Incorrect interpretation of previously published data in the paper ¿Identification, characterization, and comparative genomic distribution of the HERV-K (HML-2) group of human endogenous retroviruses¿ written by Ravi P Subramanian, Julia H Wildschutte, Crystal Russo and John M Coffin. (Anton Buzdin, 17 January 2012)
Incorrect interpretation of previously published data in the paper ¿Identification, characterization, and comparative genomic distribution of the HERV-K (HML-2) group of human endogenous retroviruses¿ written by Ravi P Subramanian, Julia H Wildschutte, Crystal Russo and John M...
read full comment
Correction of a typographical error in the abstract (Elisabeth Menu, 24 August 2011)
In the abstract, the last sentence of the results section should be replaced by : "Using HIV-1 pseudotypes, we found that HIV-1 entry step was inhibited by decidual soluble factors."
read full comment
XMRV is inserted into 472 sites in Prostate DNA (Gerwyn Morris, 06 March 2011)
In his reply to my letters of march 02 and 03 AG Miller referenced the study of Kim and others 2008. On close examination the details of the approach reported by Kim and others are revealing and challenge the conlusions of Garson et al and the accuracy of comments made by AG Miller in his most recent letter. Permission to reproduce the following sections has been granted by the authors.
"We sequenced a total of 508 authentic XMRV integration sites from DU145 cells, and 472 of these sites were mapped to unique locations in the human genome. Integration events were found in all 24 human chromosomes (22 autosomes and the sex chromosomes X and Y) (Fig. 1). The frequencies of integration of XMRV were generally proportional to chromosome size, but the overall...
read full comment
.response rebutting Miller (Gerwyn Morris, 05 March 2011)
Dr Miller you are commenting on a different study to the one I raised
I am talking about a study by Dong et al 2007 which first detected xmrv in dna taken straight from prostate tissue where they first screened the DU 145 cells to ensure that they did not harbour XMRV.
If you are going to reply to my posts at least have the courtesy of reading them first
You talk of hypothetical situations as though they were fact
As you know the DU 145 cell line environment is one of high oxidative stress and elevated levels of NF-kappa B.you also know that high NF-kappa B instigates the transcription of XMRV and stimulates its replication. If the DUi25 cell line DNA contained integrated XMRV provirus then the cell line wouldexpress XMRV.
Response to the comments by Gerwyn Morris posted 02 March and 03 March 2011 (A Dusty Miller, 04 March 2011)
You note that I have not replied to your previous comments. This is because of their voluminous nature, your inability to correctly interpret what is basically a sound article, and because I have other things to do!
In your post of 02 March, the main substantive point questions the proposed direction of contaminant transfer, from the XMRV-infected DU145 cells to the prostate cancer tissue. In the Kim et al. 2008 paper describing these studies, they infected DU145 cells with XMRV at a multiplicity of 0.1 and the cells were grown for 3 days. By this time, it is likely that all of the cells carried at least one integrated copy of XMRV, because XMRV is replication-competent and can readily spread in cultured DU145 prostate cancer cells. In contrast, the number of integrated copies...
read full comment
Response to the comment by Abigail Smith posted 02 March 2011 (A Dusty Miller, 04 March 2011)
Thanks for the citation (Mitchell et al., PLoS Biology 2:E234, 2004). While these authors did not mention observing any duplicate integrations, they do state in Materials and Methods that only novel integration site sequences were deposited at the NCBI, implying that some sites were not novel and thus were duplicates. Duplicates would not be unexpected in a single experiment, because PCR amplification results in many copies of what might have initially been a unique site, and if one clones and sequences enough sites, duplicates are bound to be found. For example, if 1,000 cells were infected with 10 of their replication-defective HIV vector particles, resulting in 10 integrated proviruses, cloning of 100 integration sites from DNA isolated from these cells would result in detection of...
