Op 20 februari was er een web broadcast tussen onderzoekers Paul Cheney en Judy Mikovits aangaande XMRV bij ME/CVS.
De video kunt u op de website van Cheney Research opnieuw bekijken.
Hieronder vindt u de transcripts van het gesprek met heel wat interessante vragen en antwoorden over XMRV bij ME/CVS. Deze transcripts werden beschikbaar gesteld door vrijwillige leden van Phoenix Rising, waarvoor dank.
door Paula Carnes, Las Vegas, NV. (c) Vertaling door Zuiderzon, ME-Gids.net
Behandelingsmogelijkheid voor XMRV
Wat met de negatieve Britse en Duitse resultaten en die VIP Dx negatieve resultaten?
Er is slechts een zeer laag gehalte XMRV in bloed op te sporen. Onderzoekers moeten alle (4) technieken gebruiken. PCR is niet efficiënt. Cultuur ook als het in lage aantallen aanwezig is in bloed. We weten nog niet waar de reservoirs van het virus zich bevinden.
Gow et al. vond in de Britse studie XMRV terug bij 4.6% van de gezonde populatie en geen bij de CVS-patiënten. Mikovits ze dat ze verschillende reagentia gebruikten en het WPI niet vraagden welk reagentia te gebruiken.
Wat te doen als je negatief testte bij het VIP Dx of als je getest wil worden?
Ga naar de WPI website en vul het vrijwilligersformulier in om deel te nemen aan hun studies. Ze verwittigen iedereen die zich aangemeld heeft voor komende studies. Ze hopen al deze patiënten verwittigd te hebben in de komende week.
Kan XMRV in de hersenen terecht komen, en in welk gebied precies?
Het komt vermoedelijk in de microglia cellen terecht die het naar de hersenen vervoert. Het kan zeker invloed hebben op het autonome zenuwstelsel. We weten niet welk deel precies van de hersenen aangedaan zijn.
Hoe wordt XMRV overgedragen?
Hou je zeker aan de HIV universele voorzorgsmaatregelen – seksuele bescherming, deel nooit scheermesjes of tandenborstels. Wees misschien ook voorzichtig met het delen van glazen, uitwisselen van speeksel. We weten het niet.
Veel CVS-patiënten hebben verhoogde RNase-L. Zou dit XMRV suggereren?
Ja, verhoogde RNase-L is een teken van een actieve virale infectie.
NK celfunctie zou verlaagd zijn en/of defect. NK cellen ruimen virussen en tumorcellen op.
CD4/CD8 ratio is abnormaal?
Mikovits zei hierover: “Dat zien we niet.”
Zou er activatie zijn van herpesvirussen – EBV, CMV, HHV6?
Ja omdat XMRV en HIV immunodeficiëntie veroorzaken. We zouden dit effect ook zien in chronische Lyme gevallen.
Zou XMRV neurologische problemen veroorzaken – stoornissen van het vestibulaire systeem?
Ja, er zou myopathie zijn, niet kunnen wandelen. Dit zou afkomstig zijn van de neurotoxiciteit van de XMRV infectie.
Veranderingen in het immuunsysteem zouden gaan over verhoogde cytokines en TGF beta.
Waren de CVS uitbraak clusters te wijten aan een retrovirus?
We denken zeker zo en zijn dit aan het onderzoeken.
Cheney bediscussieerde kort de herstelverwachting waarbij hij zei dat de leeftijd een sleutelfactor is. Mensen van over de 40 en als de patiënt langer ziek was dan 5 jaar, zouden minst kans hebben te herstellen. Ernst van de ziekte was geen punt. Je kon heel ziek en nog steeds herstellen. De graad van stress maakt het veel erger omwille van de cortisol respons. Mikovits was het eens op dit punt, cortisol voedt het virus.
Een mannelijke patiënt, met mono-achtig begin op 25-jarige leeftijd, ontwikkelde later teelbalkanker en hartritmestoornis. Zou dit allemaal gerelateerd kunnen zijn aan XMRV?
