Since the first association of the retrovirus XMRV with chronic fatigue syndrome in 2009 in the US, subsequent studies have failed to detect evidence of infection in patients from the US, Europe, and China. These studies were potentially compromised by a number of factors, such as differences in patient characterization, geographic locations, clinical samples used, and methods used to detect the virus. These and other potentially confounding conditions have been addressed in the most comprehensive study to date on the association of XMRV with CFS.
In the introduction to their paper, published in the Journal of Virology, the authors note other problems with many of the studies of XMRV in CFS patients:
- Too small control populations
- Patient and control samples collected at different times
- Investigators generally not blinded to sample identity
- PCR assays that rely on conservation of viral sequence mainly used
- Limits of detection, reproducibility, and precision of assays unknown
- Controls for each step that would identify analysis not done
- Insufficient numbers of negative controls included
- No study included positive samples from the original 2009 patient cohort of Lombardi et al.
To address these issues, the authors collected blood from 105 CFS patients and 200 healthy volunteers in the Salt Lake City area. One hundred of the patients fulfilled both the CDC-Fukuda and the Canadian consensus criteria for diagnosis of ME/CFS. The patients were selected from a clinic that specializes in the diagnosis and management of CFS and fibromyalgia.
New blood samples were also collected (by a third party) from 14 patients from the original study by Lombardi et al. The samples were blinded for subsequent study. Detection of viral nucleic acids was done using four different PCR assays. Anti-XMRV antibodies in patient sera were detected by ELISA. Finally, virus growth from clinical specimens was attempted in cell culture. The authors used the multiple experimental approaches reported by Lombardi and colleagues.
Let’s go through the results of each assay separately.
PCR for viral nucleic acids. Four different quantitative PCR assays were developed that detect different regions of the viral genome. The assay for pol sequences has been used by several groups and is the most specific PCR assay for XMRV. Three other PCR assays were also used that target the LTR, gag and env regions of XMRV DNA. These assays could detect at least 5 viral copies of XMRV DNA. The precision and reproducibility of the PCR assays, as well as their specificity for XMRV, were also demonstrated. DNA prepared from white blood cells of 100 CFS patients and 200 controls were negative for XMRV. For every 96 PCR reactions, 12 water controls were included; these were always negative for XMRV DNA.
XMRV antibodies in human sera. To detect XMRV antibodies in human serum, a portion of the viral envelope protein, called SU, was expressed in cells and purified from the cell culture medium. The SU protein was attached to plastic supports, and human serum was added. Any anti-XMRV antibodies in human sera will attach to the SU protein and can subsequently be detected by a colorimetric assay (we have discussed this type of assay previously). This assay revealed no differences in the amount of bound human antibodies for sera from CFS patients or healthy controls. Some of the patient sera were also used in western blot analysis. Recombinant XMRV SU protein was fractionated by gel electrophoresis. The protein on the gel is then transferred to a membrane which is mixed with human serum. If there are anti-XMRV antibodies in the human serum, they will react with the SU protein on the membrane, and can be detected by a colorimetric assay. When rabbit anti-XMRV serum was used in this assay, the SU protein was readily detected. None of the human sera analyzed by this method were found to contain antibodies that detect SU protein.
Infectious XMRV in human plasma. It has been suggested that the most sensitive method for detecting XMRV in patients is to inoculate cultured cells with clinical material and look for evidence of XMRV replication. The XMRV-susceptible cell line LNCaP was therefore infected with 0.1 ml of plasma from 31 patients and 34 healthy volunteers; negative and positive controls were also included. Viral replication was measured by western blot analysis and quantitative PCR. No viral protein or DNA was detected in any culture after incubation for up to 6 weeks.
Analysis of previously XMRV-positive samples. Blood was drawn from twenty-five patients who had tested positive for XMRV as reported by Lombardi et al. These samples were all found to be negative for XMRV DNA and antibodies by the PCR and ELISA assays described above. In addition, no infectious XMRV could be cultured from these 25 samples.
Presence of mouse DNA. After not finding XMRV using qPCR, serological, and viral culture assays, the authors used the nested PCR assay described by Lo et al. Although positives were observed, they were not consistent between different assays. This led the authors to look for contamination in their PCR reagents. After examination of each component, they found that two different versions of Taq polymerase, the enzyme used in PCR assays, contained trace amounts of mouse DNA.