read full comment
the study cannot demonstrate direction of transfer (Gerwyn Morris, 03 March 2011)
The authors did not follow the scientific method and demonstrate that the DU125 cells did not contain integrated DNA before the start of the experiment. If the cell line was "contaminated" with human XMRV then the results would have been exactly the same
The other problem they have is that none of the studies that identified and isolated XMRV used the the DU145 cell line in any way whatsoever
The experiment that isolated integrated XMRV directly from the prostste tissue of infected patients also did not invole the use of DU145
The question of identical insertion sites is a probabalistic argument and purely determined by sample size and the affinity of a retrovirus for GPG islands
Citation request by Dr. Miller-- (Abigail Smith, 02 March 2011)
If you do not want a list of every integration site ever (heh), Mitchell et al might be suitable citation: "Retroviral DNA Integration: ASLV, HIV, and MLV Show Distinct Target Site Preferences"
They identified 3127 insertion sites of HIV-1, ASLV, and MLV and they did not mention observing any duplicates. As far as MLV goes, their analysis of Chromosome 11 showed, at max, 3 MLV insertion sites within the same 2 Mb region.
I do not know of any published duplicated insertion sites myself. It certainly strains credulity that a lab only sequenced a handful of integrations, and found not just one duplication, but two. And the duplications just happen to have identical LTRs as well.
read full comment
The authors state that the sequences were unlikely to have been transfered into the DU125 cells from the patients examined without nothing but their biases as evidence.
Likewise they voice their belief that the other integration sites are probably caused by contamination after failing to provide any evidence despite a rigorous effort to discover said evidence.
I submit that scientists who publish unfounded opinion and not fact is the main issue here
Miller talks of unacceptable phraseology.I am therefore somewhat surprised that he has not highlighted the extract below
"we suspect that some or all of them may also be the result of...
read full comment
Response to the comment by Gerwyn Morris posted 26 February 2011 (A Dusty Miller, 02 March 2011)
Morris' criticism of the article by Garson et al. is unwarranted, and stems from a misunderstanding of the difference between retrovirus integration near a gene versus integration at exactly the same site in the whole human genome. It is true that murine leukemia viruses (MLV) can often be found within or near oncogenes involved in the progression of tumors in MLV-infected mice. However, integration within 1,000 or 10,000 nucleotides of a gene is quite different from integration at exactly the same nucleotide position in a whole mammalian genome. None of the references provided by Morris show integration of a retrovirus at the same nucleotide position.
I do agree that it would be nice to have formal support for the statement that "With the exception of a single early...
read full comment
is this the final straw to xmrv... (aidan walsh, 28 February 2011)
i propose that cfs and prostate cancer is related to 'unintentional chronic dehydration' and there may be no infection involved in the illness...also it could be very possible that these infections are involved... c.pneumonaie dr. charles stratton vanderbilt university...mycoplasmas drs. nancy and garth nicolson laguna beach california...ciguetera (epitope) toxins with now a link to low level radiation and their work has been replicated and they claim is a bio-marker for all 'auto-immune'disorders with links to myelodysplasia syndromes...also not to forget a neuro surgeon found 300 consecutive fibromyalgia patients with chiari malformation and/or stenosis of the spines in cfs patients as well and just last week from new jersey where spinal fluids in chronic lyme and cfs patients showed...
read full comment
XMRV class viruses integrate into the same sites repeatedly (Gerwyn Morris, 26 February 2011)
The authors are clearly not familiar with MLV viruses
MLV viruses have a preference for integrating within certain genes involved in the promotion or repression of tumours. A classic example would be PIM-1(1) or P53 (2) n-myc(3)is also a common integration site. Thus mulv virus' display the propery of integrating into the same sites repeatedly.It is surprising that the authors have not researched into the subject. Hence the following section of the paper is completely incorrect
"With the exception of a single early publication on avian sarcoma-leukosis virus, which was refuted by later work [10], sequencing studies of thousands of retroviral integration sites have to our knowledge never identified exactly the same site twice." ...
read full comment
If I may ask a question with regard to your article. May I ask why you have cloned a region 5kb upstream to the transcription start site (ATG) and not directly at the start site? Do you think you would have found similar results would you have repeated the experiment directly at the start site (ATG)with perhaps less divergences (enhancers and silencers)and so localizing their origins and effect on the latter binding sites. May I aslo ask what other results you found on other regions of DNA tested or/and if the other regions tested correlated with the results noted on this analysis. Was the activity of the luciferase activity greater or lesser and if so in which part of the cloned region, was the luciferase activity enhanced by its location on the cloned region, closer or...
read full comment
Robinson et al flaws in study design (Gerwyn Morris, 21 January 2011)
This article presents a methodological critique of the study carried out by Robinson et al (1). In essence this article submits that the work in question departs so profoundly from the work of other research groups that the results must be treated with caution. In particular these results are at best open to interpretation and at worst may be the product of experimentally induced artifacts.