Cheney haalde aan dat hartsymptomen afkomstig zijn van rechter ventriculaire druk en diastolische disfunctie, terug te vinden bij 97% van de CVS gevallen. Je weet dat je dit hebt wanneer je niet in een winkelcentrum kan shoppen en warmte en rechtstaan energieproblemen veroorzaakt. Dit is afkomstig van energieproblemen op cellulair niveau. Opnieuw suggereerde Mikovits dat XMRV dit zou kunnen veroorzaken.
Deel I [0 – 10 min]
transcript door Kim
Cheney…in molecular biology from George Washington University and did her PhD work in the area of retrovirology, specifically how retroviruses, and specifically HIV, infect human monocytes. She studied under the legendary Dr. Frank Ruscetti at NCI, who is considered to be the father of human retrovirology, being involved in the discovery of the first human retrovirus, HTLV I in 1981. I think it’s also true, in my opinion anyway, that Judy is a superb scientist, very good in the laboratory, and it’s perhaps no accident that it needed that kind of superb scientist, laboratory scientist, to find this virus, as it has some difficulties associated with it in terms of looking at it and finding it and measuring it and we’ll get into that. So I’d like to welcome Dr. Mikovits, Judy are you on the line?
Judy – (inaudible) thank you.
Cheney – We basically had a number of questions submitted from a large group of patients from all over this country and really, all over the world. And I sort of selected, I grouped them into different categories.
- There’s a category on infectiousness.
- There’s a category on what makes this virus tick in terms of how it might be stimulated or suppressed.
- Some of it’s biology and
- some questions about therapy.
And so we’ll try to pull relevant questions from each of these groups and although your question may not be answered specifically, hopefully it will fall into one of these groupings.
I’d like to start with Judy and ask her a couple of questions having to do with how hormones might interact with XMRV, specifically androgens &/or estrogens, or even any other hormones. Judy, can you answer that?
Judy – We know from work in the laboratories of Bob Silverman and Steven Goff from Columbia University that the retrovirus XMRV has what’s known as the cis-acting element, literally the on/off switch of the virus, two androgen and hormone responsive elements. And that means that when that virus, when the on/off switch sees certain hormones, it can turn it on &/or off, so what you would want to do is have a balance of hormones and not spikes. And we really don’t know a lot of how exactly they control the expression of the virus or the reservoirs that might be involved given the hormone sensitivities or switch of the virus, but there is a hormone responsive element to the virus that we think will be critical in understanding how it might cause disease.
Cheney – I see. We’ve been looking at hormones here for several years now using the Echo Terrain Map technology which allows us to look at redox shifts, very sensitively in CFS patients. And we see, in cases of hormone testing, both on the scan or under the tongue, a rather transient and immediate responses from a redox perspective, both positive and negative. And my concern about that is that it may not necessarily reflect what happens downstream in case of a virus, but certainly redox shifts, positive or negative, might influence the virus. In that regard, my sense, over time, has been that, perhaps, a balancing act of hormones may be the best way to go and not to rely on one particular hormone to suppress it or worry about another particular hormone activating it. But it’s more about balance than any specific hormone.
Judy – Exactly.
Cheney – That would be my impression from Echo Terrain Map technology.
There’s another question, Judy, about…there are some concerns about blood banks and whether things are moving in a direction to defend the blood supply from XMRV.
Judy – We are working here at the Institute both with the National Blood Working Group that was established as soon as our paper in Science came out in October and we are setting up an experimental design to – and very sensitive assays – that as we know from other work aren’t straightforward in order to protect the blood supply. There is a very active and very large group in this country. We have been contacted by the UK, with a group doing exactly the same thing and we are participating with them to protect the blood supply. And of course, we had said at previous talks and we recommend that, until we know more, CFS patients, whether they’ve been tested or not, simply not give blood in order to prevent spread.
Cheney – Understand.
There’s one question about how long it takes to translate scientific information from the laboratory, from the bench, to the bedside. What’s your sense for the translation time from what we’re learning at the bench or in laboratories to actual patient care?
