Transcripción escrita conferencia de Klimas sobre XMRV
Publicado: 15 Dic 2009, 14:55
Dr. Klimas's Talk on XMRV From PANDORA (Nov 2009)
Section Three: XMRV, NK and T Cells, Latent and Retroviruses
So what is this virus X-M-R-V? Well, the RV means retrovirus. So that puts it in a family of viruses, retroviruses,Dr. Klimas on XMRV and ME/CFS that we actually know quite a bit about. And the X is xenotropic. M was mouse. This virus started in a mouse. Now there’s…ya know viruses start somewhere. They’ve got to start somewhere. Like the HIV virus started in a monkey. It’s a monkey virus that eventually evolved several hundred years ago into a virus that could infect humans. So we got this lousy virus, HIV.
XMRV is in its own evolution. And it jumped from mouse to human at some point. We don’t know when, but probably not in the too terribly distant past. Well, that doesn’t mean a lot, because in Darwin terms, distant past could be 100 million years, but these guys think like that, the evolutionary biologists. That wasn’t long ago, a thousand years ago or so. But in this mouse virus, it could have been in the last century. That’s the sense of it.
About 3-4% of people have this virus and they’re not sick. And that’s another part of this. So there’s this background population. Now, I’m just saying that flat out, but you know I gotta tell you that the research on this virus is only 2 years old. And so, we don’t know very much about it. And there’s probably regional differences. There might even be continental differences. We don’t know. There’s been nothing done anywhere else. They did some studies – originally this virus was found in prostate cancer. So most of the work was done in that area and there’s two studies: one in Germany and one in Ireland that failed to find this virus in their patients. Now, whether they’re using the same technique or it’s not in Germany, it’s not in Ireland, we don’t know. So, there’s a lot of questions still to be answered with this virus.
And for those of you who aren’t in the land of science, Science is like the Mecca of publication. If you get your stuff in Science, that’s the best place you could possibly put them.
The Science Paper - This Science paper was amazing for a number of reasons. First, this team had put together such strong science that they could go for a Science paper. And for those of you who aren’t in the land of science, Science is like the Mecca of publication. If you get your stuff in Science, that’s the best place you could possibly put them. And they don’t take just anything and they sure, sure, sure don’t take something unless it’s extremely well done, validated and tested out. So they took this paper. And if you read this paper, they not only took it, they put it in Science Express. They thought it was so important, they published it on a very fast track. And so, that was important.
And if you read the paper, you’ll see they found this virus the first way they looked. They backed up and looked from a whole different angle. Still found it. Backed up and looked from another angle. Still found it. Then, in two other ways, they had five different kinds of ways they looked for this virus. And they were able to find the virus. So I think that’s why Science was so impressed. They also used a very big population. They had 100 Chronic Fatigue patients – 101. And they had more than 200 controls. So that’s usually…scientists like that kind of stuff.
And then, the interesting thing was in this paper, the first 20 patients they studied were Chronic Fatigue patients that had developed some kind of Cancer. That’s actually how they got the Cancer guys’ attention, I’m assuming. Because Dr. Peterson’s got 30 years of stuff in his freezer and dug out everybody in his whole population that had ever gone on to develop Leukemia or Lymphoma or any other kind of Cancer. They pulled those out first and that’s actually where they first found it and that’s what got their interest up. And then they went back and looked at a bunch of others. The way they looked is very sophisticated and they found 67% that way. And then they tried to find it in all these other ways, when they added everything together, they could find the virus in roughly 95% of the patients using one technique or another, but not necessarily consistently, no matter what technique they used. But it means that there’s at least 67% of people in that Reno cohort and possibly quite a bit more.
they found this virus the first way they looked. They backed up and looked from a whole different angle. Still found it. Backed up and looked from another angle. Still found it..they had five different kinds of ways they looked for this virus. And they were able to find the virus....that’s why Science was so impressed.
A Mouse Virus - So, what is this virus? It’s a mouse virus. It was first discovered in 2005. It was discovered by prostate cancer researchers looking for a virus, viral causes of Cancer. So they found it in that study in 40% of prostate cancer. Another group looked and found it in 23%. And so there have been two studies that said: the virus is in prostate cancer. Other groups though, have not found it - in Germany or Ireland – so it’s still considered somewhat controversial.
It’s a different strain than the one seen in prostate cancer. It’s not exactly the same. Okay? I’ve already had patients whose husbands had prostate cancer thinking that they somehow infected their husband. Oh my God, I gave my husband prostate cancer. Don’t think that way, okay? It’s a different strain of the virus. They’re related, they’re closely related. But we don’t know enough to even pretend to go that far with assumptions.
It’s a virus that doesn’t have a lot of mutations. And what that means to the virology world is that it doesn’t change very much, it’s not shifting around, there’s not a whole bunch of different kinds of it. Like there is with HIV, where within a few weeks of applying an antiviral, the HIV virus can mutate away and escape and go off and do its own thing. So this is a pretty stable virus. That bodes well, particularly for vaccine work. That bodes extremely well. We don’t know what that means to the antivirals yet. It just depends on how much replication is going on.
I’ve already had patients whose husbands had prostate cancer thinking that they somehow infected their husband....Don’t think that way, okay? It’s a different strain of the virus.
ME/CFS - Why does it fit into Chronic Fatigue? Well, there’s a lot of good reasons why it fits in to Chronic Fatigue. Those of you who live and breathe this stuff might have heard me talk about natural killer cells a little bit. ((laughs)) NKs are really broken in Chronic Fatigue Syndrome and natural killer cells are part of your defense that prevents latent viruses from reactivating. And they really, really don’t work well in Chronic Fatigue Syndrome. And our group has done 20 years of work to try and figure out why – and we know why. And we also extend that to say: these natural killer cells that don’t work are closely related to a different cell, cytotoxic T-cells. And they don’t work either and between the two of them, that is your antiviral, latent viral reactivation system. Both of the systems are broken.
So, enter a virus that infects and affects natural killer cell function and that’s this one. And infects and affects T-cells, cytotoxic T-cells. That’s this one. So we’re kind of keen, we don’t know for sure, I mean this so early in the work, we’ve gone all of three weeks since that paper came out. There’s going to be a lot of work to be done. But it would make a lot of sense, a good hypothesis to construct if this virus is in there mucking up cell function, and that would make a lot of sense to what’s going on.
It also is a virus that can infect tissues that aren’t white blood cells. And we’ve always thought: something like that has to go on in Chronic Fatigue Syndrome because you all have some neuro-inflammation. Your brain has a low grade level of inflammation. And you have some inflammation in the tissues that make hormones, particularly the hypothalamic-pituitary axis. And this is a virus that has some tropism or infects that type of tissue. So it starts to make the whole picture come together. Now we don’t know enough about this virus’s tropism or what stuff it likes to infect. This is just sort of the first look and some of this may change as we get more sophisticated and look with better ways. But the sense is this virus, if it’s acting like its cousin virus HIV that likes to infect those kinds of tissues, that it’s going to have receptors that let it into other places too. Anyway, I think it fits well and I’m very excited about that fit.
