Finally a Viral Cause of Chronic Fatigue Syndrome? Or Not? – How Results Can Vary and Depend on Multiple Factors

15 02 2010

Last week @F1000 (on Twitter) alerted me to an interesting discussion at F1000 on  a paper in Science, that linked Chronic fatigue syndrome (CFS) to a newly discovered human virus XRMV [1]ResearchBlogging.org.

This finding was recently disputed by another study in PLOS [2], that couldn’t reproduce the results.  This was highlighted in an excellent post by neuroskeptic “Chronic Fatigue Syndrome in “not caused by single virus” shock!

Here is my take on the discrepancy.

Chronic fatigue syndrome (CFS) is a debilitating disorder with unknown etiology. CFS causes extreme fatigue of the kind that does not go  away after a rest. Symptoms of CFS include fatigue for 6 months or more and experiencing other problems such as muscle pain, memory problems, headaches, pain in multiple joints and  sleep problems. Since other illnesses can cause similar symptoms, CFS is hard to diagnose. (source: Medline Plus).

No one knows what causes CFS, but a viral cause has often been suspected, at least in part of the CFS patients. Because the course of the disease often resembles a post-viral fatigue, CFS has also been referred to as post-viral fatigue syndrome (PVFS).

The article of Lombardi [1], published in October 2009 in Science, was a real breakthrough. The study showed that two thirds of patients with CFS were infected with a novel gamma retrovirus, xenotropic murine leukaemia virus-related virus (XMRV). XMVR was previously linked to prostate cancer.

Lombardi et al  isolated DNA from white blood cells (Peripheral Blood Mononuclear Cells or PBMCs) and assayed the samples for XMRV gag sequences by nested polymerase chain reaction (PCR).

The PCR is a technique that allows the detection of a single or few copies of target DNA by amplifying it across several orders of magnitude, generating thousands to millions of copies of a particular DNA. Nested PCR amplifies the resultant amplicon several orders of magnitude further. In the first round external primers are used (short DNA-sequences that fit the outer end of the piece of DNA to be amplified) and an internal set of primers is used for the second round. Nested PCR is often used if the target DNA is not abundantly present and to avoid the comtamination with products that are amplified as a spin-off due to the amplification of artifacts (sites to which the primers bind as well)

[I used a similar approach 15-20 years ago to identify a lymphoma-characteristic translocation in tonsils and purified B cells of (otherwise) healthy individuals. By direct sequencing I could prove that each sequence was unique in its breakpoint sequence, thereby excluding that the PCR-products arose by contamination of an amplified positive control. All tumor cells had the translocation against one in 100,000 or 1,000,000 normal cells. To be able to detect the oncogene in B cells, B cells had to be purified by FACS. Otherwise the detection limit could not be reached]

Lombardi could detect XMRV gag DNA in 68 of 101 patients (67%) as compared to 8 of 218 (3.7%) healthy controls. Detection of gag as well as env XMRV was confirmed in 7 of 11 CFS samples at the Cleveland Clinic (remarkably these are only shown in Fig 1A of the paper, thus not the original PCR-results).
In contrast, XMRV gag sequences were detected in 8 of 218 (3.7%) PBMC DNA specimens from healthy individuals. Of the 11 healthy control DNA samples analyzed by PCR, only one sample was positive for gag and none for env. The XMRV gag and env sequences were more than 99% similar to those previously reported for prostate tumor–associated strains of XMRV. The authors see this as proof against contamination of samples with prostate cancer associated XMRV-DNA.

Not only PCR experiments were done. Using intracellular flow cytometry and Western blot assays XMRV proteins were found to be expressed in PBMCs from CFS patients. CFS patiens had anti-XMRV antibodies and cell culture experiments revealed that patient-derived XMRV was infectious. These findings are consistent with but do not prove that XMRV may be a contributing factor in the pathogenesis of CFS. XMRV might just be an innocent bystander. However, unlike XMRV-positive prostate cancer cells, XMRV infection status did not not correlate with the RNASEL genotype.

