NEW: Parainfluenza Virus5 research = gene si.research by Dr.Gow

Discussion in 'Fibromyalgia Main Forum' started by karinaxx, Oct 17, 2006.

  1. karinaxx

    karinaxx New Member

    research 10/17/06 11:21 AM

    I DON'T KNOW IF ANYBODY HAS POSTED THIS ALREADY, BUT NEVER THE LESS, I CONSIDER THIS VERY IMPORTANT INFORMATION.
    THE FIRST PART IS MORE ABOUT THE POLITICS OF THE CDC, THE SECOND PART IS WHERE IT GETS INTERESTING!
    I SO HOPE THIS IS THE FINAL THING AND WE ARE FINALLY GETTING SOMEWHERE!

    i deleted the orginal post i made , because there were some comments made, which would have ended up in an ugly arguement.
    for those , especially wakemeup, who gave so constuctive
    and touching responses: i am sorry they were deleted with it. feeling with you wakemeup!
    i posted it again, because i think the conection made here by the cfids foundation, between the two independant research findings, very important!
    take care everyone
    karina





    OUTSIDE THE BOX: INSIDE PERSPECTIVE

    By Alan Cocchetto, NCF Medical Director ©2006

    As you can imagine, the NCF receives all types of communications from patients worldwide. Be it by phone, fax or email, we hear from you! We listen, support, assist, console and try to help each of you in your own way.

    With that said, my own correspondence has continued to grow and at times, often seems out of control as it appears to have a life of its own. As one of many point guards here at the NCF, there's always work to be done. Recently, a patient faxed me an article on CFIDS/ME that was published by a well-known physician. After reading this, I feel that I must comment, especially in light of the NCF's recent research. In one of my e-mails, another patient sent me information on Dr. John Gow's gene research into CFS/ME. I will comment on this as well.

    The article that was faxed to my office was titled "Wake-up call." This was published in MS Magazine this summer and was written by Dr. Nancy Klimas. Dr. Klimas primarily discussed the CDC's "hopeful new research" that showed that Chronic Fatigue Syndrome may have a genetic basis. Also, Dr. Klimas states that "this is a huge step forward in terms of diagnosing and hopefully treating CFS." In her article, I found one of Dr. Klimas' comments to be rather interesting. She stated "How I view the disease today, however, is not the way I once perceived it." As the NCF's Medical Director, you'll see why I have chosen to comment on that particular statement. Dr. Klimas also went on to discuss research money by stating that "It's difficult to raise research funding for an illness that is so misunderstood, yet lack of adequate funding has limited the kinds of studies that might yield definitive answers."

    I must admit, perhaps I was looking for more from Dr. Klimas. After all, she holds the position as the current AACFS (IACFS) president. Why do I feel so strongly about this? Well, in 1990, Dr. Klimas published an article in the Journal of Clinical Microbiology on her examination of the immunity in CFS patients. Dr. Klimas' conclusion was that "CFS is a form of acquired immunodeficiency." Simply stated, most of us reading those very words would interpret them as CFS is a form of AIDS! Now, don't get me wrong, I'm not trying to put words in Dr. Klimas' mouth. After all, she is the one who wrote those words initially and published them in a peer-reviewed medical journal. What I now find most unfortunate is that Dr. Klimas never refers to "those words" anymore. As such, I really wonder what the readership of MS Magazine would have thought if Dr. Klimas had openly stated, based on her own published medical research, that "CFS is a form of acquired immunodeficiency." My guess is that the readers would truly be astounded and that they would come to view CFS as a very severe disease. Perhaps the readers would truly begin to finally understand what their family members, friends, colleagues, or acquaintances who suffered with this disease were going through. Readers would realize that this disease is not depression nor malingering nor a hodgepodge of symptoms but a very serious immune disease whose victims lose physical functionality. Wouldn't this description really be closer to the actual truth regarding this disease? Ask anyone who has had this disease for ten years or more and I'd bet you would reach a common consensus when it comes to physical dysfunction. What I don't understand is Dr. Klimas' initial research view to publish that "CFS is a form of acquired immunodeficiency" and to now comment that "How I view the disease today, however, is not the way I once perceived it" appear to be polar opposite thoughts. Certainly, as more is learned medically in this field, our scientific models undergo greater refinement. However, I wonder what Dr. Klimas now thinks of her 1990 publication? What of the immune abnormalities? Did they go away? Do they no longer exist? Does she no longer make these statements, as she had done in 1990, because that would somehow jeopardize her NIH funding for research, upset the CDC, or make her views oppose those of her peers? Hasn't a line really been drawn in the sand? I've always been taught that you can't take something that is black and white and try to make it grey. It's akin to backtracking to retract words you've said or somehow trying to smooth out the hard edges of the truth. In farm country we often say that it's like closing the barn door after the horses have gotten out. In my mind, I find it difficult to reconcile these views, especially given prior statements...statements made in a medical journal article.