(thanks to Kim on the Phoenix Rising Forums for the transcription)
Section 4: Retroviruses and A Biomarker
Latent and Active Infections - When we talk about latent viruses, this is what we’re talking about. The guy on the top is a quiet little white blood cell hanging out doing nothing because no one has asked him, it doesn’t have a job yet. If it becomes activated, it’s because something floated into the system, some antigen, some bug that it’s supposed to respond to. And in our systems we have hundreds of millions of these little quiet cells and each individual cell only knows its one little job.
Now this one’s for Epstein Barr, that one’s for Staph, and that one is for some other bug. If that bug comes into the system, then that cell is the one that gets activated. And if it had hidden inside it, in its DNA like over there, if it has inside it this little piece of virus fragment, sitting in that DNA, that cell is turned on to make all of its stuff it knows how to make. It got activated. It’s going to make cytokines, it’s going to make interleukin 2, it’s going to make ?? , oh and by the way, it’s going to make that sneaky little virus that was tucked into its DNA too. And that’s what happens.
Retroviruses are funny because we’re just chock full of them. We have little bits and pieces of retrovirus all in our DNA.
These latent infections just sit around doing nothing until that cell is activated and then boom, they start making virus stuff. Retroviruses are funny because we’re just chock full of them. We have little bits and pieces of retrovirus all in our DNA. Talk about evolution, our great, great, great, great, great, great, great grandfathers got infected with some little piece of something, maybe a chunk from a mouse back then. But it’s not a whole virus. They have just little bits and pieces, of busted up pieces of retrovirus tucked in the DNA. We think it’s an important part of the way that we evolved. That we borrow DNA from other species this way and we transfer things around. If viruses carried little pieces of information into the genome back then. And some of it was bad and that didn’t work out. And some of it was good and it carried on or it was neutral and it carried on.
Generational Transmission? - But there are some retroviruses that can be carried generation to generation as a whole and complete virus tucked into that DNA or rather enough DNA to make a whole and complete virus when it’s turned on. And this is one of those retroviruses. It can be transferred generation to generation or what’s called vertical transmission, mother or father to child through the DNA. So we don’t know if there’s 3 or 4% of background. There’s just people who have vertical transmission or if there’s some way that you can infect people back and forth in life. We don’t know that at all, okay?
XMRV transmission and CFSBut we do know that this virus is one of the ones that is vertically transmitted. We know that from the mouse data. So it can be transmitted vertically. So the question is if you have children, do your children necessarily have it? And the answer is maybe yes or maybe not. First off,
We don’t know if it’s sexually transmitted....We know HIV is, obviously, is a sexually transmitted retrovirus. But, there’s no…you’d think in 25 years, we would have seen massive numbers of spousal pairs. And we have not.
there’s two parents not one. And each only give half of the DNA, yeah, right? So in any given child, there’s only one chance in four that you can pass on any particular piece of DNA on a good day. So you don’t worry too much about kids flat out that way. And then you say: And oh, by the way in their life, they have to come across the thing that activates the virus and turns this whole mess on. And so there’s a whole lot of reasons not to get all worried about…I mean I’m not saying it couldn’t happen to your children…Of course it’s conceivable. But what’s exciting right now is we’re getting this, we’re getting the understanding of it, and we’ll probably, knock on wood, that we will be to the position where we’re actually intervening effectively before it becomes a bigger worry. But, um, I don’t know about kids. I’m saying it is a vertically transmitted virus.
Sexual Transmission? - We don’t know if it’s sexually transmitted. I will say that there are sexually transmitted retroviruses. We know HIV is, obviously, is a sexually transmitted retrovirus. But, there’s no…you’d think in 25 years, we would have seen massive numbers of spousal pairs. And we have not. You occasionally do, occasionally we do see a spousal pair. It happens. But almost always those people both had acute infection at the same time at the onset and it’s really unclear if it was transmission between the two of them or if they had some other thing happen that kicked off the whole, the whole thing. And you see household Chronic Fatigue. I mean I do see mother-daughter, father-daughter, father-son, whatever…I’ve seen it. But, in my clinical practice in the 25 years or so, it’s not very common. It doesn’t happen a lot.
So, the next slide. This virus is not HIV. A lot of people panicked when they heard this. This virus really is not HIV. It’s in the same family, but it’s a distant, distant cousin…very very distant. And it’s not infecting or affecting the same cells. So, it’s not doing the same immunologic thing that HIV does. Okay?
it’s pretty impressive that out of 101 CFS defined by clinical case definition or a research case definition that they found 99 with virus. And if this is the case, that’s pretty exciting. It’s pretty impressive. And, oh, by the way, we have a biomarker. Not a small deal.
There are also other retroviruses that don’t do anything that we know about. There’s a virus called HTLV-2 that I have studied myself in the past, and many others have, and it’s just sitting around doing nothing. It’s really…it’s vertically transmitted, it even replicates, and it doesn’t cause much in the way of illness. So, that doesn’t necessarily mean that just because you find a retrovirus, it’s definitely the deal. And not every retrovirus is big and bad and ugly. There’s another virus called HTLV-1 that’s vertically transmitted and does cause an illness. And it causes a neurologic illness. And so, we have different bugs, different things.
HIV is a retrovirus and there’s at least 20 or more drugs directed at HIV. So, will those drugs work to control this virus? That is definitely the big question of the day. And the first thing to say is: some of them probably will. And the second thing to say is, but not all of them…you couldn’t just pick a random one and try it.
This one’s to show you mouse going to people…that basically it started out way up there as a mouse thing. Mice learned to live with it. They don’t have a receptor that allows this virus to become a big bad deal. So, mice just sit around for generations and generations of mice being a reservoir of virus, but not actually getting sick from the virus. But then the virus shifted and it became capable of jumping from species to human.
Almost All Positives - One Way or the Other - So, this was the study. They had in their freezers samples from people that weren’t from their cohort. So, these were not just Reno samples. There were samples from Florida, from California, from North Carolina, and other places. Everyone in their repository had a Chronic Fatigue diagnosis. The mean age was 55. There was two thirds women. They had this large control sample. They looked…and they looked at these patients, out of 101 patients, and they looked at the DNA, the sequences of the virus in the DNA. It’s really a sophisticated way to look and they found it in 67% and in 3.75% of the 320 controls.