Judy – Actually, we’ve already begun that process, so if you listen to some…decades – that’s really not our policy. We are a translational research institute and we’re actually working with doctors and companies and others right now to translate that. That is why we’re developing sensitive tests for diagnostics and to monitor clinical trials. We’ve actually begun talking with – and as I understand there was a question about a compound known as peptide-T and we’re actually developing drugs in other laboratories or compounds in other laboratories. So we’re laying the groundwork right now and have begun that translational process and we are confident that we can have clinical trials as early as this year, maybe as early as even when the institute opens it’s treatment facility in September.
Cheney – So, in other words, there may be research trials available at Whittemore Peterson as early as September of 2010?
Judy – That’s correct. Other doctors throughout the United States may be able to participate with cohorts. There’s not necessarily a need to come directly here. We’re working with other physicians across the U.S.
Cheney – Are these studies likely to be free to patients who are to participate?
Judy – That is our goal.
Cheney – Okay.
Why do you think peptide-T would actually inhibit XMRV? Is there a scientific basis for that? Or is just hoped that it will?
Judy – Actually, no. On that note, Candice Pert who actually developed, discovered it and runs the company that has run clinical trials with peptide-T in HIV disease had actually, more than a decade ago, run a clinical trial in men with CFS and they saw improvement. And when our paper came out, she said – and I understand why now – she contacted me immediately and said, “We have an opportunity, we have some drug that is ready and certified by the FDA, so it’s a limited amount now, but we could run some small studies and actually follow XMRV. Peptide-T is known to interact with the monocyte, which is a cell type in your innatei mmune response, that’s known to be infected in, and actually play a role in retroviral diseases. And as we mentioned, that was my PhD thesis. So, we actually had some sound scientific rationale to actually use peptide-T in this cohort with XMRV.
Cheney – I’d like to explore another sort of generic issue and that has to do with testing. And beyond that, the recent reports out of the United Kingdom of negative results for the testing by PCR of blood in CFS patients. And beyond that, the fact that some patients who have been tested at VIPdx Laboratories in Reno using the WPI, Whittemore Peterson validated testing procedures are also negative.
And so, I’d like you to comment a little bit about the reasons why you can get negative results and importance of methodologies.
Judy – The methodologies are really critical in studying XMRV because there’s as much that we don’t know about it as we do know about it. It is apparent from the UK studies as well as the German study in prostate cancer who looked at more than 500 samples and didn’t find XMRV either by PCR and some other techniques, it is clear that what we don’t know about the virus with regard to is – it’s reservoirs – what cells it’s living in, where it is in the body. As much as we do know about the virus, so unless you use all four techniques in the Science paper for isolating it and determining the presence of the virus – in that case, failure to detect it by PCR does not mean it’s not there. And even by the culture method that is used by VIPdx right now, we are working very hard to get the serology, which means that the patient would have had an immune response to the virus and we can detect that serologically in our paper, but we don’t have that test online yet as a diagnostic or a clear certified test yet, but we hope to have that test within the next month or so, as I’ve said, maybe within weeks, to be validated for clinical use. If you went just by the virus – that is, I can’t isolate it or VIP can’t isolate it by the techniques in our paper, and you have the antibody, it is evidence that you’re infected and since the retrovirus is a lifelong infection, we simply then just don’t know the reservoir where this virus is. So this is a very low copy number, meaning it is very low level in peripheral blood. And really, unless you use all four techniques that are described in our Science paper, and go to the WPI website where we have detailed the differences in the methodologies in the different studies to give you an idea of the complexity of the issues, but also what’s necessary to detect the virus. So, we will, very shortly, have all of the testing available. (ending at 11:25)
transcript door Kim en Lilly
Judy (continued): So we will very shortly have all of the testing available but for now the best way to look for the virus is to participate in research studies and
I know there was one question on: “You told us that research studies are going to be online, when are they are coming online at the WP institute?”