Given the care with which these numerous assays were developed and conducted, it is possible to conclude with great certainty that the patient samples examined in this study do not contain XMRV DNA or antibodies to the virus. It’s not clear why the 14 patients resampled from the original Lombardi et al. study were negative for XMRV in this new study. The authors suggest one possibility: presence of “trace amounts of mouse DNA in the Taq polymerase enzymes used in these previous studies”. I believe that it is important to determine the source of XMRV in samples that have been previously tested positive for viral nucleic acid or antibodies. Without this information, questions about the involvement of XMRV in CFS will continue to linger in the minds of many non-scientists.
At the end of the manuscript the authors state their conclusion from this study:
Given the lack of evidence for XMRV or XMRV-like viruses in our cohort of CFS patients, as well as the lack of these viruses in a set of patients previously tested positive, we feel that that XMRV is not associated with CFS. We are forced to conclude that prescribing antiretroviral agents to CFS patients is insufficiently justified and potentially dangerous.
They also note that there is “still a wealth of prior data to encourage further research into the involvement of other infectious agents in CFS, and these efforts must continue.”
Clifford H. Shin, Lucinda Bateman, Robert Schlaberg, Ashley M. Bunker, Christopher J. Leonard, Ronald W. Hughen, Alan R. Light, Kathleen C. Light, & Ila R. Singh1* (2011). Absence of XMRV and other MLV-related viruses in patients with Chronic Fatigue Syndrome. Journal of Virology : 10.1128/JVI.00693-11
I was wondering the same thing. They figured out what was causing polio in 1908. The etiology of TB was figured out in 1882. Numerous other diseases were figured out prior to 1950. Back then I don’t think they had 1% of the technology we have now. If they could figure out what caused Polio back then, there is no reason they can’t figure out the etiology of ME/CFS now. Especially given its fairly obvious infectious signature. Looking back over the last 30 years, the only factor that has held this back is lack of will, focus, and funding. If someone finally decides to solve this illness and can get resources, it will be solved – probably in short order.
I almost wonder if all of the modern technology and illness theory has been more of a detrimental distraction than an aide. We need to go back to the roots of scientific research on this one. Stop with the measuring all the crazy parameters that go along with secondary phenomena. The simplest solution is probably the correct one. Illness = bug. Find bug. Find how to get rid of bug or prevent bug. Done.
As a ME/CFS patient, I strongly suggest that it is time to stop debating the XMRV link. It was certainly an exciting and worthwhile hypothesis, but we now need to move on. There are lots of new potential hypothesis, particularly with the recent spinal fluid Proteome study for example.
The CDC did test WPI samples. As I reported on CFS Central on August 13, 2010, “One of the CDC slides from last week’s Blood Safety Advisory Committee meeting showed that the CDC tested 20 samples from Chronic Fatigue Syndrome (CFS) patients that the Whittemore Peterson Institute (WPI) found to be positive for the retrovirus XMRV. But, according to the slide, the CDC didn’t find any positives among those 20.”
Earlier, on August 8, 2010, I posted an article on CFS Central about how I had queried the CDC’s Dr. Stephan Monroe via email about the CDC’s negative XMRV study, including why the government agency omitted from its paper the fact that the CDC had indeed tested those 20 WPI positive samples.
Rather than answer my question, Monroe simply ran up the next question—deleting its bullet point, thereby altering the questions as posed.
Mindy Kitei
CFS Central
http://www.cfscentral.com
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If the authors of this paper wished to determine if the virus was present they should have tried replication or validated their assays. Without this, they cannot claim that they are capable of detecting HGRVs. Thus they cannot claim there is no virus present. The Lombardi PCR conditions themselves is evidence you are seeking. They lowered the stringency of the primers. This is what Lo et al did too.
Sensitivity is the problem. VP62 is not representative of HGRVs. If HIV was approached this way than any virus not matching a clone would not be HIV. Millions would be declared negative for infection. This is not how the scientific community has been approaching virology and it is not how it will continue.
The WPI has not switched their assays for the Blood Working Group. They were however asked to try and create a Whole blood assay, which they don’t use in their research.
If people don’t understand this field, then they won’t ask why the CDC was able to switch assays. They don’t have to be smart, they are relying on others being uneducated.
