Write-up of the Invest in ME conference via The Canary

[lansbergen]

Is it possible, I wonder, for a strong viral immune response to somehow wipe out bacteria in the gut and upset the balance of the microbiome?

In the old days it was assumed virus infections change the gut flora.

 

[Bob]

@Rose49, the editor responded quickly and has amended it as follows...

Davis had trouble raising funds from the usual funding bodies, so he had to collect funds privately. Unfortunately this meant he could not include the numbers originally planned for, and the pilot study consists of three severely ill ME/CFS patients (one being his son) and 43 healthy controls. He has since begun a study with 20 ME/CFS Patients and 10 healthy controls, and will collect billions of data points.

 

[Janet Dafoe]

@Rose49, the editor has amended it as follows...

Well gosh, it's not perfect but it's better than it was! I showed it to Ron. He said,"That's good enough".. Thank you.

 

[Janet Dafoe]

Hi everyone!
I had Ron read the whole Canary article. He would like everyone to know that those three things he mentioned in his talk, biotin, et al, are not "biomarkers". Biomarkers will be things that we use that will enable us to accurately diagnose ME/CFS, and will likely not be one thing. These things he mentioned were examples of metabolites that are low in some ME/CFS patients that can cause symptoms. They may be components of whatever turns out to be a biomarker, but we're not there yet. I'm not sure if it's worth trying to correct that in the article. What do you think? We can't control everything that gets printed. We just like to do our best to be sure people are getting accurate information. Ron chuckled when he saw the part about how he has "loads" of money. That would be nice and help the research go faster! The article is really great though, and sure sends the right message! NOT IN OUR HEADS! and, GOOD SCIENCE IS HAPPENING WITH HOPE FOR MORE!

 

[ukxmrv]

Hopefully the article doesn't need to be perfect and there gets to a point that both the writer and editor will want to move on. No point spending precious energy correcting things that are minor (ish!). The overall message is good as you said.

Thank you family Davis for all your amazing work.

 

[Kati]

Thank you @Rose49 for the clarification and setting the record straight so things are as clear as possible. It is extremely useful and important that the message that comes across is as accurate as possible. I understand that interpretations are sometimes difficult to correct once published, but glad you are here and making sure we understand.

 

[Forbin]

In the old days it was assumed virus infections change the gut flora.

I found this article on Vincent Racaniello's Virology Blog:

How influenza virus infection might lead to gastrointestinal symptoms
10 DECEMBER 2014

http://www.virology.ws/2014/12/10/how-influenza-virus-infection-might-lead-to-gastrointestinal-symptoms/

These results show that influenza virus infection of the lung leads to production of CCR9 positive Th cells, which migrate to the gut. These cells produce interferon gamma, which alters the gut microbiome. Numbers of Th17 cells in the gut increase, leading to intestinal injury. The altered gut microbiome also stimulates IL-15 production which in turn increases Th17 cell numbers.

[Earlier in the article...]

Th17 cells are a type of helper T cells (others include Th1 and Th2 helper T cells) that are important for microbial defenses at epithelial barriers. They achieve this function in part by producing cytokines, including IL-17A. Th17 cells appear to play a role in intestinal injury caused by influenza virus infection of the lung. The number of Th17 cells in the intestine of mice increased after influenza virus infection, but not in the liver or kidney. In addition, giving mice antibody to IL-17A reduced intestinal injury.

These results are in mice, but it is interesting how a viral infection of the lungs can alter the microbiome of the gut without the presence of replicating virus in the gut.

IL-17A was one of the cytokines that the CII found elevated in the first three years of ME.