Well we received word, we were waiting for word from our institutional review board for human assurance. We were waiting for approval of our studies, literally since October and given that this is a new human retrovirus our institutional review board went out really in every way to make sure that we protect patient privacy and now they are convinced we should have approval at the end of this month, in March for an XMRV study across a number of diseases and patient populations, next week. So if you’ve applied to the website and you’re waiting for an answer and you haven’t gotten one, we are going to start working through that list next week and begin these studies to do large-scale testing. And we at the institute can do all 4 tests, and we will know beyond a shadow of a doubt if you’re infected with XMRV.
Cheney: In one of the 2nd papers published out of the UK, I think it was the Jonathan Kerr paper they indicated a 4.6% serologic positivity in the UK population with an n-value over 500 and yet reported no such serologic evidence in CFS. Do you have any explanation for that?
Judy: They stated in their paper that the antibodies … which were not the antibody we used, and we are disappointed that they did not ask us either for clinical control virus or our reagents which could have answered that question. Not discouraged, but disappointed. At any rate the antibody was written in the paper not to detect the XMRV gag. So it’s very important to use, so they suggested it was just cross-reactivity with other mouse viruses and it implied that that’s what we were seeing as well. But we did validate our reagents and we know beyond a shadow of a doubt that they do detect XMRV. So it’s simply a matter of the reagents they used just did not detect XMRV and they said it in their paper so it’s a mystery why they published those data, knowing what they know.
Cheney: I have one question. Does XMRV get into the brain and is there a specific area of the brain it is more likely to affect?
Judy: We do not know that answer. I would hypothesize given what we just talked about, given about monocytes, the brain monocyte is called a microglial cell. So what we know from all human retroviruses is that they infect these cells of the immune response, that the traffic actually goes to the brain. So we don’t know what other cell types in the brain could be infected but we would suspect that the microglia, the brain monocyte, actually takes the virus to the brain, and those studies have been done in other retroviruses. And of course it’s much too early to know those answers with XMRV.
Cheney: One question was, specifically, could this affect the autonomic nervous system?
Judy: It certainly could.
Cheney: I’d like to move into another group of questions that have a lot of patients interested in and concerned about. This is the issue of infectiousness. They have been found to be infected by culture at VIPdx and are concerned about limiting the transmission from themselves to their loved-ones and family members, sexual partners and others and are very concerned about what they should do.
Judy: Again on our website on the presentation that I gave in Santa Barbara, we put those slides up and they detail that because we don’t know all of the details of transmission but we all know of situations in which people are infected in families and other situations. We think of using as much as possible HIV universal precautions. Those precautions are easily found on the website, but again they suggest
- that you practice safe sex,
- that don’t share toothbrushes, razors, things that could transmit blood.
- That you don’t give blood as we mentioned earlier,
- and just practice universal precautions.
There are certainly other things that we can do, as soon as possible we know the information about the mode of transmission we will publish as soon as possible and try to protect everyone. But the best way to protect is to diagnose, to know if you’re infected, and if you are infected then practice universal precautions.
Cheney: One of the comments that one of our patients had was when they read the universal precautions they tend to concentrate on ways that you might interact with people with blood. Their question was if this virus is found in body-secretions such as saliva for example, is there a concern about transmission from other body secretions other than blood itself?
Judy: Well there certainly is a concern but since we don’t have those data there is also a concern about maybe having the public panic. The only other body secretion we’ve ever isolated the virus from is prostatic secretions and again that’s in the case of the prostate cancer.
And so we simply don’t have enough data, but there are ways to protect yourself in the cases of suspecting saliva transmission.
- You know simply don’t share glasses,
- use a different setting in the dish washer mode and hot water,
- things like that.
It’s perhaps over-precautious, but certainly there’s no reason to accept that it’s not. You know HIV/Aids you can certainly kiss, hug infected people and their not spreading virus that way. So there is no reason to suspect that you can’t have normal contact with infected individuals.
Cheney: One of the things that interested me was the potential infection rate in the country of 3.8% which rounds out to about 10 million Americans who may be infected but are not sick compared to let’s say 1 million CFS patients who are infected and let’s say disabled, suggesting that the majority of people, maybe even as much as 90% of people that become infected do not get CFS, although they actually may be infected with XMRV. That being said, then that could make the relative infectiousness of this sort-of subterranean in that it could be transmitted but since it’s not causing disease, or apparent disease anyway in the great majority of those infected, it’s hard to evaluate the infectiousness of this based upon watching an isolated case and those around them. On the other hand it also suggests that if only 10 million Americans are infected after goodness maybe decades of presence that this must not be a terribly-infectious agent.
