Lipkin and Hornig go hunting for ME/CFS pathogens

Hi, Simon thanks for report. Are the first results going to be published just about general viral testing or have they actually started stage 2? Stage 2 is what I'm waiting for. I hope they keep some of the patients who are positive in stage 1, at least as controls. If we have immune deficiency, and pick up lots of viruses, eliminating the people with other viruses might get rid of your main cohort. I've never had really high titres myself, but I think we need to look at both groups.
I found Dr. Chia's video very convincing, that we need to look in the tissues. Lerner had also found viruses through biopsies. I think Lipkin said that this throughput method did not work on tissue, too complicated in make up (not if memory got that backward). Someone has been collecting tissues from patients doing standard procedures for years. I think we still have to find some way to get tissues looked at.

Is there any list of the 18 viruses they looked for?

- Afraid I have no more info on what will be published when.

- 20% of those positive in stage 1 get sequenced in stage 2 regardless so if they tend to have more viruses, that should show up. If a large group are taken out by the first stage then that would make the group very interesting indeed, and I'm sure there would be further work on it. From a few initial figures Mady showed, only a small proportions were screened out in stage 1, but it looked like early data so final results could be v different.

- I agree it would be v interesting to look at tissues too, but I suspect this study will be a (pretty-impressive) start, not the final answer.

I am sure there is, but I don't know what's on it! Though it probably includes not just viruses but bacteria too such as Borrellia bacteria that trigger lyme disease.

Not sure I was able to help a huge amount there, sorry!

Thank you so much for volunteering for that, Acer.

Yes - thanks to all those patients making the effort to be involved with good quality research.

markers for inflammation and immune dysfunction interest me far more than pathogens. It seems unlikely they'll find a pathogen, although they may find evidence that several pathogens are involved.

I'm not impressed by Klimas talking about what keeps the illness going as she talks about deconditioning and suggests using a heart monitor in a way that would mean I could hardly go upstairs.

Well, I feel a lot better if I don't go up or down a flight of stairs for a week or more. So she really might be onto something in that regard. Those little spurts of over-exertion (or overly-raised heartbeat) might be having a relatively mild effect that is resulting in worse symptoms and reduced ability to do other activities.

And her talk of deconditioning seems to put it in a rather peripheral status ... it's something to avoid if possible, but she also clearly states that PEM is not something to push through if we react badly to a certain level of exertion. And she certainly does not suggest that deconditioning has any central involvement in ME/CFS.

Simon, congrats, your article has got an endorsement from the CII:
https://twitter.com/CII722/status/308985339991715841
https://twitter.com/CII722/status/308985800098447362

Big up Simon. Nice to see that they're pleased with the articles too.

Breaking news from Invest in ME conference (tweets from Jørgen Jelstad):

1. They MIGHT have something interesting from the pathogen study, but too early to say:

2. Looks like they found a difference between CFS and controls in CSF fluid cytokines
Pretty sure these are the Peterson/Simmaron samples, 60 patients but controls inc other illness groups too

Not sure if this is based on CSF still, or on bloods, so sample size uncertain:

Thanks for the update, Simon! It's all too easy for me to lose track of what's going on in these relatively long-term studies, so it's a huge help to me when someone who's managing to keep up shares their info.

I read this today: http://www.eurekalert.org/pub_releases/2013-06/slu-slu061713.php which basically is a 'new' technique where they sequence all the DNA and RNA in the blood (as Lipkin and co are doing) and then subtract the entire human genetic sequence from the genetic material of a blood sample and identify pathogens based on what remains.
I assumed this was what Lipkin was doing with his next-gen sequencing, but it says at the bottom of this notice that its a new technique that St. Louis hope to patent. Does that mean that Lipkin isn't doing this human DNA subtraction as part of his technique, or is he doing so using some other method?

FWIW, I sent emails to Lipkin and Hornig along with a link to one of Chia's research articles. I suggested they speak with Chia, or at least ask Klimas whether she thinks his tissue investigations are worth consideration. Hornig replied that she agrees with the importance of investigating whether microbes are in tissue other than blood, and she said she has regular contact with Klimas about this and other things.

I'm a bit puzzled by this, as its exactly the approach described by Lipkin to discover unknown viruses in the past, and also my understanding of what they will do in this pathogen study. Maybe it's a twist on the technique, but don't think it's a brand new approach at all.

Yes, can anyone shed any light on this too; I'm very confused.

I would say the new technique is the amplification of genetic material which probably makes finding things either easier or more reliable with fewer samples

I just read this article today.

Thank you Simon for a great article and for your replies to the variety of questions here.

I have a very basic (probably silly) question. When they talk about finding EBV, do they mean and active EBV virus or are they talking about elevated IGG titers?

I am always confused about this because if they do find the active virus then it could explain the symptoms and might rule out ME/CFS.

My doctor, Dr. Enlander checks for antibodies for many pathogens like EBV, CMV, HHV6, M. Pneumonia, Coxsackie B, Parvovirus B19...etc I show high titers for all of these and he believes that it is part of my ME/CFS. When I show these results to my GP, he laughs at it and says we all have antibodies to many pathogens and it doesn't mean anything.

What's up with this?

Thanks, NeilK

I'm pretty sure they are looking for pathogens directly in the blood (so EBV protein or DNA), rather than elevated IGG titres, either general or specific to EBV. And of course they will be comparing the rate of EBV in patients with those in their carefully matched controls. And I think the EBV resutls will be out later this year - may well have been submitted for publication already.

Came across this earlier from Deckoff-Jones. Links to video presentation from Hornig. Don't know if you covered it before in the thread Simon but thought I would throw it out there anyway:

An article from July 22? but folder indicates 2011?... and with some new and great quotes by Lipkin and Hornig that I don't recall.

http://trialx.com/curetalk/2011/11/...equencing-and-proteomics-to-hunt-cfs-viruses/