The Power and Pitfalls of Omics: George Davey Smith’s storming talk at ME/CFS conference
Read about the talk that stole the show at a recent ME/CFS conference in Simon McGrath's two-part blog.
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Dr. Holtorf on Infectious Causes of ME/CFS and Fibromyalgia

Discussion in 'Fungal Infection (Yeast, Candida)' started by osisposis, Jul 20, 2016.

  1. osisposis

    osisposis Senior Member

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    pattismith, actup and perrier like this.
  2. osisposis

    osisposis Senior Member

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    is this junk science? or is there a possibility that theres another cause behind the seceptability to these things? would a bad chronic inhalation exposure that causes damage in the airways make you seceptable?
     
  3. Woolie

    Woolie Senior Member

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    Thanks for posting @osisposis. I used to think our problem was chronic infection (perhaps especially EBV), but now I'm not convinced. I think a huge problem with the evidence cited in this article is that what they generally measure is not the infection itself, but the immune system's response to it. So for example, we all could have normal viral loads for many of these viruses, but be overproducing antibodies etc. to them. On most of the tests, you can't tell the difference between these two possibilities.

    I'm thinking now that our problem is less likely to be ongoing infection, and more likely to be some ongoing weirdness in our immune response. There were a few things that tipped the balanced for me. One was how diverse everyone's initial infections were - even if you just look at people whose illness started with an acute viral illness. It seems many roads can lead to the same outcome.

    Another thing for me was the tales from responders to rituximab. If the problem were something like viral load (perhaps EBV infecting the B cells), then removing a large portion of the infected cells should lead to a lasting recovery. But even in ritux responders, the recovery is short-lived. Once a new panel of B cells is produced, the problem returns. If the problem were chronic viral infection, why would it come back so readily after wiping out such a large number of the infected host cells? Okay, so maybe whatever infected host cells remained were able to gain a foothold and proliferate. But then you have to explain why this doesn't happen in "normal" people, who also carry EBV infected B cells. How come the virus doesn't gain a foothold in them? t all boils down to some abnormality in our immune system.

    But maybe someone who's more expert can comment?
     
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  4. msf

    msf Senior Member

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    Because the initial factor that allowed the virus to flourish in the ME patients isn´t present in normal people?
     
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  5. osisposis

    osisposis Senior Member

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  6. osisposis

    osisposis Senior Member

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  7. Woolie

    Woolie Senior Member

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    Yea, it could be that, @msf and @osisposis. That some immune problem causes us to be more susceptible to infection, and its the infection that's making us ill.

    But then, the problem with that explanation for me is that we feel so ill. People who were HIV positive - in the days before good drugs - seemed to go on for years with all sorts of viruses proliferating, and they didn't feel ill till quite close to the end.

    But this all makes sense if you think about what actually makes you feel ill when you have an infection. Its not the viral infection itself, but our body's response to it - all the antibodies, cytokines and interferon we produce to fight the virus. The illness experience is caused by the immune reaction, rather than the underlying infection itself.

    We feel very ill most of the time. And yet we don't show any of the outward signs of chronic infection that HIV people show. Okay, you could say we have a "milder' case than them. But then why do we feel more ill?

    For me, it all still points back towards some sort of immune overreactivity.
     
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  8. osisposis

    osisposis Senior Member

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  9. w john martin

    w john martin

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    Dr. Holtorf’s article provides 11 references to “stealth adaptation” of viruses (References 28-38). Many CFS patients are dismissive of this concept, in part because it was not embraced by public health authorities. Yet it is a valuable indication of the body having a non-immunological defense mechanism for suppressing both stealth adapted and conventional viruses. A good deal of progress has been made on linking this non-immunological anti-virus defense mechanism to an alternative cellular energy (ACE) pathway. A wider understanding of the ACE pathway will likely facilitate recruitment of CFS patients into clinical trials. I would, therefore, like to recommend reading and discussing the cited references in Dr. Holtorf’s article and learning more about the ACE pathway from the Internet. Kind regards, W. John Martin, MD, PhD.
     
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  10. Mij

    Mij Senior Member

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    Every year during allergy season my immune system goes all haywire, my body feels as though I have reactivating viruses during this time, but I finally realized after many years that it's actually my immune system that is over reacting.and not functioning properly.
     
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  11. osisposis

    osisposis Senior Member

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  12. osisposis

    osisposis Senior Member

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  13. osisposis

    osisposis Senior Member

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  14. osisposis

    osisposis Senior Member

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    I know what got me here, many may not, but many do
     
  15. osisposis

    osisposis Senior Member

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    just some stuff I looked at, diffenertial diagnoses is very interesting to me.

    Regulatory CD4+CD25+ T Cells Dampen Inflammatory Disease in Murine Mycoplasma Pneumonia and Promote IL-17 and IFN-? Responses


    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4866680/

    [Differential diagnosis of pulmonary mycobacterial infection; radiological findings mimicking tuberculous or nontuberculous mycobacterial pneumonia].
    Radiological imaging is one of the important clues for diagnosis of pulmonary mycobacterial infection. Differential diagnosis of pulmonary tuberculosis and nontuberculous mycobacterial infection is following; bacterial pneumonia, bronchopneumonia, mycoplasma pneumonia, pulmonary fungal infection, diffuse panbronchiolitis, sinobronchial syndrome, sarcoidosis, Wegener's granulomatosis, bronchiolealveolar carcinoma, pulmonary malignant lymphoma, and pneumoconiosis. Characteristic findings of bronchial tuberculosis are chronic productive cough with no radiological finding, lobar atelectasis, or mucoid impaction of bronchi. Radiologic findings of pulmonary mycobacterial infection are multiple infiltration, centri-lobular nodules which sometime adhere, cavity, and solitary nodule, however, these findings mimic bacterial pneumonia and bronchopneumonia especially in case of immunosuppressive patients. Pulmonary tuberculosis predominantly appears in upper lobe and the top of lower lobe of S6. Nontuberous mycobacterium pulmonary infection predominantly affects middle lobe and lingual lobe, accompanying with bronchial wall thickness and bronchiectasis. It is difficult to diagnose pulmonary mycobacterial infection using pulmonary imaging alone, therefore bacterial examination from sputum or bronchoalveolar lavage fluid should be necessary.

    http://www.ncbi.nlm.nih.gov/pubmed/19764464

    Necrotizing granulomatous inflammation: what does it mean if your special stains are negative?

    http://www.nature.com/modpathol/journal/v25/n1s/full/modpathol2011155a.html

    Mycobacterium avium Complex Cervical Lymphadenitis in an Immunocompetent Adult▿
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2944454/
     
  16. osisposis

    osisposis Senior Member

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    Relapses of primary cutaneous anaplastic large-cell lymphoma in a female immunocompetent patient with persistent chlamydophila pneumoniae and human herpesvirus 8 infection.

    http://www.ncbi.nlm.nih.gov/pubmed/27382410
     
  17. wastwater

    wastwater Senior Member

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    uk
    Prompted me to look at sv-40 again
     

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