Deel III – [20 min – 30 min]
transcript door Lily
Cheney: If it were, we’d see a lot more than 10 million Americans infected with it, so there must be something that’s inhibiting the effective transmission of that agent given those numbers. Ten million versus let’s say one million. And also many people infected simply don’t get sick. At least they don’t get sick with CFS.
I’d like to turn next to that which I thought was a very interesting and very broad question, Judy, having to do with what is it about the biology and the pathophysiology of a retrovirus – let’s say it that way rather than XMRV it’s self – what is it about the biology and the pathophysiology of a retrovirus that fits with the syndrome of CFS? What is it that overlaps what we know about CFS and the possibility that a retrovirus might actually be causing this illness? Is there something about XMRV or a retrovirus in general, that fit with what we’re seeing? And I’ve made a sort of a list of things and maybe I’ll just go through them, Judy, and see if you either agree or disagree and want to add to it?
Number one: We found evidence of elevated RNase-L activity in the Lake Tahoe epidemic of CFS way back in 1985. RNase-L activity suggests the presence of a viral infection.
Judy: That’s correct, I’ve checked. It can’t do it’s job and it can do a lot of bad things and overactive RNase-L will cause the cell to die and apoptosis and split it’s self immediately into the blood stream.
Cheney: The very presence of RNase-L suggests viral etiology for that epidemic.
Judy: That’s correct.
Cheney: NK function seems to define the illness. The very first paper on this was out of Japan back in 1987 describing what they said was low NK Syndrome which is CFS back in Japan. And low NK syndrome has been a feature of this disease. Do you think basically, XMRV can cause low NK function?
Judy: Absolutely. A Natural Killer cell’s job is to clear viral infected cells and to clear tumor cells. So if you have a retrovirus present which unchecked, it’s continually expressed, and the NK cell can’t clear it, it [NK cell] eventually becomes exhausted and of course, the virus can do something to the NK cell to allow it to persist. So cells whose job it is to kill virus infected cells can’t kill XMRV or can’t clear it, would then have defective NK cells, a persistent marker of infection.
Cheney: In the Lake Tahoe epidemic many years ago, but also here in my clinic in Ashville, we frequently see an elevated CD4 to CD8 ratio, primarily due to CD8 depletion, and I wonder if you might comment. Is CD8 depletion something that XMRV might be able to cause?
Judy: We don’t see XMRV as a cytotoxic virus, thus far. Certainly, it is possible through indirect effects, through mediators or what’s known as cytokines, we could see dysregulation of the adaptive immune response which is the CD8 cell. But we don’t see direct cytopathic. More this virus seems to be like HTLV-1 and not kill it’s cells like HIV.
Cheney: The CFS is highly associated with activation of herpes group viruses, especially EBV, HHV-6 and CMV. I was wondering if XMRV infection is consistent with the activation of other human herpes viruses that they are already infected with.
Judy: Yes, because XMRV, because the hypothesis is that the virus creates an underlying immune deficiency, se as you just said, the NK and maybe the CD8 cells don’t work so you’ve got an underlying immune deficiency, so if your immune system can’t do it’s job, so that viruses that you harbor in your body like EBV and CMV which are near ubiquitous around the world, are not able to be controlled by an immune system that is not functioning up to par and actually immune deficient so, the hypothesis is, just like HIV/AIDS, it creates an underlying immune deficiency. So, as you know, CMV retinitis is an AIDS defining illness, as is chronic EBV and EBV malignancy. So it makes perfect sense how a retrovirus can cause an underlying immune deficiency. Essentially, we see what we see in this disease, not only herpes viruses but things like chronic lyme, which are also found in CFS cohorts.
