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The Infectious Etiology of Chronic Diseases (from an IOM workshop)

WillowJ

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4,940
Location
WA, USA
http://books.nap.edu/openbook.php?record_id=11026&page=R1

http://iom.edu/Reports/2004/The-Inf...-Mitigating-the-Effects-Workshop-Summary.aspx

This report summarizes a two-day workshop held by the Institute of Medicine's Forum on Microbial Threats on October 21-22, 2002, to address this rapidly evolving field.


Invited experts presented research findings on a range of recognized and potential chronic sequelae of infections, as well as on diverse pathogenic mechanisms leading from exposure to chronic disease outcomes. Cancers, cardiovascular disease, demyelinating syndromes, neuropsychiatric diseases, hepatitis, and type 1 diabetes were among the conditions addressed.

Participants explored factors driving infectious etiologies of chronic diseases of prominence, identified difficulties in linking infectious agents with chronic outcomes, and discussed broad-based strategies and research programs to advance the field.
 

halcyon

Senior Member
Messages
2,482
There is a chapter on enteroviruses.
Interesting discussion starts on page 53. Talks about the same challenges that Dr. Chia talks about with detection, which led him to tissue testing instead.

Despite the advantages of enterovirus detection by RT-PCR, challenges remain. In the case of chronic diseases, the virus may act indirectly (e.g., through immune-mediated pathology). The virus may be cleared well before disease onset or virus may be present in the patient but not in the diseased tissue. Even in acute illnesses, the titer is relatively low in all specimens. As a result, a conventional single-step RT-PCR amplification may not be sensitive enough for direct detection from the original clinical specimen. Designing a prospective study and collecting multiple specimens, at multiple time points throughout the duration of the study, may overcome some of these problems; however, the only way to solve the sensitivity problem is by increasing the sensitivity of the detection method.

I really hope Dr. Lipkin knows what he's doing. As best I can tell he's looking at stool, and as mentioned in this report, enteroviral shedding in stool only lasts between 2 to 8 weeks after infection. I'm terrified he's going to turn up false negatives and then it's back in the closet with us for another few decades.
 

Sidereal

Senior Member
Messages
4,856
I really hope Dr. Lipkin knows what he's doing. As best I can tell he's looking at stool, and as mentioned in this report, enteroviral shedding in stool only lasts between 2 to 8 weeks after infection. I'm terrified he's going to turn up false negatives and then it's back in the closet with us for another few decades.

I'm worried about that too.
 

Hip

Senior Member
Messages
17,824
I really hope Dr. Lipkin knows what he's doing. As best I can tell he's looking at stool, and as mentioned in this report, enteroviral shedding in stool only lasts between 2 to 8 weeks after infection. I'm terrified he's going to turn up false negatives and then it's back in the closet with us for another few decades.

I think Dr Lipkin's main forte is as a pathogen hunter. He likes discovering new pathogens, and has great expertise in this area. I believe Lipkin interest is in finding possibly new pathogens associated with ME/CFS, more than working out a theory on how pathogens already known to be associated with ME/CFS — pathogens such as enterovirus or EBV — might trigger ME/CFS and give rise to ME/CFS symptoms.

When it comes to figuring out the biochemistry and immunology that would explain how a pathogen, known or unknown, can give rise to ME/CFS and its symptoms, that may be a different skill set.

In this respect, I think the work Dr Michael VanElzakker is excellent. His vagus nerve infection hypothesis (VNIH) of ME/CFS is the first theory I have seen with the power to explain how an infection can give rise to the symptoms found in ME/CFS.

The VNIH is the first theory of ME/CFS that starts at the very beginning of the etiological chain — with the infection — and then posits the mechanism by which that infection can give rise to the symptoms that appear in ME/CFS — symptoms that are at the very end of the ME/CFS causal chain. So the scope of the VNIH is extraordinary: it provides a testable theory of the whole pathophysiology of ME/CFS from beginning to end.


I would like to see more theories like the VNIH. For example, if we look at the autopsies showing that the brains of ME/CFS patients are infected with enteroviruses (whereas in the control group, no brains were so infected), the issue here is the biochemical and immunological mechanisms by which these brain infections could give rise to the symptoms of ME/CFS.

The mechanism of how a brain infection leads to ME/CFS symptoms may well be exactly the same as the one VanElzakker proposes in his VNIH: namely that inflammatory cytokines resulting from the infection switch on the sickness behavior response, which then causes the ME/CFS symptoms (sickness behavior symptoms are very similar to those of ME/CFS).
 
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