    Dr. Klimas does state that "it is difficult to raise research funding for an illness that is so misunderstood." If I were able to ask Dr. Klimas one basic question, it would be this: "Did you ever think that, perhaps, one of the very reasons that the disease is so misunderstood is simply because you failed to use the very words that you openly used sixteen years ago....that "CFS is a form of acquired immunodeficiency?" Aren't these the very words that can help to erase such misunderstandings about this disease? Aren't these the very words that help to imply severity? Should the disease then be viewed as "severe" among the medical community, then wouldn't this
    honest description perhaps assist those who are trying to obtain appropriate research funding from either the private or public sector?

    Let me now comment and provide additional inside perspective regarding the NCF's
    current ongoing research.

    The NCF has found the primary etiologic infectious agent that is operative in this disease - Parainfluenza Virus-5 or PIV-5. It was the SER strain that was isolated and that strain came from swine with PRRS disease. It appears that this strain has moved from swine to humans. The immunodeficiency that comes with CFIDS/ME is a result of PIV-5 damaging the immune system. It does so by directly infecting bone marrow B-cells, which act as the viral reservoir, and by directly antagonizing the effects of interferon thus altering innate host immunity. PIV-5 is a master of viral evasion. It acts as a slow viral infection that plays hide and seek with the host's antiviral response via alterations involving key interferon-based pathways. In the months ahead, the NCF will focus on some of the consequences of PIV-5 infection. You will also learn of new efforts by the Foundation that are directly aimed at finding therapies for this infection. We have been a very busy bunch here working for you, the patient community.

    Let me provide you with some hints from our current efforts to review the recent advances in CFIDS research. The NCF firmly believes that all roads will ultimately coincide and therefore complement our scientific findings. Thus, with time, we would expect that additional research, performed by other scientists around the globe, should serve to illuminate the work that has already been completed by the NCF.

    Here is perhaps the newest example of this. As readers may be aware, Dr. John Gow, from Glasgow University in Scotland, has announced the gene signature his research group has identified from patients with CFIDS/ME. Those who have an interest can refer to his World Patent that was just issued on August 10 (WO2006082390). This was sent to me via email from a fellow CFIDS patient. The patent discloses a number of genes that are identified which are expressed at abnormal levels in patients affected by CFS/ME as compared to normal healthy individuals. According to Dr. Gow, "The genes identified provide objective disease markers that may be used in diagnostic tests to support the diagnosis of CFS/ME."

    Let's take a look at one of the gene markers that Dr. Gow is very interested in. After the NCF explains its connection to PIV-5, we're certain that the readers will begin to appreciate this specific connection to the Foundation's research.

    In his patent, Dr. Gow expressed his interest in the ATPase system. According to his patent, "At the cellular level, fatigue has been linked with alterations in the cell membrane ion-channel traffic and ATPase system. ATPases are also linked with neurotransmitter release (e.g . dopamine) and cellular energy metabolism via creatine phosphatase. Increased ATPase activity has been reported in muscle biopsies from patients with CFS. Previous work has raised the possibility that patients with CFS may have an ion channel dysfunction. This dysfunction might be induced by changes in the ion channel function, neurotransmitters involved in "gating" the channel or by a shift in the balance of the cellular "energy charge", i.e - the ratio between ATP and ADP that is normally a function of the ATPase activity."