The XMRV /XAND Pages
Now of the negative, these 33 negatives, they went on and looked in other ways. And they found 19 of those had antibody in their plasma, so that was more than half of those negatives. But this is the big number: 30 of the negatives had virus they could identify by taking the serum of those cells, the serum from the plasma, and infecting a cell line and then growing the virus in that cell line. So they could transfer from the plasma, virus to the cell line. Now that has a lot of implications and it’s certainly the reason why, in part, the CDC, the NIH, and others that really care about the blood industry are looking long and hard at this. They found the virus, a transmissible virus, in the plasma and they were able to infect cell lines. So it is suggestive of an infective component, at least in the blood. And then there were other ways, so they worked out that they were able to find 99 of the 101 patients in that way.
Now think about that for a minute. We define an illness by a bunch of symptoms. Now, I’ll say Dr. Peterson is a really fine doctor, and I’m quite certain that he’s not misdiagnosing Chronic Fatigue Syndrome. He’s really splendid. So, it could be that he has a really clean, tight population of folks in his freezer. But I would say, I think I’m pretty damn good, and I think if I pulled out stuff from my freezer, there might be a couple of MSs in there or something else that evolved down the line. I mean, I’m not sure. But it’s pretty impressive that out of 101 CFS defined by clinical case definition or a research case definition that they found 99 with virus. And if this is the case, that’s pretty exciting. It’s pretty impressive. And, oh, by the way, we have a biomarker. Not a small deal. A biomarker – the virus itself. No better biomarker than something that’s clearly, tightly associated with an illness.
(thanks again to Kim on the Phoenix Rising Forums for the transcription)
Section 6: Virus Life Cycle, Immune Modulators (Antivirals)
And here’s the real compelling question: will antivirals work? This is a virus that’s sort of coming in to a white blood cell and it’s hunting for its receptor. And then it’s going to attach to this cell. This is a retrovirus attaching to the cell. Now in this virus, we don’t know what that receptor is yet in human. We actually sort of have an idea from the mouse work, but we don’t know for sure. But there’s an attachment step. And then the virus enters the cell. It fuses to the cell. In HIV there’s these entry inhibitors and fusion inhibitors that prevent that so there are potential therapies if it were the same receptor. I kind of doubt it. I don’t think we’ll be using those particular HIV drugs.
Then it gets into the cell and when it gets into the cell, it dumps its RNA into the cell. It pokes a little hole and the virus comes in. And then that RNA comes out. And we’re DNA, not RNA. The nucleus of our cells is DNA, so it has to be turned into DNA. And to do that, it uses an enzyme called reverse transcriptase and that turns the (see I knew before that thing before it told me. I am smart). Anyway, it turns RNA into DNA and that is a wonderful target for this virus…the reverse transcriptase inhibitors…because then the DNA can integrate into the cell. Now we have integrase integration inhibitors also…in HIV…integrase inhibitors. But they are fairly selective for HIV. I don’t know that they would be effective in another retrovirus.
..there are literally thousands of compounds in the pharmaceutical companies’ shelves that they developed for HIV that weren’t as good as things for HIV that approved that might be the very perfect thing for this virus. So, we’re not starting from scratch here with this virus – at all!
And then, when the cell is activated and its DNA starts making stuff like this, it has to be…it makes these great big long proteins and those proteins have to be cleaved into little pieces (see I’m sinking here). And that’s the protease inhibitor line in HIV, the proteases that cleave are inhibited and that prevents that piece from being torn up. And then all these bits and pieces assemble themselves over on the cell wall and they bud off – BOP – and there’s a virus. And that’s how viruses are made.
So, we have entry inhibitors, we have reverse transcriptase inhibitors, we have integrase inhibitors, we have protease inhibitors. And then all those put together is the whole repertoire of drugs that have been developed over the last 20 years or so for HIV.
But, be it known that there are literally thousands of compounds in the pharmaceutical companies’ shelves that they developed for HIV that weren’t as good as things for HIV that approved that might be the very perfect thing for this virus. So, we’re not starting from scratch here with this virus – at all! The other thing about this virus, and this is just from what Dr. Coffin said at the Chronic Fatigue meeting on Friday (I’m not a retrovirologist as brilliant as these guys) but I can parrot them pretty well. Dr. Coffin said – because this virus doesn’t seem to mutate very much, it’s a great target for vaccine trials.
And when you ask - what about antibodies? – if we vaccinated people to this virus that already had the virus, we could goose up their immune response to this particular virus. That’s what they’re doing in HIV trials, they vaccinate infected people. So you might suppress the virus with an antiviral and then goose up the immune system with vaccines, so it could really work hard on this virus and then reduce it. So you could start postulating. Isn’t it fun to be able to postulate therapies…I mean, it’s great. I’m loving this. I’m lying awake at night thinking of all these things. It’s like – oooh,we could do this – oooh, we could do that. Good stuff. I know, I know, I’m an immunologist, what can I say?
Isn’t it fun to be able to postulate therapies…I mean, it’s great. I’m loving this. I’m lying awake at night thinking of all these things. It’s like – oooh,we could do this – oooh, we could do that. Good stuff. I know, I know, I’m an immunologist, what can I say?
Ampligen - Of course one of the things I think about is immunomodulators – drugs that would either quiet immune activation or enhance cell function are very appropriate. Okay, so what’s already out there? Well, Ampligen, Ampligen’s an interesting drug. And they actually showed – they had 8 patients that had Ampligen data – that they showed at the CFSAC meeting that Dan showed. And it had a mixed result. In some cases, Ampligen was very effective in suppressing this virus, and in some cases it was not – in those 8 patients. That’s not very many. But Ampligen sounds kind of promising because it’s an antiviral that’s an immunomodulator that enhances natural killer cells and cytotoxic T-cell function. It’s even more intriguing than before in my mind, I think Ampligen’s got some real potential.
Immunovir (Isoprinosine) - some of my patients are on this medication. It’s only had phase 2 trials, it hasn’t had phase 3 trials. But it’s more or less a nutraceutical, it’s an amino acid. But it is also an NK cell enhancer and a cytotoxic T-cell enhancer that may have some antiviral effect.
Cell Therapy - this cell therapy – I referred to this ex-vivo cell therapy – some of you were in this study – It was in 1993 or…it was 1993. Well we took a lymph node from a patient and we grew the cells in a laboratory and we made literally a transfusion of white blood cells. Max did that. He was busy, busy transfusing my patients with white blood cells – their own white blood cells. But in the test, in the laboratory, we had grown them, fixed sort of what was broken about them, and then we got some very very nice clinical responses in that Phase 1, that study that never got to go to a Phase 2 study for lack of funding. And then finally, this makes cytokines that are either directly antiviral or immune enhancing more interesting.