The Erlwein study was published within 3 months after the first article. It is much simpler in design. DNA was extracted from whole blood (not purified white blood cells) and subjected to a nested PCR using another set of primers. The positive control was an end-point dilution of the plasmid. Water served as a negative control. None of the 186 CSF samples was positive.

The question then is: which study is true? (although it should be stressed that the Science paper just shows a link between the virus and CFS, not a causal relationship)

Regional Differences

Both findings could be “real” if there was a regional difference in occurrence of the virus. Indeed XMRV has previously been detected in prostate cancer cells from American patients, but not from German and Irish patients.

Conflict of Interest

Lombardi’s clinic [1] offers $650 diagnostic test to detect XMRV, so it is of real advantage to the authors of the first paper that the CSF-samples are positive for the virus. On the other hand Prof. Simon Wessely of the second paper has built his career on the hypothesis that CFS is a form of psychoneurosis, that should be treated with cognitive behavior therapy. The presence of a viral (biological) cause would not fit in.

Shortcomings of the Lombardi-article [1]

Both studies have used nested PCR to detect XMRV. Because of the enormous amplification potential, PCR can easily lead to contamination (with the positive control) and thus false positive results. Indeed it is very easy to get contamination from an undiluted positive into a weakly positive or negative sample.

Charles Chiu who belongs to the group detecting XMRV in a specific kind of hereditary prostate cancer, puts it like this [5]:

In their Dissenting Opinion of this article, Moore and Shuda raise valid concerns regarding the potential for PCR contamination in this study. Some concerns include 1) the criteria for defining CFS/ME in the patients and in controls were not explicitly defined, 2) nested PCR was used and neither in a blinded nor randomized fashion, 3) the remarkable lack of diversity in the six fully sequenced XMRV genomes (<6 nucleotide average difference across genome) — with Fig. S1 even showing that for one fully sequenced isolate two of the single nucleotide differences were “N’s” — clearly the result of a sequencing error, 4) failure to use Southern blotting to confirm PCR results, and 5) primary nested PCR screening done in one lab as opposed to independent screening from start to finish in two different laboratories. Concerns have also been brought up with respect to the antigen testing

Shortcomings of the Erlwein-article [2]

Many people have objected that the population of CSF patients is not the same in both studies. Sure it is difficult enough to diagnose CSF (which is only done by exclusion), but according to many commenters of the PLOS study there was a clear bias towards more depressed patients. Therefore, a biological agent is less likely the cause of the disease in these patients. In contrast the US patients had all kinds of physical constraints and immunological problems.

The review process was also far less stringent: 3 days versus several months.

The PLOS study might have suffered from the opposite of contamination: failure to amplify the rare CSF-DNA. This is not improbable. The Erlwein group did not purify the blood cells, used other primers, amplified another sequences and did not test DNA of normal individuals. The positive control was diluted in water not in human DNA. The negative control was water.

Omitting cell purification can lead to a lower relative amount of the XMRV-DNA or to inhibition (often seen this with unpurified samples). Furthermore the gel results seem of poor quality (see Fig 2). The second round of the positive PCR sample results in an overloaded lane with too many aspecific bands (lane 9), whereas the first round leads to a very vague low molecular band (lane 10). True that the CSF-samples also run two rounds, but why aren’t the aspecific bands seen here? It would have been better to use a tenfold titration of the positive control in human DNA (this might be a more real imitation of the CSF samples: (possibly) a rare piece of XMRV DNA mixed with genomic DNA) and to use normal DNA as control, not water.Another point is that the normal XMRV-incidence of 1-3,7% in healthy controls is not reached in the PLOS study, although this could be a matter of chance (1 out of 100).

Further Studies

Anyway, we can philosophize, but the answer must await further studies. There are several ongoing efforts.