Initially the results of the study by Robinson et al appear unremarkable. The detection rate by PCR is in line with that reported by Danielson et al but some 400% lower than that achieved by IHC using XMRV specific probes (2, 3). This of course means that any conclusion made by PCR alone regarding the association of XMRV and mouse DNA is profoundly unsafe. One must...
read full comment
lombardi et al advised not to use one step kits (Gerwyn Morris, 21 January 2011)
If the Sato and others had read the original study by Lombardi et al(2009) they would have noted that the authors of that study advised(in the text) against the use of one step kits because mouse contamination had been detected in such kits. It seems strange that Sato and others have attemped to "reinvent the wheel" in their study by presenting information that was already in the public domain
read full comment
Dr. Naoki Mori submitted this article for retraction without my agreement. Although I agree to retract our paper(Retrovirology 2006, 3:22), I have not agree to share responsibility with Dr. Mori.
read full comment
Baysian knowledge is not Scientific knowledge (Gerwyn Morris, 13 January 2011)
A consideration of Hue et al, 2010
The paper states
"To consider the provenance of XMRV we sequenced XMRV from the cell line 22Rv1, which is infected with an MLV-X that is indistinguishable from patient derived XMRV."
The virus expressed by the 22Rv1 cell line has been sequenced and has the unique nucleotide sequences in the env and gag regions which identify it as XMRV 123, therefore it is the same virus. The cell line originates from a patient suffering from prostate cancer in 1993(4). Taking the evidence as a whole the explanation that the origin of XMRV expressed by these cells in that patient, in which case the difference in sequence was not derived from replication in an immortalised cell line but was representative of wild type XMRV in 1993 and...
read full comment
Sato et al missed a trick (Isabel Greenwood, 12 January 2011)
A number of retrovirologists have expressed a belief that the recent discovery of MLV related viruses in people with Myalgic Encephalomyelitis also called Chronic Fatigue Syndrome (ME/CFS) and Prostate Cancer Patients are in fact contaminants. Four studies were posted simultaneously in this journal in Dec 2010 where the authors offered their interpretation of their findings as evidence in support of their hypothesis. Others have argued that alternative explanations of their findings are readily available. They argue that even without other lines of evidence, not considered in these studies, an alternative interpretation argues against the advocates of contamination argument. This letter focuses on a critique of one of these papers namely the one authored by Sato and others (1). The...
read full comment
XMRV in CFS subjects? (A Dusty Miller, 29 December 2010)
After solving the contamination problem reported in this article, do you find any XMRV RNA in sera from chronic fatigue syndrome patients in Japan?
read full comment
is this really the final straw? (aidan walsh, 21 December 2010)
for the past year all efforts have been placed soley on xmrv! let us all hope that this paper puts a final end to this retrovirus infection theory! there are numerous other serious ongoing research with regards to the following... c.pneumonaie,dr.charles stratton vanderbilt university...drs. garth/nancy nicolson mycoplasma with 45% of the hiv virus envelope,institute for molecular medicine, california... ciguetera 'epitope' toxins university of hawaii with a link to low level radiation...also a prominent neuro surgeon in the u.s.a. found 300 consecutive cfs/fibro patients with chiari malformation and/or cervical spinal stenosis and last dr.a.martin lerner on herpes viral ebv,cmv and hhv-6 causing heart muscle problems and successfully treated with herpes antivirals...it is now time to put...
read full comment
The Lo/Alter team (FDA/NIH) have tested these samples (Tom Kindlon, 24 August 2010)
We now have more evidence suggesting the absence of positives in this study could be a cohort issue.
As I previously pointed out, I do not believe the samples in this study are representative of Chronic Fatigue Syndrome (CFS) patients as normally defined, particularly those that attend specialist clinics [1,2].