Neutraceuticals - The nutraceuticals, they have less work done. Omega-3s are anti-inflammatory, the mushroom extracts that the Japanese use to enhance natural killer cell function, but these aren’t studies that had placebo control data and looked promising. CoQ10 at roughly 100 twice a day – that was really anti-fatiguing and enhanced cell functions. TNF inhibitors, we have a couple few patients on TNF inhibitors and I’m seeing some nice responses if they’re cytokines are way wacked out and they’re super revved up.
That’s a natural killer cell, the little guy killing that target cell. That’s an Epstein Barr virus infected target. And there’s that little white blood cell doing its job. That’s what we’re trying to do. So the white blood cells infected with virus and you want these cells to go in there and kill that cell. So, the other question with this is: okay you’ve got one virus, but what if you’ve got this virus plus a couple of other viruses? What’s the role of all these viruses all together? What about HHV-6, EBV, enteroviruses, and this virus. If we say that all these viruses are doing their work together, it might be necessary to treat more than one virus. It might be necessary to design a study that has the retrovirus piece and a Herpes virus piece because sometimes viruses lend each other machinery to make their infections more potent and damaging.
(thanks once again to Kim for the transcription)
Section : Testing for XMRV: Q&A
if I ordered a blood test on you right now and it was negative, what would happen to your soul?....yet it might not really be negative..(the) tests are going to be improved on
Ordering A Blood Test? - So, there are some issues here. That blood test only identified 67% so if I ordered a blood test on you right now and it was negative, what would happen to your soul? You know, and yet it might not really be negative, in fact it’s got a one chance in three of being wrong. The blood test that we don’t have yet that we will have very shortly, those tests are going to be improved on.
When the first HIV blood test came out it wasn’t any good either. You know, it went through stages and stages and stages before we got a really good one. Don’t rush to get the test. Why, because you’re not going to act on that test quite yet. The knowledge of being positive is not going to give you an anti viral prescription from anyone right now because we don’t know which one to give and if it’s safe or if it’s toxic. The HIV drugs are not been gentle, OK, and you guys are really tender. So, if you knew your status today it really wouldn’t change anything.
If they are right 99% of you are positive. And if they are wrong then 95% of you are positive.
Don’t rush to get the test. Why.. The knowledge of being positive is not going to give you an anti viral prescription from anyone right now... The HIV drugs are not been gentle, OK, and you guys are really tender.
So when? Soon, really soon. But you wouldn’t be able to bear the false negative right now so be careful OK. There are kits already out there, they want cash and there’s no reimbursement from your insurance provider yet. I was talking to this XMRV and Chronic fatigue syndromegreat scientist at the VA and he said, you know, my lab develops tests. That’s what we do. What’s wrong with the tests you got? Oh, I could fix that and he got all jazzed and I’m thinking, damn, get another guy in the field and you know, and he’s fixed your test, that’s great. So these people, they’re already out there and they know how to do it and tests will improve.
If you don’t have this virus – what if you didn’t. Well, you know, that’s good news too because that puts you in a different group and we know not to do all that toxic stuff to you. So that’s an important thing to do too. So don’t be discouraged even if you’re negative.
We talked about these other people that might also actually be infected. We don’t know. These are just people we are going to be looking at. The Gulf War Illness group I’m desperate to see right away because it could change the whole direction of that work and they have a fair amount of money to do that work.
So the conclusion, it really is a big thing. It’s a big thing. You should be very excited. It’s a very hopeful thing. Yeah, the research is already underway, more to come. The more we can get funded the more focused and intense we will be in getting this work done as quickly as possible. That work we were already doing plays right into this. All the genomics work and all the immunology work. That is all critical to the better understanding of this illness and how this virus plays into it.
it really is a big thing. It’s a big thing. You should be very excited. It’s a very hopeful thing.
Those of you that are in my good day bad day study, it’s nice because we’ve got your stuff already in the freezer and we’ll be looking at this virus as quickly as we can get access to the assay. That study, that’s a really important study. It looks at people in relatively better times and worse times and we’ll know if viral load is causing that. If there’s anything about this virus. We’re already looking at all the immune parameters and endocrine parameters and everything under sun. But we’re trying to understand what mediates relapse.
There are people in this room that have been in my genomics study where we put people on a bike and made them sick on purpose and then watched why they got sick. That was a heroic thing to do, we appreciate it, we’ve learned a tremendous amount from that study. We want to continue doing that study. We’re fundraising to do the last of the chronic fatigue group. We’re going to run 15 more chronic fatigue patients and then we ran out of money. I’m looking to finish that study. You can be sure we’ll look at viral expression now that we know that we should be looking for viral expression.
So, all these thing are important. They all tie together,
If any of you guys know someone that’s too sick to get out of the house and so discouraged that they look like they are going to give up , make them feel optimistic. That’s your job.
You can make a difference. You can make a difference by volunteering for studies, you can make a difference by spreading this word. If any of you guys know someone that’s too sick to get out of the house and so discouraged that they look like they are going to give up , make them feel optimistic. That’s your job. OK, this is not a good time to give up. And then finally be charitable and find charitable people to help you with that. Give, we need funds, we really do.
I’m going to stop my official talk and take questions and answers.
(Question from the audience) Over time as you discover and find the blood tests to test your patients and then you find that patients who’ve done better over time actually do have the virus. What does it mean for those types of patients?
(Answer) Patients who are recovering despite having the infection. Well, I can tell you what I would anticipate – that their immune systems are recovering. I would anticipate that people who could control their viral infection will do better. So, what you’ll hear in people’s histories very frequently, that have had this illness for a long time and had long, long, long periods of recovery, is that they tend to only get ill again if they are recovering, during times when they have a massive infection of some sort or some big immune event.
Now I’ve had it flip the other way. I’ve had more than one patient who were just very ill and just cruising on very ill and they got something terrible like a pneumonia that put them in the hospital with a high fever and huge immune
If you look at their immune systems, they are better because their immune system is better. And that has clinically been my experience. The natural killer cells are behaving better, their immune activation is less and activation drives the virus.
response and when they came out of it they were much better from their chronic fatigue. It’s like getting their immune system so… maybe it was the fever, maybe it was the immune system response, maybe with all the cytokines but sometimes you’ll see the flip of that.
But I think that people that are remit, relapse, remit, relapse - most of you guys know your pattern. Most of you guys relapse because you do too much and you crash. You’re all crashers. Because you don’t know when you are feeling well to stop acting like you are 100% because when you are feeling well you are not 100%. But, that’s a little different. That’s your body being out of balance and you don’t have the reserves of a normal person, you literally use them up and you crash.
The best question is the flip. If people are getting better over time, why are they better? If you look at their immune systems, they are better because their immune system is better. And that has clinically been my experience. The natural killer cells are behaving better, their immune activation is less and activation drives the virus.