If as you say ” it’s wholly illogical that they actually abondened their working assay” then why did they switch assays?
The evidence does not support the rest of your remark.
A clone is not wild-type virus.
Are you suggesting that this virus has magically appeared? What were the clones created from?
The point is that regulators are never going to allow someone to claim their assay works if they have never demonstrated that it can. Clinically positive samples are required.
The CDC in their study didn’t say Lombardi used Nested PCR. Does that help you?
The scientific method has not been tried and tested for thousands of years. It has been in developmenent for more than a thousand years, but modern scientifc methodology is really relatively young.
Furthermore, if this is indeed the normal way in which science progresses, I am sure that you can point us to a couple of those “exact replication studies” in this field?
You will not find any, for the reason that it is not the way science progresses. It’s a construct made up on the forums to explain away all current and future negative results.
When a “replication study” proves WPI wrong, you will argue that it apparently didn’t fully replicate the WPI’s methods because, if it did, the results would have been the same.
No, they didn’t. Read the paper.
Read the bit before.
This is a pedigreed negative sample! 😉 And when you (falsely) detect XMRV in a pedigreed negative sample, it must mean that your assay is not well calibrated.
How would you know WPI is rightfully detecting XMRV in those patients and Singh is wrong in not finding XMRV?
Thank you for demonstrating the point.
There wasn’t that much of a disincentive to reporting those results since 99.9+% of people will never hear of it. They will just hear the press release of CDC saying their study didn’t find XMRV. CDC can’t be relied on at all to tell the truth or do bona fide science in the area of ME. This is well established over the past 27 years.
“Please answer this: if the CDC didn’t want to detect those “known positives”, why did they report them? Reporting positives and then “switching assays” doesn’t seem like a smart thing to do when you are covering up evidence….”
It was 10 years after the discovery that they isolated HIV. HIV was discovered in 1983. A blood test was available in 1985.
“The U.S. Food and Drug Administration (FDA)
approved the first antiretroviral drug, zidovudine
(AZT; Retrovir), in 1987.”
http://www.hivandhepatitis.com/recent/lipo/treatment_naive/Treatment_Naive_HIV_10.pdf
When they don’t replicate they use clinically positive samples.
I’d say, given the extensive methodology used (with F. Ruscetti helping her), doing PCR, antibody and culturing for 42 days, the parsimonious conclusion is that somehow WPI got it wrong. Consistently not finding it in the blood of patients or controls implies that XMRV is not present in those samples (and the general population).
You keep arguing in circles. Please answer: if the WPI’s results are wrong, how could an independent scientist ever offer proof for this? Any false finding in the history of retrovirology could never be corrected by fellow scientists with your methodology, as any failure to find the same as the scientists that reported the false finding, could be explained away with your circular logic. Do you at least not see that is the implication from your line of reasoning?
I agree. CDC has been dispensing Tenofovir (also effective against XMRV, at least in vitro) to large numbers of HIV-negative people in Africa for years and now in San Francisco to study its potential in preventing HIV infection. There’s been little toxicity reported. But according to CDC and other enemies of ME science, Tenofovir is too toxic for ME patients to take!
I am a layperson, but I don’t understand the argument that I have heard from you and from a scientist at the ME SoK conference that pwME taking a course of ARVs will not produce any useful data and will probably be harmful to the science. What if, say 100 pwME took Tenofovir and on message boards and blogs, say 50% reported dramatic improvement over the course of a year and only, say 5% reported significant side effects. This seems like extremely useful information. If this were the case, I would go on ARVs.
For all the shouts of proper scientific methodology, it doesn’t worry you one bit that you cannot find me one single example where scientists actually used your proposed methodology?
In fact, neither Mikovits, Ruscetti, Alter, Lo nor anyone involved in the positive XMRV studies have never done a proper replication study (by your definition) in their lives.
And you’re dead wrong: the methodology I propose is the normal way of validating findings and there will be plenty of new scientific discoveries. As I have explained before, the scientific method as we now know it has not been working for thousands of years, but your circular way of affirming dogmatic beliefs has.