References

  1. Lombardi VC, Ruscetti FW, Das Gupta J, Pfost MA, Hagen KS, Peterson DL, Ruscetti SK, Bagni RK, Petrow-Sadowski C, Gold B, Dean M, Silverman RH, & Mikovits JA (2009). Detection of an infectious retrovirus, XMRV, in blood cells of patients with chronic fatigue syndrome. Science (New York, N.Y.), 326 (5952), 585-9 PMID: 19815723
  2. Erlwein, O., Kaye, S., McClure, M., Weber, J., Wills, G., Collier, D., Wessely, S., & Cleare, A. (2010). Failure to Detect the Novel Retrovirus XMRV in Chronic Fatigue Syndrome PLoS ONE, 5 (1) DOI: 10.1371/journal.pone.0008519
  3. http://f1000biology.com/article/yxfr5q9qnc967kn/id/1166366/evaluation/sections
  4. http://neuroskeptic.blogspot.com/2010/01/chronic-fatigue-syndrome-in-not-caused.html
  5. Charles Chiu: Faculty of 1000 Biology, 19 Jan 2010 http://f1000biology.com/article/id/1166366/evaluation

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19 responses

15 02 2010
John

Best review I’ve read so far(both pros and cons). Good job and thank you.

Also here’s a second negative UK study which came out today-
‘Absence of xenotropic murine leukaemia virus-related virus in UK patients with
chronic fatigue syndrome’
Retrovirology 2010, 7:10 doi:10.1186/1742-4690-7-10
http://www.retrovirology.com/content/pdf/1742-4690-7-10.pdf

16 02 2010
laikaspoetnik

Thanks John, for the compliment and for informing me about the new study. With (good) science you’re always one (or two) steps behind.

16 02 2010
oregano

The UK study obviously did not replicate the WPI study, so there is really no point in comparing them. The UK study was rushed to print to refute scientific evidence of organic cause because the authors’ personal bias is that, despite reems of biological evidence, ME/CFS is mental, to quote one of the UK study’s authors, the result of ‘illness behaviors’ and malingering.

The misinformation that XMRV has not been found in UK should cease. The WPI study included patients from UK, Ireland, Germany and Australia. Since the WPI study came out, 2 groups of patients have had their blood tested by WPI and about 50% have tested positive. If the UK study had been real science, they would have found at least some positives. That they found none is just another indication that that is what they set out to find. One of the authors of the UK study has written that doctor’s are disgusted by ME patients. No bias there, eh?

16 02 2010
laikaspoetnik

In good science two studies investigating the “same” (here the presence of XMRV in CFS patients) should always be compared. Just to get at the truth.

Yes, the UK study didn’t use the same conditions. And Yes, the UK psychiatrist involved in the study may be biased towards nonbiological causes of ME. Perhaps you missed it, but I mentioned both.

Furthermore the US study has its own bias. To me it seems rather premature to “sell tests for XMRV” that have not been unequivocally shown to demonstrate XMVR. Furthermore, even if true, causation is far from established.

And, as you could read in the comments (thanks John), the UK study is now seconded by another UK-study that couldn’t demonstrate any XMRV either.

Here are two excellent post describing the new findings:

http://www.virology.ws/2010/02/15/xmrv-not-found-in-170-additional-uk-chronic-fatigue-syndrome-patients/

http://scienceblogs.com/erv/2010/02/xmrv_and_chronic_fatigue_syndr_9.php
(HATTIP: http://twitter.com/bora)

The latter summarizes:

- 170 more CFS samples from two different cohorts.

- 395 more healthy controls.

- No Simon Wesseley.

- No XMRV by regular PCR, boosted PCR, or qRT-PCR on DNA or cDNA.

- No meaningful anti-XMRV antibodies.

- Still no XMRV in the Europe.

But they did find people with a neutralizing antibody response to XMRV.

….. In 25 healthy controls.

….. And one CFS patient.

*blink*

18 02 2010
John

The WPI just responded to the second UK XMRV negative study. Their take is that the step of cultering the sample is crucial to finding XMRV.

******************************
http://www.facebook.com/notes.php?id=154801179671

February 18, 2010: WPI is aware of the recent UK study that was unable to detect the presence of XMRV in any CFS patient samples. Although researchers at the WPI were not involved in this project, our work in XMRV continues with researchers around the world. We look forward to the results of studies which replicate the methods used in the original research described in the journal Science in October, 2009.

