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Dr. Holtorf on Infectious Causes of ME/CFS and Fibromyalgia

Messages
3,263
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?
 

msf

Senior Member
Messages
3,650
Because the initial factor that allowed the virus to flourish in the ME patients isn´t present in normal people?
 

osisposis

Senior Member
Messages
389
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?


interesting that you brought up B cells
 
Messages
3,263
Because the initial factor that allowed the virus to flourish in the ME patients isn´t present in normal people?
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.
 

osisposis

Senior Member
Messages
389
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.


it was a bad environmental exposure ( a high moisture moldy water damaged home that pushed my immune system over the edge, infection followed
 
Messages
31
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.
 

Mij

Messages
2,353
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.


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.
 

osisposis

Senior Member
Messages
389
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.



pretty positive that mast cells are playing a hudge roll in our illness. at least some of us but maybe all of us.
 

osisposis

Senior Member
Messages
389
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.


not sure what to think about the ACE pathway, haven't looked into it much tho. as far as hidden or dormant viruses or bacterias being brought out and re-activated because of a bad environmental exposure, I can see that, but from where I'm setting and what I've been through, for me the seceptability to other infections post the immune breakdown and inflammatory disease and initial infection all cause by a bad water damaged building/home, where I know mast cells were heavily involved and continue to be involved still with my severe allergic and non-allergic hypersensitivities, and a whole lot of new info. on loss of homeostasis with mast cells being main players is very convienceing for me that I know how I ended up with ME/CFS. LOSS OF HOMEOSTASIS IS WHERE IT'S AT FOR ME.
 

osisposis

Senior Member
Messages
389


environmental exposure studies with identical twins has basicly shown that you can have bad genetics that make you more seceptable to certain illnesses but they may never come into play without a environmental exposure to bring them about. in the same sence, a bad environmental exposure could bring out dorment or hidden viruses,bacterias, ect. but first the environmental exposure does the damage that gets us here, at least a group of us, and weither or not old hidden things become active again or and/or we have just become seceptable to these thing now that we have loss of homeostasis, witch lead to major and multiple/total bodily injury including the brain is secondary to the cause
 

osisposis

Senior Member
Messages
389
I know what got me here, many may not, but many do

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/