(Thanks to Fds66 from the Phoenix Rising Forums for transcribing this. Photos and Headings supplied by Cort)
For video's of Dr. Klimas Lecture on ME/CFS Community Center
Section Three: XMRV, NK and T Cells, Latent and Retroviruses
So what is this virus X-M-R-V? Well, the RV means retrovirus. So that puts it in a family of viruses, retroviruses,Dr. Klimas on XMRV and ME/CFS that we actually know quite a bit about. And the X is xenotropic. M was mouse. This virus started in a mouse. Now there’s…ya know viruses start somewhere. They’ve got to start somewhere. Like the HIV virus started in a monkey. It’s a monkey virus that eventually evolved several hundred years ago into a virus that could infect humans. So we got this lousy virus, HIV.
XMRV is in its own evolution. And it jumped from mouse to human at some point. We don’t know when, but probably not in the too terribly distant past. Well, that doesn’t mean a lot, because in Darwin terms, distant past could be 100 million years, but these guys think like that, the evolutionary biologists. That wasn’t long ago, a thousand years ago or so. But in this mouse virus, it could have been in the last century. That’s the sense of it.
About 3-4% of people have this virus and they’re not sick. And that’s another part of this. So there’s this background population. Now, I’m just saying that flat out, but you know I gotta tell you that the research on this virus is only 2 years old. And so, we don’t know very much about it. And there’s probably regional differences. There might even be continental differences. We don’t know. There’s been nothing done anywhere else. They did some studies – originally this virus was found in prostate cancer. So most of the work was done in that area and there’s two studies: one in Germany and one in Ireland that failed to find this virus in their patients. Now, whether they’re using the same technique or it’s not in Germany, it’s not in Ireland, we don’t know. So, there’s a lot of questions still to be answered with this virus.
And for those of you who aren’t in the land of science, Science is like the Mecca of publication. If you get your stuff in Science, that’s the best place you could possibly put them.
The Science Paper - This Science paper was amazing for a number of reasons. First, this team had put together such strong science that they could go for a Science paper. And for those of you who aren’t in the land of science, Science is like the Mecca of publication. If you get your stuff in Science, that’s the best place you could possibly put them. And they don’t take just anything and they sure, sure, sure don’t take something unless it’s extremely well done, validated and tested out. So they took this paper. And if you read this paper, they not only took it, they put it in Science Express. They thought it was so important, they published it on a very fast track. And so, that was important.
And if you read the paper, you’ll see they found this virus the first way they looked. They backed up and looked from a whole different angle. Still found it. Backed up and looked from another angle. Still found it. Then, in two other ways, they had five different kinds of ways they looked for this virus. And they were able to find the virus. So I think that’s why Science was so impressed. They also used a very big population. They had 100 Chronic Fatigue patients – 101. And they had more than 200 controls. So that’s usually…scientists like that kind of stuff.
And then, the interesting thing was in this paper, the first 20 patients they studied were Chronic Fatigue patients that had developed some kind of Cancer. That’s actually how they got the Cancer guys’ attention, I’m assuming. Because Dr. Peterson’s got 30 years of stuff in his freezer and dug out everybody in his whole population that had ever gone on to develop Leukemia or Lymphoma or any other kind of Cancer. They pulled those out first and that’s actually where they first found it and that’s what got their interest up. And then they went back and looked at a bunch of others. The way they looked is very sophisticated and they found 67% that way. And then they tried to find it in all these other ways, when they added everything together, they could find the virus in roughly 95% of the patients using one technique or another, but not necessarily consistently, no matter what technique they used. But it means that there’s at least 67% of people in that Reno cohort and possibly quite a bit more.
they found this virus the first way they looked. They backed up and looked from a whole different angle. Still found it. Backed up and looked from another angle. Still found it..they had five different kinds of ways they looked for this virus. And they were able to find the virus....that’s why Science was so impressed.
A Mouse Virus - So, what is this virus? It’s a mouse virus. It was first discovered in 2005. It was discovered by prostate cancer researchers looking for a virus, viral causes of Cancer. So they found it in that study in 40% of prostate cancer. Another group looked and found it in 23%. And so there have been two studies that said: the virus is in prostate cancer. Other groups though, have not found it - in Germany or Ireland – so it’s still considered somewhat controversial.
It’s a different strain than the one seen in prostate cancer. It’s not exactly the same. Okay? I’ve already had patients whose husbands had prostate cancer thinking that they somehow infected their husband. Oh my God, I gave my husband prostate cancer. Don’t think that way, okay? It’s a different strain of the virus. They’re related, they’re closely related. But we don’t know enough to even pretend to go that far with assumptions.
It’s a virus that doesn’t have a lot of mutations. And what that means to the virology world is that it doesn’t change very much, it’s not shifting around, there’s not a whole bunch of different kinds of it. Like there is with HIV, where within a few weeks of applying an antiviral, the HIV virus can mutate away and escape and go off and do its own thing. So this is a pretty stable virus. That bodes well, particularly for vaccine work. That bodes extremely well. We don’t know what that means to the antivirals yet. It just depends on how much replication is going on.
I’ve already had patients whose husbands had prostate cancer thinking that they somehow infected their husband....Don’t think that way, okay? It’s a different strain of the virus.
ME/CFS - Why does it fit into Chronic Fatigue? Well, there’s a lot of good reasons why it fits in to Chronic Fatigue. Those of you who live and breathe this stuff might have heard me talk about natural killer cells a little bit. ((laughs)) NKs are really broken in Chronic Fatigue Syndrome and natural killer cells are part of your defense that prevents latent viruses from reactivating. And they really, really don’t work well in Chronic Fatigue Syndrome. And our group has done 20 years of work to try and figure out why – and we know why. And we also extend that to say: these natural killer cells that don’t work are closely related to a different cell, cytotoxic T-cells. And they don’t work either and between the two of them, that is your antiviral, latent viral reactivation system. Both of the systems are broken.
So, enter a virus that infects and affects natural killer cell function and that’s this one. And infects and affects T-cells, cytotoxic T-cells. That’s this one. So we’re kind of keen, we don’t know for sure, I mean this so early in the work, we’ve gone all of three weeks since that paper came out. There’s going to be a lot of work to be done. But it would make a lot of sense, a good hypothesis to construct if this virus is in there mucking up cell function, and that would make a lot of sense to what’s going on.
It also is a virus that can infect tissues that aren’t white blood cells. And we’ve always thought: something like that has to go on in Chronic Fatigue Syndrome because you all have some neuro-inflammation. Your brain has a low grade level of inflammation. And you have some inflammation in the tissues that make hormones, particularly the hypothalamic-pituitary axis. And this is a virus that has some tropism or infects that type of tissue. So it starts to make the whole picture come together. Now we don’t know enough about this virus’s tropism or what stuff it likes to infect. This is just sort of the first look and some of this may change as we get more sophisticated and look with better ways. But the sense is this virus, if it’s acting like its cousin virus HIV that likes to infect those kinds of tissues, that it’s going to have receptors that let it into other places too. Anyway, I think it fits well and I’m very excited about that fit.