Information Regarding XMRV Studies

1. The authors of the Science paper established the existence of XMRV as an infectious human blood borne retrovirus for the first time in blood of patients diagnosed with Chronic Fatigue Syndrome (CFS). Previous studies had established the presence of XMRV sequences and protein in human prostate tissue.

2. In the Science paper, the presence of XMRV in well-characterized patients with CFS was established using multiple technologies:

a) PCR on nucleic acids from un-stimulated and stimulated white blood cells;
b) XMRV protein expression from stimulated white blood cells;
c) Virus isolation on the LNCaP cell line; and
d) A specific antibody response to XMRV.

3. The authors of the two UK studies did not attempt to “replicate” the WPI study. Replication requires that the same technologies be employed. The WPI sent reagents and information to several groups of researchers in an effort to support their replication studies. Neither UK study requested positive control blood, plasma or nucleic acids from the WPI.

4. The collection, preparation and storage of DNA were completely different between the Science and UK papers. The latter studies do not show data on blood harvesting or storage. Nor do the studies disclose the quantity of isolated cells. Insufficient number of cells analyzed may result in failure to detect a low copy virus like XMRV, regardless of the sensitivity of the assay. Neither UK study provides detail to allow interpretation of how many white blood cells were analyzed.

5. Patient population selection may differ between studies.

6. The UK authors were unable to detect XMRV, even though 4% of healthy individuals were found to be infected in the US. Japanese scientists detected XMRV in 1.7% in healthy blood donors in Japan. The two previously identified human retroviruses have distinct geographical distributions.

7. Perhaps the most important issue to focus on is the low level of XMRV in the blood. XMRV is present in such a small percentage of white blood cells that it is highly unlikely that either UK study’s PCR method could detect it using the methods described. Careful reading of the Science paper shows that increasing the amount of the virus by growing the white blood cells is usually required rather than using white blood cells directly purified from the body. When using PCR alone, the Science authors found that four samples needed to be taken at different times from the same patient in order for XMRV to be detected by PCR in freshly isolated white blood cells. More importantly, detection methods other than PCR showed that patients whose blood lacks sufficient amount of XMRV detectable by PCR are actually infected. This was proven by the isolation of viral proteins and the finding of infectious XMRV isolated from the indicator cell line LNCaP. The authors of the Retrovirology paper admit that their neutralization assay did not detect bacterially expressed XMRV gag and that positive control sera was needed to validate their assay. The WPI’s monoclonal antibodies specifically and sensitively completed the immune response demonstrating the assays sensitivity and specificity for XMRV envelope.

Simply stated the only validated reliable methods for detecting XMRV in CFS patients, to date, are the methods described in Science. Failure to use these methods and validated reagents has resulted in the failure to detect XMRV. A failure to detect XMRV is not the same as absence of this virus in patients with CFS.

source
http://www.wpinstitute.org/news/news_current.html

19 02 2010
ERV

Perhaps the most important issue to focus on is the low level of XMRV in the blood. XMRV is present in such a small percentage of white blood cells that it is highly unlikely that either UK study’s PCR method could detect it using the methods described.
Bull hockey.

Second UK paper used name brand reagents and the exact primer sets WPI used. They did the same things any lab in the country would do when attempting to replicate another labs findings.

Furthermore, WPI is saying that: 1) few cells are infected, 2) these cells only produce virus when cultured just right in their hands, 3) there is little/no circulating virus, 4) people infected with this virus dont develop leukemia (their immune cell profiles appear normal) like mice/gene therapy patients, but this odd, vague, hard-to-define illness.

This also requires a large number of working retrovirologists to ‘not know what theyre doing’.

Bull hockey.

19 02 2010
John

“Furthermore, WPI is saying that: 1) few cells are infected, 2) these cells only produce virus when cultured just right in their hands, 3) there is little/no circulating virus, 4) people infected with this virus dont develop leukemia (their immune cell profiles appear normal) like mice/gene therapy patients, but this odd, vague, hard-to-define illness.”