    Dr. Gow continued, "A group at the University of UIm, Germany, has recently suggested that a pentapeptide (QYNAD) with Na+ channel-blocking function could be a biological marker of certain inflammatory and immunological disorders of the nervous system. The inventors asked whether or not the pentapeptide identified by the German group might play a role in CFS. Samples of serum were sent to the University of UIm for analysis. The 15 samples included 5 normal controls, 5 patients with CFS and 5 disease controls including two patients with MS. Samples were numbered 1-15 and the German group were not informed what the samples were, or which samples were which, until the experiment was concluded. When the code was broken, the results showed that the disease control group had levels of the pentapeptide which were 2.3X those of the normal controls (similar to the published data) and the CFS samples had levels which were 3X higher than the healthy controls....The German group was unable to identify an endogenous gene which encodes the pentapeptide. The inventors carried out NCBI BLAST and EMBL-Heidelberg Bioccelerator amino acid alignments for the pentapeptide QYNAD....A number of cloned nucleotide sequences were found and when these were run through the nucleotide databases, only one clone showed full-length homology to any human gene. This gene was a human ion-channel gene - the vacuolar proton pump H+ ATPase (v-ATPase)." Dr. Gow then stated "The inventors next asked whether the v-ATPase represents a candidate gene for a diagnostic test for CFS....the patient samples have a significantly higher level of v-ATPase mRNA than the healthy controls. Thus the v-ATPase gene appears to represent a genuine biomarker for CFS/ME."


    Two items are of interest. First is that Dr. Gow looked at sodium channel function. This
    is of importance because of Dr. Hokama's research on the ciguatera-epitope has also been shown to alter sodium channel function. Next, however, is another big find. Dr. Gow considers the dramatic up-regulation of vacuolar ATPase to represent a genuine biomarker for CFS/ME. That sounds great to us here at the NCF! Why is this important. Let me now explain. Dr. Richard Compans, who has the NIH grant for the SER strain of PIV-5, published a paper on the viral fusion process associated with this parainfluenza virus ("Activation of fusion by the SER virus F protein: a low-pH-dependent paramyxovirus entry process", Seth S, Vincent A, Compans RW; J Virol. 2003 Jun;77(11):6520-7). In this paper, Dr. Compans states that the "SER virus is a recently identified virus that was isolated from aborted pigs with porcine respiratory and reproductive syndrome. This virus belongs to the family Paramyxoviridae, genus Rubulavirus, and is very closely related to SV5 but replicates without causing syncytium formation.... Virus replication was found to be completely inhibited in cells infected with SER virus in the presence of BFLA1 (bafilomycin A1) at concentrations as low as 0.1 microM." Dr. Compans further stated that there is "high specificity of bafilomycin A1, BFLA1, in the inhibition of vaculolar ATPase."

    This sounds like a match made in heaven to me! Here we have Dr. Gow who found a biomarker for high levels of vacuolar ATPase, v-ATPase, in CFS/ME and then we have Dr. Compans who found that SER viral replication was inhibited by a compound (bafilomycin A1) that inhibited vacuolar ATPase. This implies that SER replication is directly tied to v-ATPase and that its inhibition alters viral replication. As such, Dr. Gow has found a biomarker that further supports our NCF research findings for SER viral involvement in CFIDS. For those readers who may be wondering, Dr. Compans only found this replication effect for v-ATPase for the SER strain and not for other strains of PIV-5.

    Furthermore, Dr. Gow states in his patent that "The v-ATPase is known to be involved in regulation of a number of metabolic functions which are deranged in CFS/ME. v-ATPase upregulation could therefore provide an explanation for a number of the symptoms observed. For example, increased v-ATPase activity could explain the intracellular acidosis in exercising muscles, chest pain (syndrome X), altered neurotransmitter (dopamine) function and abnormal regulation of hypothalamic hormones. In addition, it could explain the increased energy expenditure and fatigue associated with the condition."