(thanks to Kim on the Phoenix Rising Forums for the transcription)
Section 4: Retroviruses and A Biomarker
Latent and Active Infections - When we talk about latent viruses, this is what we’re talking about. The guy on the top is a quiet little white blood cell hanging out doing nothing because no one has asked him, it doesn’t have a job yet. If it becomes activated, it’s because something floated into the system, some antigen, some bug that it’s supposed to respond to. And in our systems we have hundreds of millions of these little quiet cells and each individual cell only knows its one little job.
Now this one’s for Epstein Barr, that one’s for Staph, and that one is for some other bug. If that bug comes into the system, then that cell is the one that gets activated. And if it had hidden inside it, in its DNA like over there, if it has inside it this little piece of virus fragment, sitting in that DNA, that cell is turned on to make all of its stuff it knows how to make. It got activated. It’s going to make cytokines, it’s going to make interleukin 2, it’s going to make ?? , oh and by the way, it’s going to make that sneaky little virus that was tucked into its DNA too. And that’s what happens.
Retroviruses are funny because we’re just chock full of them. We have little bits and pieces of retrovirus all in our DNA.
These latent infections just sit around doing nothing until that cell is activated and then boom, they start making virus stuff. Retroviruses are funny because we’re just chock full of them. We have little bits and pieces of retrovirus all in our DNA. Talk about evolution, our great, great, great, great, great, great, great grandfathers got infected with some little piece of something, maybe a chunk from a mouse back then. But it’s not a whole virus. They have just little bits and pieces, of busted up pieces of retrovirus tucked in the DNA. We think it’s an important part of the way that we evolved. That we borrow DNA from other species this way and we transfer things around. If viruses carried little pieces of information into the genome back then. And some of it was bad and that didn’t work out. And some of it was good and it carried on or it was neutral and it carried on.
Generational Transmission? - But there are some retroviruses that can be carried generation to generation as a whole and complete virus tucked into that DNA or rather enough DNA to make a whole and complete virus when it’s turned on. And this is one of those retroviruses. It can be transferred generation to generation or what’s called vertical transmission, mother or father to child through the DNA. So we don’t know if there’s 3 or 4% of background. There’s just people who have vertical transmission or if there’s some way that you can infect people back and forth in life. We don’t know that at all, okay?
XMRV transmission and CFSBut we do know that this virus is one of the ones that is vertically transmitted. We know that from the mouse data. So it can be transmitted vertically. So the question is if you have children, do your children necessarily have it? And the answer is maybe yes or maybe not. First off,
We don’t know if it’s sexually transmitted....We know HIV is, obviously, is a sexually transmitted retrovirus. But, there’s no…you’d think in 25 years, we would have seen massive numbers of spousal pairs. And we have not.
there’s two parents not one. And each only give half of the DNA, yeah, right? So in any given child, there’s only one chance in four that you can pass on any particular piece of DNA on a good day. So you don’t worry too much about kids flat out that way. And then you say: And oh, by the way in their life, they have to come across the thing that activates the virus and turns this whole mess on. And so there’s a whole lot of reasons not to get all worried about…I mean I’m not saying it couldn’t happen to your children…Of course it’s conceivable. But what’s exciting right now is we’re getting this, we’re getting the understanding of it, and we’ll probably, knock on wood, that we will be to the position where we’re actually intervening effectively before it becomes a bigger worry. But, um, I don’t know about kids. I’m saying it is a vertically transmitted virus.
Sexual Transmission? - We don’t know if it’s sexually transmitted. I will say that there are sexually transmitted retroviruses. We know HIV is, obviously, is a sexually transmitted retrovirus. But, there’s no…you’d think in 25 years, we would have seen massive numbers of spousal pairs. And we have not. You occasionally do, occasionally we do see a spousal pair. It happens. But almost always those people both had acute infection at the same time at the onset and it’s really unclear if it was transmission between the two of them or if they had some other thing happen that kicked off the whole, the whole thing. And you see household Chronic Fatigue. I mean I do see mother-daughter, father-daughter, father-son, whatever…I’ve seen it. But, in my clinical practice in the 25 years or so, it’s not very common. It doesn’t happen a lot.
So, the next slide. This virus is not HIV. A lot of people panicked when they heard this. This virus really is not HIV. It’s in the same family, but it’s a distant, distant cousin…very very distant. And it’s not infecting or affecting the same cells. So, it’s not doing the same immunologic thing that HIV does. Okay?
it’s pretty impressive that out of 101 CFS defined by clinical case definition or a research case definition that they found 99 with virus. And if this is the case, that’s pretty exciting. It’s pretty impressive. And, oh, by the way, we have a biomarker. Not a small deal.
There are also other retroviruses that don’t do anything that we know about. There’s a virus called HTLV-2 that I have studied myself in the past, and many others have, and it’s just sitting around doing nothing. It’s really…it’s vertically transmitted, it even replicates, and it doesn’t cause much in the way of illness. So, that doesn’t necessarily mean that just because you find a retrovirus, it’s definitely the deal. And not every retrovirus is big and bad and ugly. There’s another virus called HTLV-1 that’s vertically transmitted and does cause an illness. And it causes a neurologic illness. And so, we have different bugs, different things.
HIV is a retrovirus and there’s at least 20 or more drugs directed at HIV. So, will those drugs work to control this virus? That is definitely the big question of the day. And the first thing to say is: some of them probably will. And the second thing to say is, but not all of them…you couldn’t just pick a random one and try it.
This one’s to show you mouse going to people…that basically it started out way up there as a mouse thing. Mice learned to live with it. They don’t have a receptor that allows this virus to become a big bad deal. So, mice just sit around for generations and generations of mice being a reservoir of virus, but not actually getting sick from the virus. But then the virus shifted and it became capable of jumping from species to human.
Almost All Positives - One Way or the Other - So, this was the study. They had in their freezers samples from people that weren’t from their cohort. So, these were not just Reno samples. There were samples from Florida, from California, from North Carolina, and other places. Everyone in their repository had a Chronic Fatigue diagnosis. The mean age was 55. There was two thirds women. They had this large control sample. They looked…and they looked at these patients, out of 101 patients, and they looked at the DNA, the sequences of the virus in the DNA. It’s really a sophisticated way to look and they found it in 67% and in 3.75% of the 320 controls.