1) Correct, they are saying few cells are infected, 2) Incorrect(and bizarre), they didn’t say they had to be the ones to culture the samples, but rather that the samples needed to be cultured, as a direct consequence of 3) Correct, 4)possibly incorrect for at least a subgroup- Dr. Peterson has been following a cohort of patients who developed Mantle Cell Lymphoma for quite some time now. The only problem is when someone develops cancer, even if they had CFS for many years prior, they no longer qualify as a CFS diagnosis, therefore they don’t appear in the CFS literature, and 4) immune abnormalities are one of the most consistant findings in CFS, the problem is that different patients have different profiles. Why is this? A good question, and one that has been awfully hard to answer with the extremely little research funding made available thus far for this ‘odd, vague, [and] hard-to-define illness’.

ERV, I for one think it would be neat if you could ask your professors about the history of AIDS research and maybe give a little history lesson on the discovery of HIV. From what I hear, there was quite the controversy re: finding the HIV virus in the early days when labs did not follow each other’s protocols but instead assumed the techniques they had been using were sufficient.

20 04 2010
laikaspoetnik

I’m rereading the articles, but I can’t find that WPI cultures the PBML before doing PCR.

They say: we isolated nucleic acids from PBMCs and assayed the samples for XMRV gag sequences by nested polymerase chain reaction (PCR) (5, 6). Of the 101 CFS samples analyzed, 68 (67%) contained
XMRV gag sequence. Detection of XMRV was confirmed in 7 of 11 WPI CFS samples at the Cleveland Clinic by PCR-amplifying and sequencing
segments of XMRVenv [..] and gag (736 nt) in CFS PBMC DNA (Fig. 1A)

The funny thing is, they only show the results of the WPI samples tested by the Cleveland Clinic in the first round:
[legend Fig 1a] : XMRV sequences in PBMC DNA from CFS patients. Single-round PCR results for gag, env, and gapdh sequences in PBMCs of (A) CFS patients.
Whereas a nested PCR was needed to detect the virus???

In the materials and methods section it says:
The PBMC (approximately 2 x 107 cells) were centrifuged at 500x g for 7 min and EITHER stored as unactivated cells in 90% FBS and 10% DMSO at -80 ºC for further culture and analysis OR resuspended in TRIzol (..) and stored at -80 ºC for DNA and RNA extraction and analysis.

So no need for culture to demonstrate the virus by PCR…

Another funny thing: one of their negative PCR samples scores positive in other tests.

Requirements for virus isolation is something else.

5 03 2010
atopos

I am not a scientist and have difficulty in determining the significance of these various studies.
Background:
I’m aware that science normally progresses via questions and conflict – if all is agreed and obvious then there is nothing new and no new science. I don’t have the tools to evaluate the procedures used in these studies other than one element.

That element is having contracted something which has been labeled “CFID” or M.E. depending on who writes the dx. It is indeed a confusing illness; the severity varies with some predictable and some unknown triggers and perhaps biological processes I have no control over. I do not know the initial cause, though it had a rapid, flu-like onset.

It is also confusing to diagnose, since
i) there multiple definitions of it, ranging from meaningless catch-all categories such as “unexplained fatigue lasting over 6 months” (= patient is sick for unknown reason) to sets of both observable and measurable signs, at least some of which occur in all patients. The latter is used only by physicians who have seen and practiced with many patients.
ii) the same patient’s outward symptoms vary dramatically over time

iii) there are numerous biological markers (ask Dr. Paul Cheney, who has worked with this since the Incline Villiage incident) but most tests are not covered by insurance and not widely known. There are distinct and repeatable tests developed by a handful (literally, less than 10) physicians nationwide who deal with this cohort. These tests are not yet known outside the specialty.

iv) given that many, though not all symptoms are common to many severe, chonic diseases there is probably more than one underlying disease in the patient cohort. The issue has never been studied with the scale or precision required, so we don’t know what subgroups exist.

iv) immune dysfunction is a common element; by definition: If one has a 100% functioning immune system one does not have CFID. There may be people with overlapping sets of symptoms from unknown causes who are labeled as “Chronic Fatigue” cases, but those are one or more other diseases than what we’re discussing. Wessely etc would disagree, as they use the terms “CFS” and “ME” to describe a different – and quite controversial – disease.