    Given the surging interests into gene studies, done by the CDC and other research groups, the NCF feels that Dr. Gow's finding for this specific biomarker is in agreement with our research finding for PIV-5 involvement in CFIDS. Hopefully in the next Forum, we will be discussing other biomarkers and their possible therapeutic implications. The NCF has contacted several new research scientists who have expressed interest in working for the Foundation. This is particularly exciting because all of our new research activity will be aimed at therapeutic intervention by increasing our understanding of several unique pathways that are involved in the disease. Our "out of the box" scientific approach has allowed us to make great progress to date. Please help us to help you! By donating to the NCF's Research Grant Program, you become a partner with us to continue our research momentum towards a therapeutic solution for CFIDS/ME. Together, we can reach this goal!




    [This Message was Edited on 10/17/2006]
  2. Smiffy

    Smiffy Member

    Fascinating article, thank you so much. My symptoms started with really bad flu 20 year ago.
  3. mezombie

    mezombie Member

  4. karinaxx

    karinaxx New Member

    thanks for bubming it and for your insightfull comments previously made.
    i bumb it one more time, for others to see it and again sorry to the others, which took time and energy to put some additional info here and now it got deleted with the previous posting.
    i will take some time of the board, need a brake.
    take care everyone
    love
    karina
  5. findmind

    findmind New Member

    This is a vitally important document. I get the Forum and have been fascinated by how all this research is coming together! I believe they will be the group who actually lets us all know what treatment(s) will be available.

    I hope ProHealth is working on a product that will seek out and kill this SER strain of the Parainfluenza 5 virus (PIV-5). They, to me, will be a major source of hope to all of us here on this board.

    I say this because I can't see the Medicaid system, HMOs, or the VA system giving interferon treatments to anyone.

    You know, I was very, very sick back in 91-92, and while I was at the drs, I glanced down at a progress note my dr. had written, and I saw "HIV-1?". I am not HIV positive, and I wondered if the VA system thought that CFS was a type of "acquired immunodeficiency", as this new research has shown, and that Dr. Klimas was sure of in her medical journal report.

    The Forum had a "quote box" in their last issue that said, "Animals without STATl lack the other half of the immune system, known as innate immunity. Innate immunity kicks in immediately to fight infection, in part by causing cells to produce anti-viral molecules known as interferons. Mice that lack STAT1 cannot respond efficiently to interferon and lose most of their innate immune response." (Science, March 2003)

    Many studies have proven the lack of STAT1 in CFS; other studies have shown that the SER strain of the PIV-5 kills STAT1. This makes CFS and "acquired condition", and Dr. Klimas knew that back in 1990.

    Now she is part of the CDC group that is "branding" the name CFS across the country and to physicians. Why?

    I am royally sick at scientists and researchers who are using their findings in a "corporate" manner; geting patents, not publishing the information so others can further the research into meaningful therapies; and opeming businesses to do specialized testing for those who can afford it.

    I can only hope that current research, being funded solely by patients and others who believe the NCF is heading in the right direction, including myself, will find the answers and treatments we need.

    Getting testing and treatments will probably take an act of God: everybody, keep praying!

    There's always hope!
    findmind

  6. NyroFan

    NyroFan New Member

    karinex:

    Yes, it is a very interesting article. It is definitely thought provoking.

    Thank you for posting it.

    nyrofan
  7. fight4acure

    fight4acure Member

  8. karinaxx

    karinaxx New Member

    i was a few days of the board and did not expect any one still seeing this, so i am glad it got to you in time.

    findmind, indeed it is incredible, how research on different level is coming together.
    you said everything there is to say, i agree on everything.


    just add this for clarification, for others to see:

    Patent Application for CFS Diagnostic Test



    In mid-August, Dr. John Gow and Dr. Abhijit Chaudhuri of the University of Glasgow submitted an application to the European Patent Office describing a diagnostic tool for CFS. The “invention” (as it's termed in the application) covers “materials and methods for diagnosis and treatment of CFS,” based on genetic biomarkers observed by Gow and Chaudhuri during their extensive genetic research into the illness.

