epidemic surveillance, and/or effective treatments.

    3. This news of the dedicated efforts by NCF-funded researchers and others underscores the importance of contributions to CFS research. We at Pro Health are proud to report that as a patient-owned company we have raised and donated more than $2.5 million to CFS and Fibromyalgia research to date, and contribute a portion of all our product sales to this cause.

  19. Slayadragon

    Slayadragon New Member

    This is all very interesting, but the part that I found to be "new" was the idea that the body doesn't bother to put resources into fighting off regular colds/flu (e.g. through congestion, fever, diarrhea) because it's sort of "given up."

    Obviously most americans think that those symptoms are caused by the cold, and thus try to get rid of them.

    Another hypothesis is that they are the body's mechanisms to help rid itself of the cold or flu. For example, congestion expels germs. So does diarrhea. Fever burns off germs.

    I'm not absolutely sure if that's true, but a lot of people think so. In Denmark, remedies to treat cold like we have here are not available. This is not because they are perceived to be too dangerous, but rather because the Danish believe themselves to be health-oriented and thus think that it's best to let the body do its job. (They're also not work-obsessed, and so stay home when they're sick rather than drugging themselves up and plunging on.)

    In my case (as measured by a recent test), my body is already teeming with viruses. (40x the high-normal value) If my body can't fight off those viruses (many of which probably are causing a lot more damage than a cold virus), why should it take a huge amount of its energy up in fighting on that one little cold by producing mucus etc.?

    If this is indeed the case, then the comment stated by most CFS patients (including myself) of "I don't get colds" would be incorrect. The correct statement would be "My body does not actively fight off colds."

    I am going to have to start watching for what my body does when I am actively exposed to cold viruses (e.g. when my husband is sick). It may be that I feel a lot worse during those times (because my viral load has gone up even higher than usual) but that I'm not noticing it.

    The other possibility is that there may be a limit to the amount of viruses that can be present in the body, and that at some point no more can survive because all the resources are already being absorbed. Does that seem to be true? I don't know enough about this subject yet to say.
  20. karinaxx

    karinaxx New Member