Dear Vincent,
I am sure you will discuss this on TWiV. Please could you also comment upon:
Analysis of cerebrospinal fluid from chronic fatigue syndrome patients for multiple human ubiquitous viruses and xenotropic murine leukemia-related virus
1. Steven E. Schutzer MD1,*,
2. Megan A. Rounds MS3,
3. Benjamin H. Natelson MD1,2,4,
4. David J. Ecker PhD3,
5. Mark W. Eshoo PhD3
Article first published online: 6 APR 2011
DOI: 10.1002/ana.22389
Annals of Neurology
Volume 69, Issue 4, pages 735–738, April 2011
Thanks.
There is no link to those mentioned slides. The CDC have tested those 20 samples for XMRV and mouse contamination. They found neither.
van Kuppeveld
“We would also like to report that WPI researchers have previously detected XMRV in
patient samples from both Dr. Kerr’s and Dr. van Kuppeveld’s cohorts prior to the
completion of their own studies, as they requested. We have email communication that
confirms both doctors were aware of these findings before publishing their negative
papers. In addition, Dr. van Kuppeveld asked for and received reagents and a positive
patient sample to determine if his testing procedures could in fact detect XMRV in a
positive blood sample before he published his paper. We wonder why these materials
were not used in his study which also failed to detect XMRV.”
http://www.wpinstitute.org/news/docs/DearDrMcClureaw4.pdf
The antibody test was not non specific. It was for an MLV virus.
I agree that dramatic improvement with ARVs anecdotally reported in a small number of people does not mean that XMRV is associated with ME. However, it does very strongly suggest that one or more retroviruses susceptible to the particular ARVs used is/are the ‘but for’ cause of ME in these patients. This is extremely important information and at some threshold point would persuade me to take ARVs regardless of the lack of a study.
They don’t know the reason for those results, but it has been suggested that the virus breaking up makes it easier to detect in older blood.
You’ll have to write WPI about that that statement is not correct only 2 were positive not 14 . Ila Singh has misspoke .
The study was not thorough or well designed. It used novel unvalidated assays. It doesn’t matter how many you have, as there are multiple parameters and an infinite amount of variations. The authors can say that they could not detect a known clinically positive sample. They cannot state, that if they used previously proven methods, or if they had calibrated to known clinically positive samples, that those people tested were negative or positive. Let’s replicate and see what the results are. That is how the scientific method works.
Yet, she the paper found no positives in the general population using unvalidated novel assays.
The only way to do it is to replicate. It is standard practice to use known clinically positive samples to calibrate an assay. There is no other way to know that a test works.
The first question is where is the evidence that they have ever been found positive? The second, is if they have and the data has not been published, then do you accept it or ignore it? Currently, even though the WPI, NCI and others are reporting finding poly’s, xeno’s and modified poly’s, those who have a belief that this must be contamination (no evidence), refuse to take into account when conducting their research what others are doing and finding in their research and reporting in conferences. They can’t have it both ways.
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You are making less and less sense:
“Sensitivity is the problem. VP62 is not representative of HGRV”
The second sentence contradicts the first.
Please bear in mind that, if sensitivity were indeed the problem, the Lombardi findings would already have been invalidated (in your eyes) as far more sensitive assays have found nothing.
The issue is specificity as (in your eyes) the non-Lombardi assays are specific for VP62 and will not detect non-VP62 strains of XMRV. Thus, they are too specific.
You’re welcome.
This is “well established” on the forums, where crazy conspiracy theories are met without much critisicm.
Your assertion that there isn’t much of an disincentive for the CDC to report these results is really illogical. They know that these results will be reported by various news outlets and journals (for instance, even ScienceMag reported these CDC’s positives of WPI’s samples). It would have been very simple to just say ‘uh, we didn’t find anything’ but instead, they found XMRV, decided to switch assyays to cover this up in the future , but still reported these positives AND reported that they have switched assays?
I don’t want to offend, but that’s crazy. Why would the CDC even acknowledge that they had switched assays if their objective was to “bury” their earlier findings?
I did. When you look above you’ll read the quotes from the paper and the SOM. There is no bit before that implies otherwise
So I guess you do think that Lombardi et al. are lying when they clearly state they have used nested PCR?
Gob, we just love how you mysteriously imply that you know just a little bit more than the rest of us (while making error upon error).
At least I am glad that you or Gerwyn are not asserting or implying anymore that the original 67% Science result was obtained using culturing before doing PCR.