    In the application, Gow and Chaudhuri identify a number of genes that are expressed at abnormal levels in CFS patients compared to healthy individuals. In contrast to earlier studies from various sources, the researchers claim to have been able to use the expression patterns of these genes to establish functional models of CFS pathology, explaining some of the symptoms observed in affected individuals. If accurate, this could provide a rational basis not only for diagnosing CFS but also for classifying CFS patients according to the biochemical basis for their symptoms, thereby enabling appropriately targeted therapies.

    The researchers carefully point out that, taken alone, the profile generated by this test may not provide an absolute diagnosis of CFS. They suggest that a clinician should also take into account the patient’s physical or psychological symptoms in order to reach a diagnosis. But they state that the gene expression profile this test generates could provide useful data to help confirm or reject a preliminary diagnosis based on physical and psychological symptoms alone. In other words, a test result indicating that one or more of the identified genes is upregulated—meaning that the gene in question shows at least a two-fold increase in expression as compared to unaffected individuals—would provide support for a diagnosis of CFS. Similarly, a normal gene profile could potentially rule out the illness.

    According to the patent application, Gow and Chaudhuri believe that CFS is not a genetic disease caused by gene defects but an acquired condition where there’s a shift in the functionality of a select number of genes regulating specific biological activities—specifically those involved in infection and immunity, cell membrane function and cell cycle. Based on the expression patterns they’ve observed, they’ve established a model of affected "hub" and "network" genes, with the hub genes acting as control centers and the network genes acting largely as the implementers. This set of hub and network genes defines the functional shift in the biological systems of patients who continue to have symptoms due to CFS.

    Gow and Chaudhuri go on to relate the affected genes to specific sets of CFS symptoms, like recurrent infections and tender lymph nodes, restricted mobility and atopic/allergic reactions, providing clues for targeted treatment options.

    The time taken to obtain a patent varies substantially from country to country, but European patent applications typically take four years or more to be granted. In the meantime, Gow and Chaudhuri can continue research on the subject, potentially leading to further refinement. Others from around the world are also deeply involved in genetic CFS research. As advances emerge—and as more news surfaces on this patent and the process it describes—the CFIDS Association will keep you posted.



    take care everyone
    love
    karina










  9. karinaxx

    karinaxx New Member

    familiar with this research and Dr.Meirleirs findings, i put some research into context under my profile: put some research together.....part1-3
    ciou
    karina
  10. karinaxx

    karinaxx New Member

    and since i am showing MS like symptoms and the HHV-6 beeing a possible factor in MS, it is again an intresting research question.




    Human herpes viruses 6 - HHV-6

    Abstract

    HHV-6 has two variants, A and B.

    HHV-6A seems to be implicated in ME, with significantly higher abnormal levels seen in sufferers than to healthy controls. It works by attacking some of the major defenses of the immune system, for example T cells, as in the case of HIV/AIDS, which has lead researchers to propose that HHV-6 could also act as a cofactor in the progression of AIDS.

    Three possibilities for the link between ME and HHV-6:-

    it causes ME

    it causes ME only when linked with another virus;

    it does not cause ME but is taking advantage of the sufferers weakened immune system.



    HHV-6

    Human herpes viruses 6 (HHV-6), as its name suggests, is a member of the herpes family. There are two variants, HHV-6A and HHV-6B.As far as one can tell, HHV-6B is the more ‘common’ one of the two. It is a common cause of the viral disease roseola that is seen in over 95% of young children by the age of 2 - a self-limited fever and rash. Much like chicken pox and shingles, the virus can be reactivated in adults that were infected as children. The virus persists after the initial infection in a latent ('hibernating') form in the cells of the central nervous system, bone marrow and immune system and it can then reactivate and begin replicating again (Fig. 1).