A paper has just been published by researchers from the FDA and NIH which found MLV-like virus gag gene sequences in 32 of 37 (86.5%) of their CFS patients compared with only 3 of 44 (6.8%) healthy volunteer blood donors[3].
In accompanying material[4], they mention the following: "10. How are the differences between the CDC and FDA study results being evaluated?
Differences in the results could reflect differences in the...
read full comment
Clarificaiton on Herpesviruses (Monica Tomaszewski, 26 July 2010)
Is there a particular reason why the authors choose to make a distinction between HCMV and HHV-5, as CMV is the 5th human herpesvirus?
read full comment
Methodological deficiencies in the study by Switzer et al (Gerwyn Morris, 23 July 2010)
A number of people here have already commented (quite eloquently) on the inappropriateness of using the Reeves 2005 criteria to diagnose people with ME/CFS. Indeed, using a selection criteria which has roughly the same chance of separating people with this illness from a generally fatigued population as tossing a coin is not the most auspicious of starts. That said however there are also some serious shortcomings with the methodology of the Switzer et al. paper which would make the detection of an in vivo virus highly unlikely, if present, in the people included in this study, regardless of the patient criteria used.
The terms analytical sensitivity and diagnostic sensitivity, although often used interchangeably, have entirely different meanings. Analytical...
read full comment
What patient group are they studying? (Robin Durham, 23 July 2010)
I am a patient. I was given the diagnosis 15 years ago using the original Fukuda definition (which does include tender lymphadenopathy despite what the authors of the study say). I also meet the criteria for the Canadian Consensus definition. I would have been excluded from this study because I have some of the physical findings of the Canadian definition. If I don't have CDC defined CFS, what do I have?
read full comment
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Latest comments
Incorrect interpretation of previously published data in the paper ¿Identification, characterization, and comparative genomic distribution of the HERV-K (HML-2) group of human endogenous retroviruses¿ written by Ravi P Subramanian, Julia H Wildschutte, Crystal Russo and John M Coffin. (Anton Buzdin, 17 January 2012)
Incorrect interpretation of previously published data in the paper ¿Identification, characterization, and comparative genomic distribution of the HERV-K (HML-2) group of human endogenous retroviruses¿ written by Ravi P Subramanian, Julia H Wildschutte, Crystal Russo and John M... read full comment
Comment on: Subramanian et al. Retrovirology, 8:90
Correction of a typographical error in the abstract (Elisabeth Menu, 24 August 2011)
In the abstract, the last sentence of the results section should be replaced by : "Using HIV-1 pseudotypes, we found that HIV-1 entry step was inhibited by decidual soluble factors." read full comment
Comment on: Marlin et al. Retrovirology, 8:58
Email address update (Mario Chin, 11 March 2011)
Current corresponding author email address for M.P.S. Chin: mpschin@amvetbio.com
read full comment
Comment on: Ristic et al. Retrovirology, 7:73
XMRV is inserted into 472 sites in Prostate DNA (Gerwyn Morris, 06 March 2011)
In his reply to my letters of march 02 and 03 AG Miller referenced the study of Kim and others 2008. On close examination the details of the approach reported by Kim and others are revealing and challenge the conlusions of Garson et al and the accuracy of comments made by AG Miller in his most recent letter. Permission to reproduce the following sections has been granted by the authors.
"We sequenced a total of 508 authentic XMRV integration sites from DU145 cells, and 472 of these sites were mapped to unique locations in the human genome. Integration events were found in all 24 human chromosomes (22 autosomes and the sex chromosomes X and Y) (Fig. 1). The frequencies of integration of XMRV were generally proportional to chromosome size, but the overall... read full comment
Comment on: Garson et al. Retrovirology, 8:13
.response rebutting Miller (Gerwyn Morris, 05 March 2011)
Dr Miller you are commenting on a different study to the one I raised
I am talking about a study by Dong et al 2007 which first detected xmrv in dna taken straight from prostate tissue where they first screened the DU 145 cells to ensure that they did not harbour XMRV.