The XMRV /XAND Pages
Now of the negative, these 33 negatives, they went on and looked in other ways. And they found 19 of those had antibody in their plasma, so that was more than half of those negatives. But this is the big number: 30 of the negatives had virus they could identify by taking the serum of those cells, the serum from the plasma, and infecting a cell line and then growing the virus in that cell line. So they could transfer from the plasma, virus to the cell line. Now that has a lot of implications and it’s certainly the reason why, in part, the CDC, the NIH, and others that really care about the blood industry are looking long and hard at this. They found the virus, a transmissible virus, in the plasma and they were able to infect cell lines. So it is suggestive of an infective component, at least in the blood. And then there were other ways, so they worked out that they were able to find 99 of the 101 patients in that way.
Now think about that for a minute. We define an illness by a bunch of symptoms. Now, I’ll say Dr. Peterson is a really fine doctor, and I’m quite certain that he’s not misdiagnosing Chronic Fatigue Syndrome. He’s really splendid. So, it could be that he has a really clean, tight population of folks in his freezer. But I would say, I think I’m pretty damn good, and I think if I pulled out stuff from my freezer, there might be a couple of MSs in there or something else that evolved down the line. I mean, I’m not sure. But it’s pretty impressive that out of 101 CFS defined by clinical case definition or a research case definition that they found 99 with virus. And if this is the case, that’s pretty exciting. It’s pretty impressive. And, oh, by the way, we have a biomarker. Not a small deal. A biomarker – the virus itself. No better biomarker than something that’s clearly, tightly associated with an illness.
(thanks again to Kim on the Phoenix Rising Forums for the transcription)
Section 6: Virus Life Cycle, Immune Modulators (Antivirals)
And here’s the real compelling question: will antivirals work? This is a virus that’s sort of coming in to a white blood cell and it’s hunting for its receptor. And then it’s going to attach to this cell. This is a retrovirus attaching to the cell. Now in this virus, we don’t know what that receptor is yet in human. We actually sort of have an idea from the mouse work, but we don’t know for sure. But there’s an attachment step. And then the virus enters the cell. It fuses to the cell. In HIV there’s these entry inhibitors and fusion inhibitors that prevent that so there are potential therapies if it were the same receptor. I kind of doubt it. I don’t think we’ll be using those particular HIV drugs.
Then it gets into the cell and when it gets into the cell, it dumps its RNA into the cell. It pokes a little hole and the virus comes in. And then that RNA comes out. And we’re DNA, not RNA. The nucleus of our cells is DNA, so it has to be turned into DNA. And to do that, it uses an enzyme called reverse transcriptase and that turns the (see I knew before that thing before it told me. I am smart). Anyway, it turns RNA into DNA and that is a wonderful target for this virus…the reverse transcriptase inhibitors…because then the DNA can integrate into the cell. Now we have integrase integration inhibitors also…in HIV…integrase inhibitors. But they are fairly selective for HIV. I don’t know that they would be effective in another retrovirus.
..there are literally thousands of compounds in the pharmaceutical companies’ shelves that they developed for HIV that weren’t as good as things for HIV that approved that might be the very perfect thing for this virus. So, we’re not starting from scratch here with this virus – at all!
And then, when the cell is activated and its DNA starts making stuff like this, it has to be…it makes these great big long proteins and those proteins have to be cleaved into little pieces (see I’m sinking here). And that’s the protease inhibitor line in HIV, the proteases that cleave are inhibited and that prevents that piece from being torn up. And then all these bits and pieces assemble themselves over on the cell wall and they bud off – BOP – and there’s a virus. And that’s how viruses are made.
So, we have entry inhibitors, we have reverse transcriptase inhibitors, we have integrase inhibitors, we have protease inhibitors. And then all those put together is the whole repertoire of drugs that have been developed over the last 20 years or so for HIV.
But, be it known that there are literally thousands of compounds in the pharmaceutical companies’ shelves that they developed for HIV that weren’t as good as things for HIV that approved that might be the very perfect thing for this virus. So, we’re not starting from scratch here with this virus – at all! The other thing about this virus, and this is just from what Dr. Coffin said at the Chronic Fatigue meeting on Friday (I’m not a retrovirologist as brilliant as these guys) but I can parrot them pretty well. Dr. Coffin said – because this virus doesn’t seem to mutate very much, it’s a great target for vaccine trials.
And when you ask - what about antibodies? – if we vaccinated people to this virus that already had the virus, we could goose up their immune response to this particular virus. That’s what they’re doing in HIV trials, they vaccinate infected people. So you might suppress the virus with an antiviral and then goose up the immune system with vaccines, so it could really work hard on this virus and then reduce it. So you could start postulating. Isn’t it fun to be able to postulate therapies…I mean, it’s great. I’m loving this. I’m lying awake at night thinking of all these things. It’s like – oooh,we could do this – oooh, we could do that. Good stuff. I know, I know, I’m an immunologist, what can I say?
Isn’t it fun to be able to postulate therapies…I mean, it’s great. I’m loving this. I’m lying awake at night thinking of all these things. It’s like – oooh,we could do this – oooh, we could do that. Good stuff. I know, I know, I’m an immunologist, what can I say?
Ampligen - Of course one of the things I think about is immunomodulators – drugs that would either quiet immune activation or enhance cell function are very appropriate. Okay, so what’s already out there? Well, Ampligen, Ampligen’s an interesting drug. And they actually showed – they had 8 patients that had Ampligen data – that they showed at the CFSAC meeting that Dan showed. And it had a mixed result. In some cases, Ampligen was very effective in suppressing this virus, and in some cases it was not – in those 8 patients. That’s not very many. But Ampligen sounds kind of promising because it’s an antiviral that’s an immunomodulator that enhances natural killer cells and cytotoxic T-cell function. It’s even more intriguing than before in my mind, I think Ampligen’s got some real potential.
Immunovir (Isoprinosine) - some of my patients are on this medication. It’s only had phase 2 trials, it hasn’t had phase 3 trials. But it’s more or less a nutraceutical, it’s an amino acid. But it is also an NK cell enhancer and a cytotoxic T-cell enhancer that may have some antiviral effect.
Cell Therapy - this cell therapy – I referred to this ex-vivo cell therapy – some of you were in this study – It was in 1993 or…it was 1993. Well we took a lymph node from a patient and we grew the cells in a laboratory and we made literally a transfusion of white blood cells. Max did that. He was busy, busy transfusing my patients with white blood cells – their own white blood cells. But in the test, in the laboratory, we had grown them, fixed sort of what was broken about them, and then we got some very very nice clinical responses in that Phase 1, that study that never got to go to a Phase 2 study for lack of funding. And then finally, this makes cytokines that are either directly antiviral or immune enhancing more interesting.
Neutraceuticals - The nutraceuticals, they have less work done. Omega-3s are anti-inflammatory, the mushroom extracts that the Japanese use to enhance natural killer cell function, but these aren’t studies that had placebo control data and looked promising. CoQ10 at roughly 100 twice a day – that was really anti-fatiguing and enhanced cell functions. TNF inhibitors, we have a couple few patients on TNF inhibitors and I’m seeing some nice responses if they’re cytokines are way wacked out and they’re super revved up.