Pingback: Study Finds No Link Between XMRV and Chronic Fatigue Syndrome | DnBillBoard
Prof. R, you said:
“it is possible to conclude with great certainty that the patient samples examined in this study do not contain XMRV DNA or antibodies to the virus… I believe that it is important to determine the source of XMRV in samples that have been previously tested positive for viral nucleic acid or antibodies. Without this information, questions about the involvement of XMRV in CFS will continue to linger in the minds of many non-scientists.”
I take your statement to mean that you are certain that XMRV did not exist in these samples or even in tissues of the patients from whom the samples were derived. Is that correct?
I am a layperson and have a very incomplete understanding of the science that has been done in this area. But it seems to me that, considering the possibility that detection methods may not be totally perfect, the below evidence, plus the mountain of circumstantial evidence that a retrovirus(es), likely including HGRVs are involved in ME, it seems to me that it is unlikely that XMRV is meaningfully related to ME, but that it is not certain. This is an important distinction given the stakes for patients. And that even if XMRV proper is not associated with ME, that it is likely that one or more other retroviruses, especially HGRVs, are associated with ME. What do you think?
Gob said: “One of those patients was the source of a sequenced infectious clone and the famous EM image of the budding virus.”
I did and there is nothing there that implies otherwise. Lomardi et al. performed nested PCR and got their 67% result. Please don’t play the “I know more than you do but I won’t tell exactly what” game here.
State what is exactly wrong with that or concede that you are wrong in asserting that “The Lombardi et al results were not based on Nested PCR” (<–statement by Gob)
Still not found a single example, Gob? Not one example of a true relication study in the field of (retro)virology, nor an example of a validation study that assumed the findings of the study it was trying to validate were correct beforehand? Please enlighten us with just a single historical example….
How can this then be the “only normal way in which science progresses”?
You are digging your own hole here, Gob.
With those samples you now refer to, Van Kuppenveld DID detect XMRV. In other words, in your circular methodology, his assay was VALIDATED through clinical samples provided to him by WPI!
From the very same letter you incorrectly referred to earlier:
“…our findings were based on solid, sensitive PCRs (described in detail in our paper) that
efficiently detected XMRV in a cell line, as well as in positive samples that were provided to us
by Dr. Judy Mikovits”
Thank you for this report. Also, thank you very much for the previous Twiv interviewing Dr. Singh. She came across as a very careful and methodical researcher from Columbia. ( My niece just got her graduate degree from there. I get the impression that is a fine institution there.)
I wonder what this means for the future of XMRV in prostate cancer. ..Will stay tuned…
It’s standard practice but you cannot provide us with a single replication study that uses said (circular) methodology.
In fact, replicating the original study would mean that you cannot calibrate your assays to the results of the original study, as you would then not be independently replicating it. Remember that the original study also did not calibrate its own assays to its positives results (as the universe would then collapse 😉 ).
Dear Vincent,
It would be great to see this topic be discussed on TWiv. This kind of research into possible infectious agents involved in CFS could be an example and opportunity to discuss how scientists can search for an unknown pathogen in a disease with suspected infectious aetiology. Available techniques and difficulties.
In the case of CFS there is immunological evidence which supports the possibility of an infectious aetiology. How can virologists (or microbiologists in general) use the information gained by immunologists to direct their search for the virus (or other pathogen) possibly causing this disease?
The following are a review of the immunology in CFS, and a more recent and very interesting study using a systems biology approach to study cytokine expression profiles.
1) Lorusso L, Mikhaylova SV, Capelli E, Ferrari D, Ngonga GK, Ricevuti G.
Immunological aspects of chronic fatigue syndrome. Autoimmun Rev. 2009
Feb;8(4):287-91. Epub 2008 Sep 16. Review. PubMed PMID: 18801465.
2) Broderick G, Fuite J, Kreitz A, Vernon SD, Klimas N, Fletcher MA. A formal
analysis of cytokine networks in chronic fatigue syndrome. Brain Behav Immun.
2010 Oct;24(7):1209-17. Epub 2010 May 4. PubMed PMID: 20447453; PubMed Central
PMCID: PMC2939140.
And a third study that may ad to the paper pointed out by JEV P20778 in the post above.