Cheney: There’s a lot of brain involvement in CFS and it comes in the form of neuro-cognitive complaints; it comes in the form of neuro-behavioral shifts; it comes in the form of abnormal MRI scans that are typically non-specific but abnormal; it comes in the form of subtle neurological findings on exams such as hyper-reflexia and disturbances of the vestibular apparatus. So my question is, do you think XMRV could be be causing neurological problems like this?
Judy: Oh absolutely, and again we go back to other retroviruses, HTLV-1, in addition to leukemia that it is causative for, has associated with it a disease called HTVL-1 associated myelopathy, where it is a myelopathy type disease. The patients stagger, can’t walk, end up in wheelchairs, and it is related directly to viral load but they don’t understand all of the mechanisms. Importantly, in XMRV family members in animals the envelope protein actually is a neurotoxin, so parts of the viruses by themselves, without all the infectious replicating virus, can cause neurotoxicity. We are actually investigating the envelope protein of this virus as potentially a neurotoxin.
Cheney: A lot of these patients, if you investigate their immune system, there’s evidence of significant activation of the immune system of almost any parameter that you look at, particularly cytokine elevations of various kinds and evidence of TGF beta 1 activations. Suggesting the immune system is really activated and there’s kind of a counter response trying to tone it down. Is immune activation, which we almost see universally by cytokine markers consistent with XMRV infection?
Judy: Well yes, and every other retroviral infection, absolutely. Again, it goes unchecked, so the immune system is trying to do it’s job, clear the virus, keep the virus down, and when the virus goes unchecked, it causes the kind of things we discussed with elevated T cells as the problem. So in the face of chronic inflammation you develop immune deficiency.
Cheney: And this is sort of a cross-over from the biology and pathophysiology to infectiousness issue. We see CFS occurring in clusters. We’ve seen cluster formations for 25 years. We were involved in a cluster in Lake Tahoe; a cluster in Yearington; a cluster in Placerville; and David Bell was in a cluster in Lyndonville, NY. We see clusters in school systems. We see clusters in families. We see clusters in airline attendants. This is interesting. Is it possible that these clusters could be driven by a retrovirus?
Judy: Absolutely. It’s highly possible and we are actively investigating it.
Transcript door OvertheHills
Well here is my attempt at part IV. There are one or two words I couldn’t get (indicated by ??) and probably many more where I got it wrong, so I will be pleased to get corrections from anyone. It’s pretty technical at times (as well as hard to hear), so I’ve kept it close to verbatim although that makes it a little rambling and repititious, sorry.
Q. Paul Cheney: Let me move on.These are some questions Judy, that are probably more directed at me. What kind of risk factors are there in either extended illness, or in getting ill, in terms of prognosis basically, does age matter? does length of illness matter? does severity of illness matter?
A. Paul Cheney: Its my opinion that the most important thing that matters is age. It seemed to me that the younger that people are the better chance they have of getting over at least significant illness such as chronic fatigue syndrome but as you age and get older and older and older it seems its tougher and tougher and tougher to recover from an illness especially after you’ve had it for more than about five years. So length of illness seems to be a variable in prognosis but especially age is a variable.
I have not found that severity is an important determinant of prognosis. I’ve seen very, very sick people both young and old that have been sick for several years who seem to get over this syndrome of chronic fatigue. But if they’ve had it for longer than five years and they are older, and old here is over forty, then it seemed to be tougher and tougher to see a complete cure, though people do get substantially better.
One of the variables that seems to also be in play in prognosis and in how severe the illness is, is the degree of stress in ones life and the chaos, the psychosocial chaos one is in and I just wanted to ask Judy if stress, and specifically the accompanying steroid hormone response such as cortisol during stress.
Q. Paul Cheney: Does cortisol, which is activated in the stress response system, could it play a role in activating XMRV?
A. Judy Mikovits: Yes, part of that switch I mentioned at the beginning of the talk there is a cortisol responsive on-switch for the virus. Every time cortisol is present in the cells when the virus is present, it can turn it on, so you’re spreading the virus ever so slowly throughout your healthy immune cells and the idea is the more cells that get sick, the more clinical symptoms you see.