That’s a natural killer cell, the little guy killing that target cell. That’s an Epstein Barr virus infected target. And there’s that little white blood cell doing its job. That’s what we’re trying to do. So the white blood cells infected with virus and you want these cells to go in there and kill that cell. So, the other question with this is: okay you’ve got one virus, but what if you’ve got this virus plus a couple of other viruses? What’s the role of all these viruses all together? What about HHV-6, EBV, enteroviruses, and this virus. If we say that all these viruses are doing their work together, it might be necessary to treat more than one virus. It might be necessary to design a study that has the retrovirus piece and a Herpes virus piece because sometimes viruses lend each other machinery to make their infections more potent and damaging.
(thanks once again to Kim for the transcription)
Section : Testing for XMRV: Q&A
if I ordered a blood test on you right now and it was negative, what would happen to your soul?....yet it might not really be negative..(the) tests are going to be improved on
Ordering A Blood Test? - So, there are some issues here. That blood test only identified 67% so if I ordered a blood test on you right now and it was negative, what would happen to your soul? You know, and yet it might not really be negative, in fact it’s got a one chance in three of being wrong. The blood test that we don’t have yet that we will have very shortly, those tests are going to be improved on.
When the first HIV blood test came out it wasn’t any good either. You know, it went through stages and stages and stages before we got a really good one. Don’t rush to get the test. Why, because you’re not going to act on that test quite yet. The knowledge of being positive is not going to give you an anti viral prescription from anyone right now because we don’t know which one to give and if it’s safe or if it’s toxic. The HIV drugs are not been gentle, OK, and you guys are really tender. So, if you knew your status today it really wouldn’t change anything.
If they are right 99% of you are positive. And if they are wrong then 95% of you are positive.
Don’t rush to get the test. Why.. The knowledge of being positive is not going to give you an anti viral prescription from anyone right now... The HIV drugs are not been gentle, OK, and you guys are really tender.
So when? Soon, really soon. But you wouldn’t be able to bear the false negative right now so be careful OK. There are kits already out there, they want cash and there’s no reimbursement from your insurance provider yet. I was talking to this XMRV and Chronic fatigue syndromegreat scientist at the VA and he said, you know, my lab develops tests. That’s what we do. What’s wrong with the tests you got? Oh, I could fix that and he got all jazzed and I’m thinking, damn, get another guy in the field and you know, and he’s fixed your test, that’s great. So these people, they’re already out there and they know how to do it and tests will improve.
If you don’t have this virus – what if you didn’t. Well, you know, that’s good news too because that puts you in a different group and we know not to do all that toxic stuff to you. So that’s an important thing to do too. So don’t be discouraged even if you’re negative.
We talked about these other people that might also actually be infected. We don’t know. These are just people we are going to be looking at. The Gulf War Illness group I’m desperate to see right away because it could change the whole direction of that work and they have a fair amount of money to do that work.
So the conclusion, it really is a big thing. It’s a big thing. You should be very excited. It’s a very hopeful thing. Yeah, the research is already underway, more to come. The more we can get funded the more focused and intense we will be in getting this work done as quickly as possible. That work we were already doing plays right into this. All the genomics work and all the immunology work. That is all critical to the better understanding of this illness and how this virus plays into it.
it really is a big thing. It’s a big thing. You should be very excited. It’s a very hopeful thing.
Those of you that are in my good day bad day study, it’s nice because we’ve got your stuff already in the freezer and we’ll be looking at this virus as quickly as we can get access to the assay. That study, that’s a really important study. It looks at people in relatively better times and worse times and we’ll know if viral load is causing that. If there’s anything about this virus. We’re already looking at all the immune parameters and endocrine parameters and everything under sun. But we’re trying to understand what mediates relapse.
There are people in this room that have been in my genomics study where we put people on a bike and made them sick on purpose and then watched why they got sick. That was a heroic thing to do, we appreciate it, we’ve learned a tremendous amount from that study. We want to continue doing that study. We’re fundraising to do the last of the chronic fatigue group. We’re going to run 15 more chronic fatigue patients and then we ran out of money. I’m looking to finish that study. You can be sure we’ll look at viral expression now that we know that we should be looking for viral expression.
So, all these thing are important. They all tie together,
If any of you guys know someone that’s too sick to get out of the house and so discouraged that they look like they are going to give up , make them feel optimistic. That’s your job.
You can make a difference. You can make a difference by volunteering for studies, you can make a difference by spreading this word. If any of you guys know someone that’s too sick to get out of the house and so discouraged that they look like they are going to give up , make them feel optimistic. That’s your job. OK, this is not a good time to give up. And then finally be charitable and find charitable people to help you with that. Give, we need funds, we really do.
I’m going to stop my official talk and take questions and answers.
(Question from the audience) Over time as you discover and find the blood tests to test your patients and then you find that patients who’ve done better over time actually do have the virus. What does it mean for those types of patients?
(Answer) Patients who are recovering despite having the infection. Well, I can tell you what I would anticipate – that their immune systems are recovering. I would anticipate that people who could control their viral infection will do better. So, what you’ll hear in people’s histories very frequently, that have had this illness for a long time and had long, long, long periods of recovery, is that they tend to only get ill again if they are recovering, during times when they have a massive infection of some sort or some big immune event.
Now I’ve had it flip the other way. I’ve had more than one patient who were just very ill and just cruising on very ill and they got something terrible like a pneumonia that put them in the hospital with a high fever and huge immune
If you look at their immune systems, they are better because their immune system is better. And that has clinically been my experience. The natural killer cells are behaving better, their immune activation is less and activation drives the virus.
response and when they came out of it they were much better from their chronic fatigue. It’s like getting their immune system so… maybe it was the fever, maybe it was the immune system response, maybe with all the cytokines but sometimes you’ll see the flip of that.
But I think that people that are remit, relapse, remit, relapse - most of you guys know your pattern. Most of you guys relapse because you do too much and you crash. You’re all crashers. Because you don’t know when you are feeling well to stop acting like you are 100% because when you are feeling well you are not 100%. But, that’s a little different. That’s your body being out of balance and you don’t have the reserves of a normal person, you literally use them up and you crash.
The best question is the flip. If people are getting better over time, why are they better? If you look at their immune systems, they are better because their immune system is better. And that has clinically been my experience. The natural killer cells are behaving better, their immune activation is less and activation drives the virus.
(Thanks to Fds66 from the Phoenix Rising Forums for transcribing this. Photos and Headings supplied by Cort)
For video's of Dr. Klimas Lecture on ME/CFS Community Center