    HHV-6, MS and ME
    The other strain, however, HHV-6A, is the one implicated in AIDS, MS and ME, amongst other diseases. In the case of MS, a direct link has been found between it and HHV-6A [1]. In addition, Dr. Dharam Ablashi, co-discoverer of HHV-6 and Scientific Director of the HHV-6 has summarised from existing literature that when lab methods detecting the presence of active HHV-6A infection are used, an exceptionally strong, statistically significant association between HHV-6A and both multiple sclerosis and ME is consistently seen. From what I’ve found, it seems that it is not a case of HHV-6A being reactivated in an adult like I explained before but people with MS, ME etc. acquiring it as a primary infection. So, they haven’t been infected as children etc. Using the chicken pox ‘analogy’ again, it’s like when adults suffer from the chicken pox (not having caught it as children), and of course it can be a lot worse when this happens. They haven’t built up immunity to it.



    Fig. 1. Demonstrating latency and reactivation of the virus. [2]

    T-cell killer

    But what does HHV-6 actually do? HHV-6A is known to be a cytopathic pathogen with a powerful ability to infect and kill cells. It can directly infect or interfere with the function of several elements of the immune system including CD4 and CD8 T-cells, NK-cells, some B-cells, and mononuclear phagocytes. Basically, it’s messing with some of the major defences your body has towards pathogens in your body, interrupting the normal function of the immune system. T cells, for example, are regarded as the ‘generals’ of the immune system. So this is where the problems could arise and cause ME.
    See Fig. 2 on the next page for an illustration of the progression of HHV-6.



    SIDENOTE - HHV-6 and HIV/AIDS

    The cells HHV-6 targets have brought about connections being made with HIV/AIDS as HIV destroys the same kind blood cells - CD4 T cells (helper cells). Findings have lead to proposals that HHV-6 acts can be a cofactor in the progression of AIDS and in the switch of HIV from the latent to the replicative state. Ultimately, HHV-6 can be a cause of death in AIDS patients. HHV-6, however, does not cause AIDS if the person is not infected with HIV. Of course, there is a lot more information on that subject but I could write a whole book alone on this area!



    Fig 2. Illustrating a progression from infection to the clinical disease [3]

    Neurotropism The tendency to affect, be attracted to, or attack nervous tissue
    Vasculopathy - Disease of the blood vessels



    In the end, there are three ways that HHV-6 could be related to ME:

    ME is caused by this virus. a. Perhaps causing a persistent viral infection of HHV-6.

    HHV-6 causes ME when it comes into contact with another virus, for example parvovirus. a. HHV-6 could be relatively harmless on its own but when it comes into contact with another specific virus it is then when the trouble occurs. i. For example, in the case of bird flu, if a human infected with influenza virus also acquires H5N1, a mutant strain of bird flu that can be transmitted from human to human could form. It is an opportunistic pathogen that takes advantage of an already weakened immune system. Whatever the case is, there is quite a lot of significant data showing HHV-6 in ME patients compared to healthy controls.



    References cited:


    [1] http://www.hhv-6foundation.org/pressrelease_nov.pdf


    [2] http://www.wisconsinlab.com/images/reactivation_diagram.jpg


    [3] http://www.cfsresearch.org/cfs/research/viruses/2.htm




    More information

    See Cort Johnson's description here.

    5th International Conference on HHV-6 & 7

    http://www.wisconsinlab.com/cfs.htm

  11. foxglove9922

    foxglove9922 New Member

    Thanks for posting karina,,,,,,,,,I truly believe Dr. Gow/Kerr/and possibly now the CDC are seaching in the right direction regarding this illness.

    Too bad a central data bank wasn't available for these researchers to draw upon each other since gene expression seems to be a huge factor with CFS/FM.

    Bumping for others to see.

    Foxglove
  12. winsomme

    winsomme New Member

    is there reason to think that interferon is active against this PIV-5 virus?

    the reason i ask is because there is a DR in CA name John Chia who does use Interferon on his patients with some success.

    i think he believes that it is an enterovirus like Coxsackie or Echovirus that is the cause, but if the treatment helps, i guess it doesn't matter as much which virus it is that is causing it.

    hopefully, down the road we can get a test for this PIV-5 virus.

    but is there an article that talks about interferon working against PIV-5?

    thanks
    bill
  13. Cromwell

    Cromwell New Member

    It would be really helpful if someone could condense this down to some short paragraphs as those of us with bad brain fog could have a hard time following this important information.