Whether or not this disease is related to or caused by XMRV or any specific virus (it could be akin to a combination lock), I believe it presents a significant avenue to understand the human body. Something in these patients is causing a systemic collapse, starting in the immune system. Medicine today does not understand the body well enough to understand the pathology in detail or to effectively manage this disease, much less reverse and cure it. Understanding the processes involved with CFID will yield better management for the effects of many chronic diseases and probably treatments for some.

I hope those researching this issue will think beyond the details of lab assays or one particular virus and to the larger set of medical unknowns it has revealed.

20 04 2010
Matilda

I wonder who Erv really is and what major health insurer is paying him. Also wonder how he gets such a high google ranking.

Propaganda is rife in the health insurance industry and indeed right through the increasingly corporate media.

i.e. In the Iraq war there was a group of about 25 retired generals who were touted by major news organisations as independant and retired. They were always giving a supposedly impartial view on the war. Turned out they were all on the Pentagon Payroll. Corporations have major PR (propaganda) budgets and I am very suspicious of ERV. None of us know who the hell he really is.

20 04 2010
laikaspoetnik

Erv is just a well known blogging scientist, I suppose. The Science platform does help with regard to Google Ranking.

With anonymous bloggers conflict of interest may be a point. But I listen to what they say/write and whether that looks sensible or not.
In this case I have no reason to believe that erv has anything to do with this particular XMRV-research nor that he is on the payroll of an insurer (?)

21 04 2010
Matilda

The most stunningly ommitted and important piece of information which Erv and the UK scientists must be aware of as I’v commented about it on his blog only to have that comment removed. That makes me very suspicious of this creep.

Im not a scientist but heres a very basic description of the point that troubles me. They managed to infect Monkeys with XMRV and cause viremia intitially. When the poor creatures were harvested and examined very little and often no XMRV was found remaining in the blood or plasma. PCR detected no XMRV in Serum. However it was found to be widespread through the Lymph organs the digestive tract and the Lungs.
Its no surprise then that finding this virus in human blood or serum is probably a totally different kettle of fish to finding this virus in prostate tissue. A recent study into prostate samples found even when present in prostate tissue none found in serum.
This does not prove the case for XMRV in CFS but makes the conclusions of all the negative blood studies null and void as to whether CFS is caused by XMRV.
I think they need to start looking at tonsils. I don’t know if tonsils were exmained for XMRV in monkeys but I can tell you the sore throats of CFS can be horrible. Would be best to either biospy or swab tonsil. The lone female monkey in the study was also found to have XMRV in the vagina and cervix so cervical smear tissue could be looked at.
Why waist money looking at blood when there isnt much virus in that tissue.
I already know of a lab that have taken this into account and are now going to try techniques similar to Mikivits. They get it. They are not doing a study but are trying to develop testing for patients and I guess if they find it and develop a good test for it, then it might just pay off. Thats all I’m saying on that one. I don’t know much but once they knew about the monkey study they like any sane scientist knew that they would need a very sensitive test indeed to make a blood or plasma test work for XMRV and maybe it wont work if the rarety of virus found in the monekey is the same for humans which the prostate study testing both tissue and serum showed.

In the monkeys it was found to be widespread in the lymph organs and either rare or completely absent from serum and blood.

That doesnt prove the case for an XMRV CFS connection but until other tissues are looked at XMRV cannot be discounted in CFS unless you are ERV and can delete important imformationn from your blog.