If you are going to reply to my posts at least have the courtesy of reading them first
You talk of hypothetical situations as though they were fact
As you know the DU 145 cell line environment is one of high oxidative stress and elevated levels of NF-kappa B.you also know that high NF-kappa B instigates the transcription of XMRV and stimulates its replication. If the DUi25 cell line DNA contained integrated XMRV provirus then the cell line wouldexpress XMRV.
Mutations... read full comment
Comment on: Garson et al. Retrovirology, 8:13
Response to the comments by Gerwyn Morris posted 02 March and 03 March 2011 (A Dusty Miller, 04 March 2011)
You note that I have not replied to your previous comments. This is because of their voluminous nature, your inability to correctly interpret what is basically a sound article, and because I have other things to do!
In your post of 02 March, the main substantive point questions the proposed direction of contaminant transfer, from the XMRV-infected DU145 cells to the prostate cancer tissue. In the Kim et al. 2008 paper describing these studies, they infected DU145 cells with XMRV at a multiplicity of 0.1 and the cells were grown for 3 days. By this time, it is likely that all of the cells carried at least one integrated copy of XMRV, because XMRV is replication-competent and can readily spread in cultured DU145 prostate cancer cells. In contrast, the number of integrated copies... read full comment
Comment on: Garson et al. Retrovirology, 8:13
Response to the comment by Abigail Smith posted 02 March 2011 (A Dusty Miller, 04 March 2011)
Thanks for the citation (Mitchell et al., PLoS Biology 2:E234, 2004). While these authors did not mention observing any duplicate integrations, they do state in Materials and Methods that only novel integration site sequences were deposited at the NCBI, implying that some sites were not novel and thus were duplicates. Duplicates would not be unexpected in a single experiment, because PCR amplification results in many copies of what might have initially been a unique site, and if one clones and sequences enough sites, duplicates are bound to be found. For example, if 1,000 cells were infected with 10 of their replication-defective HIV vector particles, resulting in 10 integrated proviruses, cloning of 100 integration sites from DNA isolated from these cells would result in detection of... read full comment
Comment on: Garson et al. Retrovirology, 8:13
the study cannot demonstrate direction of transfer (Gerwyn Morris, 03 March 2011)
The authors did not follow the scientific method and demonstrate that the DU125 cells did not contain integrated DNA before the start of the experiment. If the cell line was "contaminated" with human XMRV then the results would have been exactly the same
The other problem they have is that none of the studies that identified and isolated XMRV used the the DU145 cell line in any way whatsoever
The experiment that isolated integrated XMRV directly from the prostste tissue of infected patients also did not invole the use of DU145
The question of identical insertion sites is a probabalistic argument and purely determined by sample size and the affinity of a retrovirus for GPG islands
XMRV has been demonstrated a greater... read full comment
Comment on: Garson et al. Retrovirology, 8:13
Citation request by Dr. Miller-- (Abigail Smith, 02 March 2011)
If you do not want a list of every integration site ever (heh), Mitchell et al might be suitable citation: "Retroviral DNA Integration: ASLV, HIV, and MLV Show Distinct Target Site Preferences"
They identified 3127 insertion sites of HIV-1, ASLV, and MLV and they did not mention observing any duplicates. As far as MLV goes, their analysis of Chromosome 11 showed, at max, 3 MLV insertion sites within the same 2 Mb region.
I do not know of any published duplicated insertion sites myself. It certainly strains credulity that a lab only sequenced a handful of integrations, and found not just one duplication, but two. And the duplications just happen to have identical LTRs as well. read full comment
Comment on: Garson et al. Retrovirology, 8:13
response to Miller (Gerwyn Morris, 02 March 2011)
in response to the letter by Miller
Would he argue with the points below?
The authors state that the sequences were unlikely to have been transfered into the DU125 cells from the patients examined without nothing but their biases as evidence.
Likewise they voice their belief that the other integration sites are probably caused by contamination after failing to provide any evidence despite a rigorous effort to discover said evidence.