    As I have brain fog...any volunteers???

    Thank you for this posting. I truly link my flu shot with this dd and I am usually pro vaccs. Also I recall a few years back having the live spray up nose vac.

    Anne
  14. findmind

    findmind New Member

    Hi, Bill...

    From what I've read about PIV5, the virus actually prevents the body's own interferon from working! So, I find it hard to see how interferon treatments could kill it. One has to read the article in the latest issue of the Forum (ncf-net.org to order) to understand how PIV5 is working in the body. It hides out in the bone marrow, infecting the newly made cells.

    So, maybe you all have read how we have early cell death (apoptosis)? I read it to mean the virus is already in the cells forming in the bone marrow, so they enter the body already infected, causing them to malfunction. The body's defenses then kill them off...if it is functioning normally!

    If, however, co-infections are depleting the body's immune system, especially cutting the RnaseL factor, so it doesn't work properly, then we are indeed in trouble.

    This may be why anti-virals and antiobiotics work for many; they allow more healthy cells to survive and eventually lessen the bacterial and viral loads, making us feel better.

    The problem, as I see it is this: there are many studies delineating these problems, but the science is not getting to the physicians, therefore we are not getting appropriate treatment.

    I still believe there must be a class-action lawsuit against the AMA in order for us to get proper care. I don't think we should wait 5 years for patents to be approved when the correct, simple blood tests exist to identify most of these culprits.

    The FFCs are doing these tests: a lawsuit would make it proper protocol for all drs to do them, or they would be guilty of negligence.

    SOMEBODY here must know a group of medical malpractice lawyers who could advise us of how to do this!

    There's always hope (if nothing else)...
    findmind
  15. karinaxx

    karinaxx New Member

    i was thinking about a law suit for the swiss goverment, since in switzerland the situation is even more hopeless, than in the US.
    there is no doctor which is knowledgeable with ME/CFIDS in kids, in the entire country!
    kids are the one who suffer the most, beeing forced to school and draged into psychiatric treatments and their parents often accused of beeing the one making the kids sick!
    the kids are made worse and left untreated untill they end up as severe cases, often unable to even eat by themselve and traumatized by the whole experience with school officials, doctors and social goverment people, sometimes even removed from their parents!
    THIS IS CRIMINAL AND BARBARIC!
    the suffering and injustice done to the kids is unbelievable.
    karina
  16. findmind

    findmind New Member

    That is SO sad! My 18 y.o. grdau got CFS at age 15, and her regular Dr said she had "chronic EBV, something we are realizing is more than mono". She has missed the last 3 years of school. Is now determined to go to college, but with her still bad symptoms after any exertion whatsoever, I doubt she'll make if for very long.

    Noone is treating her! They just sent her home to "rest"!

    There will be the piper to be paid someday; I just don't know WHOM to hold responsible for such travesties: the CDC, AMA, or NIH.

    findmind
  17. ulala

    ulala New Member

  18. findmind

    findmind New Member

    Bump

    findmind
  19. karinaxx

    karinaxx New Member

    sorry to hear that your grand daughter has to go through this. I hope she understands that she has to pace herself also mentally, we undererstimate the neurological implications in this illness to often. i read that the brain is taking up 30% of our daily energy used! and in kids the brain is still developing.

    does she know that their is a virtual school online, which is for chronically ill kids and they have a special programm for kids with ME/CFIDS? some of their teachers are ME sufferes themself.
    she could contact Jane Colby, the head of the tymestrust.org, which specializes in helping kids with ME in their education and she can refere her to the school.she is very nice and suffered of ME herself. i was in contact with her several times and she was also a speaker of the MAI- ME- Conference in the UK.
    try the link above.
    take care and give her my love
    karina
  20. karinaxx

    karinaxx New Member

    how are you?
    still doing so good?
    ciou karina

    [This Message was Edited on 10/26/2006]