Q. Paul Cheney: I have one sort of interesting question, it came to some extent from out of left field. He said he had a testicular cancer, in his case a seminoma, he’s had Chronic Fatigue syndrome for 24 years, beginning as a mono-like illness young in life (I believe he was 25 years old). Many years later he developed a seminoma, he also developed a syndrome known as Brugada’s Syndrome [http://en.wikipedia.org/wiki/Brugada_syndrome] which is a disorder of cardiac rhythm disturbances that can lead to ventricular fibrillation and sudden death. His question is, could XMRV possibly explain both the testicular cancer that erupted years later and also a disturbance of cardiac rhythm?
A. Judy Mikovits: Yes it can be postulated and very testable hypothesis for us, certainly there are many symptoms and we do have evidence that XMRV can infect cardiac myocytes and pericytes so there is reason to suspect that and I don’t know clinically about the development of seminoma, but if inflammation is involved and these stromal cells can promote the progression of a tumour, that’s a testable hypothesis, that could indeed explain all three conditions.
A: Paul Cheney: One of the interesting things about Brugada’s Syndrome, assuming you don’t have a genetic defect, and only 20% of cases have a genetic defect, 80% do not appear to [have one]. On echocardiography we see evidence of increased right ventricular strain which is a compensatory mechanism for diastolic dysfunction common to CFS patients. Increased strain on the RV (right ventricle) could possibly cause a Brugada-like Syndrome since the (a)etiology of some of the rhythm problems appeared to be around the right ventricular area and there’s right ventricular disturbances on pathology seen. So I think the link could be there.
In the case of diastolic dysfunction which is really about energy problems, it is known that HIV can affect oxygen-handling enzyme systems which would result in an energy loss and that could then translate into diastolic dysfunction which we see in a whopping 97% of cases.
Interesting compensatory mechanisms to a lack of left ventricular filling, is you use your left atrium to contract more and you use your right ventricle to contract more, to help fill the left ventricle which is not properly filling by(because of) energy issues.
It is also important to note that diastolic dysfunction would make you very sensitive to orthostatic intolerance (OI) the inability to stand for a long time, to window-shop in a mall, would be severely limited due to diastolic dysfunction. The interesting thing about diastolic dysfunction is one of the seminal clinical indicators is the inability to stand for any length of time, the inability to get hot and stand, inability to do well with hot showers is all an indication of diastolic dysfunction, which is a filling defect which would be made worse by either getting hotter or standing up. Again this diastolic dysfunction is linked with energy problems at the cell level which could arise hypothetically if XMRV interferes with these oxygen-handling enzyme systems. That’s certainly a testable hypothesis.
Q. Paul Cheney: We are getting near the end of this session, so Judy are there any more comments you would like to make either on XMRV or the future work of the WPI ?
A. Judy Mikovits: Oh yes, so the institute is moving forward, we wanted to thank everybody who asked questions through our website or through Paul’s website. We will endeavour to answer those that we didn’t answer and some who asked me more specific questions I will answer.
We’re moving forward in better diagnostics and therapeutic opportunities on several fronts, from the development of anti-retrovirals to the development of immune modulators and understanding how the immune system, how the host, the human, interacts with the virus.
We are continually encouraged by everything and all the support we get from you, and from the patients, and the patient support groups worldwide, and we certainly appreciate it.
Please keep your questions coming in we endeavour (although we fail) to answer every one in a timely manner. But we will have that research approval finally for that study next week, so do look for that, as we’ll be calling you and asking for your participation and we certainly appreciate it, to unravel all the mysteries of XMRV and its role in CFS and other diseases, so thanks again for all your support.
Paul Cheney: I think we’ve about exhausted our patients, they only last about 40 minutes anyway, so I’ll draw this to a conclusion. I’d like to thank very much Judy for being here today and answering all of these questions. For the audience, this will be available for rebroadcast on the public blog section of the Cheney research website. We plan to do these again in the future either monthly or bi-monthly on various topics that come up. We’ll let you know more about that through our newsletter. Thanks for joining [Recording Terminates 38.40]
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