27 04 2010
laikaspoetnik

@Matilda. The point is not that XMRV might not be real, nor that it might not play a role in CFS. But the point is (here) whether the WPI findings are real and what they implicate.
Your point about the blood not being the best place to find the virus is a good one. The problem only is that the Science paper is about the detection of XMRV in PBMCby PCR. The latest UK paper and The Dutch paper also enriched for PBMC and used an even more sensitive PCR than the WPI. Still they didn’t find any sign of XMRV. Now WPI says they have found XMRV in those negative samples (so it is not the difference in criteria and region). It makes you wonder…
Plus WPI does not seem to use blood cells directly (as stated in the Science paper), but need to culture it now. Plus XMRV is now also found in a number of other diseases. I’m really becoming very skeptical about WPI and its research.

27 04 2010
oregano

Why not direct some skepticism towards those studies that failed to find ANY XMRV? They can find it in Japan; UK patients’ blood has been tested in the US and found to be positive in about 50%, so why couldn’t the European studies find it?

WPI continued to research XMRV after they finished writing the paper that was published in Science (called “as good as it gets for a first paper” by Dr John Coffin, well respected retrovirologist.) So of course, their opinions and methods have evolved. They have at least 10 other studies going on, trying to find the cause of CFS.

As you mentioned, WPI also found XMRV in 3 out of 7 samples from one of the Failure to Find studies, but the study authors failed to mention that and broke off contact once they were told that some of their samples had tested postitive. Have you considered that manufacturing your skepticism is exactly what they intended?

As for ERV, she seems to have a personal rage against Dr Mikovits and judging by her (ERV’s) foul language, may be suffering from Tourette’s Syndrome. Or maybe that is just how virology students from back-water schools in Oklahoma all talk. To call her a well-respected scientist while expressing skepticism about WPI is absurd. ERV gets hits to her blog because she says outrageous, incredibly unprofessional things, not because she can think or write well.

27 04 2010
Three Studies Now Refute the Presence of XMRV in Chronic Fatigue Syndrome (CFS) « Laika's MedLibLog

[...] months ago I wrote about two contradictory studies on the presence of the novel XMRV retrovirus in blood of patients [...]

30 04 2010
Matilda

“As for ERV, she ”

Is there any evidence to support the notion that ERV is female and is indeed who she says she is. Unless we know ERV’s true identity for all we know she could be Myra McClure or even Simon Wesley. Its pretty basic really. To make any assumption about ERV’s identity is unscientific because we don’t have a clue. Do we?

I wouldn’t mind betting that ERV person is actually on a corporate PR (propaganda) payroll. A multi national health insurer maybe? But like the rest of us I don’t really know.

I also think it really suspect that ERV is always at the top of Google search engine results.

Etcetera

-this comment is truncated. this is the 3rd time that you post about Erv while the post is not about Erv. Only the statements or links in her posts that could be checked have been referred to here. Because it is only about what she says. Please start a blog about Erv so you can tell the world about your suspicion about her there. I’m not allowing any misuse of my blog for this any longer.

Everyone: from now on I’m only allowing comments that try to respond to my posts.

11 05 2010
oregano

Still “skeptical” about WPI and its research into XMRV?

Inform yourself:

http://www.iacfsme.org/BULLETINSPRING2010/Spring2010MikovitsLetter/tabid/427/Default.aspx

Drs Coffin and Ruscetti, eminent retrovirologists, speak up at International Retrovirology Conference in Prague:
http://listserv.nodak.edu/cgi-bin/wa.exe?A2=ind1005a&L=co-cure&T=0&F=&S=&P=1724

30 08 2010
Does the NHI/FDA Paper Confirm XMRV in CFS? Well, Ditch the MR and Scratch the X… and… you’ve got MLV. « Laika's MedLibLog

[...] defined CFS-population, had used old and/or too few samples (discussed in two previous posts here and here). In a way,  negative studies, failing to reproduce a finding, are less convincing [...]

2 06 2011
Science Asks to Retract the XMRV-CFS Paper, it Should Never Have Accepted in the First Place. « Laika's MedLibLog

[...] I repeat my concerns expressed in earlier posts [13 and 14]. (please read these posts first, if you are unfamiliar with [...]

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