Sullivan PF, Allander T, Lysholm F, Goh S, Persson B, Jacks A, Evengård B,
Pedersen NL, Andersson B. An unbiased metagenomic search for infectious agents
using monozygotic twins discordant for chronic fatigue. BMC Microbiol. 2011 Jan
2;11:2. PubMed PMID: 21194495; PubMed Central PMCID: PMC3022642.
I really look forward to listening to a TWiV this.
And thank you for the many things I already learned through listening to TWiV.
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I used to think that Ila Singh was “on our side”. Now she’s involved in poor testing techniques that can’t even find XMRV in WPI’s patients’ +ve samples. Use of wrong culture cells, refrozen samples, wrong PCR reagents, annealing temperatures – there’s so many places to go wrong. I’m sure Judy M will be easily able to shoot holes in this paper. Just WHY DON”T these people use exactly the same techniques etc as WPI?
And as for “… encourage further research into the involvement of other infectious agents in CFS, and these efforts must continueâ€, this is evidence to say that this team has been nobbled by the Dark Forces, in that they are trying to divert attention away from XMRV and into various blind alleys.
Perhaps a clinical trial of antiretrovirals is the best way to go from here. We have a number of anecdotes saying that patients have improved markedly after some months on ARV’s. How many anecdotes constitute scientific proof? 10? 100? We’ve known it’s a retrovirus for 25 years, so why not try ARV’s? They’re no worse than long-term antibiotics, and my son has been on a tetracycline for over a year – for acne.
No, it is beyond cavil that the m.o. of CDC re ME has generally been anti-science and anti-patient over the past 27 years. I have studied this subject for years. It’s all well documented, especially in the two federal government reports of malfeasance and nonfeasance at CDC and NIH from 1999 and 2000 and in the 700 page Osler’s Web which I have read 5 times. This is like saying the assertion that the earth is round is a crazy theory. It is proven beyond all doubt.
Like I said, 99.9%+ of people do not read sciencemag. They read USA today, the Chicago Tribune, watch CNN, etc. CDC knows they don’t have to convince every single person, just a good majority of decision makers. No legislator reads sciencemag.
If you lie too much, it’s easier to get caught. Here was an instance where they could tell the truth and not have it make much of an impact.
The fact they told the truth once, does not prove they never lie. Just as the fact that many conspiracy theories are crazy does not prove that some conspiracies do not exist. They do. This is one.
Don’t confuse “I feel better” with the phrase “I am functioning for the first time in 5 years”. It’s like all those comparisons used by ME sufferers, such as “comparing fatigue with ME is like comparing a gentle breeze with a hurricane” and “fatigue is to ME as a match is to a nuclear bomb”. Someone who is 99% dysfunctional who improves on therapy to 90% is ten times better albeit still not right.
It was a strange day yesterday. William Switzer did find (some) XMRV in the tissue of PC patients (1,9%) and found strains of XMRV that were more diverse than previously reported:
http://www.plosone.org/article/info:doi/10.1371/journal.pone.0019065#abstract0
I guess all the “contamination theorists” (like me) will now have to emphasize that Switzer is “just” a MPH and doesn’t hold a PhD? I suppose you don’t take the results of this scientist very seriously, Gob? 😉
Oh and sadly, it was only a quick and dirty PlosOne study, so I suppose the forums will not take these findings seriously.
10 year ME-CFS patient here too. I have no clear hypothesis as to what is the cause for ME/CFS, I even doubt that there is a single cause in my case or a single cause to explain all cases of ME/CFS even when using the Canadian Consensus Criteria.
Why is it is so hard to accept that the original study could be wrong? Yes, a retrovirus would fit the bill nicely, but there are a lot of negative studies for every positive one. It ain’t over yet, the research into XMRV must continue if only for prostate cancer. Let Lipkin do his job, but in the meanwhile let us move on. There are other studies (spinal fluid, ….). An anonymous poll among Dutch-speaking ME/CFS patients shows that less than 50% is XMRV/MLV positive (mix of PCR, co-culture and serology). They only got the test after an initial bloodtest showed immunological abnormalities.
And we are very gratefull that you are the one to uncover it.
If I were you, with that conclusive information of a vast government conspiracy, I would be very, very afraid and I would certainly not post this information on public forums.