I submit that scientists who publish unfounded opinion and not fact is the main issue here
Miller talks of unacceptable phraseology.I am therefore somewhat surprised that he has not highlighted the extract below
"we suspect that some or all
of them may also be the result of... read full comment
Comment on: Garson et al. Retrovirology, 8:13
Response to the comment by Gerwyn Morris posted 26 February 2011 (A Dusty Miller, 02 March 2011)
Morris' criticism of the article by Garson et al. is unwarranted, and stems from a misunderstanding of the difference between retrovirus integration near a gene versus integration at exactly the same site in the whole human genome. It is true that murine leukemia viruses (MLV) can often be found within or near oncogenes involved in the progression of tumors in MLV-infected mice. However, integration within 1,000 or 10,000 nucleotides of a gene is quite different from integration at exactly the same nucleotide position in a whole mammalian genome. None of the references provided by Morris show integration of a retrovirus at the same nucleotide position.
I do agree that it would be nice to have formal support for the statement that "With the exception of a single early... read full comment
Comment on: Garson et al. Retrovirology, 8:13
is this the final straw to xmrv... (aidan walsh, 28 February 2011)
i propose that cfs and prostate cancer is related to 'unintentional chronic dehydration' and there may be no infection involved in the illness...also it could be very possible that these infections are involved... c.pneumonaie dr. charles stratton vanderbilt university...mycoplasmas drs. nancy and garth nicolson laguna beach california...ciguetera (epitope) toxins with now a link to low level radiation and their work has been replicated and they claim is a bio-marker for all 'auto-immune'disorders with links to myelodysplasia syndromes...also not to forget a neuro surgeon found 300 consecutive fibromyalgia patients with chiari malformation and/or stenosis of the spines in cfs patients as well and just last week from new jersey where spinal fluids in chronic lyme and cfs patients showed... read full comment
Comment on: Garson et al. Retrovirology, 8:13
XMRV class viruses integrate into the same sites repeatedly (Gerwyn Morris, 26 February 2011)
The authors are clearly not familiar with MLV viruses
MLV viruses have a preference for integrating within certain genes involved in the promotion or repression of tumours. A classic example would be PIM-1(1) or P53 (2) n-myc(3)is also a common integration site.
Thus mulv virus' display the propery of integrating into the same sites repeatedly.It is surprising that the authors have not researched into the subject. Hence the following section of the paper is completely incorrect
"With the exception of a single early publication on avian
sarcoma-leukosis virus, which was refuted by later work [10], sequencing studies of
thousands of retroviral integration sites have to our knowledge never identified exactly the
same site twice."
... read full comment
Comment on: Garson et al. Retrovirology, 8:13
comment (Paule Morbois, 21 January 2011)
If I may ask a question with regard to your article.
May I ask why you have cloned a region 5kb upstream to the transcription start site (ATG) and not directly at the start site?
Do you think you would have found similar results would you have repeated the experiment directly at the start site (ATG)with perhaps less divergences (enhancers and silencers)and so localizing their origins and effect on the latter binding sites.
May I aslo ask what other results you found on other regions of DNA tested or/and if the other regions tested correlated with the results noted on this analysis. Was the activity of the luciferase activity greater or lesser and if so in which part of the cloned region, was the luciferase activity enhanced by its location on the cloned region, closer or... read full comment
Comment on: Desfarges et al. Retrovirology, 6:O20
Robinson et al flaws in study design (Gerwyn Morris, 21 January 2011)
This article presents a methodological critique of the study carried out by Robinson et al (1). In essence this article submits that the work in question departs so profoundly from the work of other research groups that the results must be treated with caution. In particular these results are at best open to interpretation and at worst may be the product of experimentally induced artifacts.
Initially the results of the study by Robinson et al appear unremarkable. The detection rate by PCR is in line with that reported by Danielson et al but some 400% lower than that achieved by IHC using XMRV specific probes (2, 3). This of course means that any conclusion made by PCR alone regarding the association of XMRV and mouse DNA is profoundly unsafe. One must... read full comment
Comment on: Robinson et al. Retrovirology, 7:108
lombardi et al advised not to use one step kits (Gerwyn Morris, 21 January 2011)
If the Sato and others had read the original study by Lombardi et al(2009) they would have noted that the authors of that study advised(in the text) against the use of one step kits because mouse contamination had been detected in such kits. It seems strange that Sato and others have attemped to "reinvent the wheel" in their study by presenting information that was already in the public domain read full comment
Comment on: Sato et al. Retrovirology, 7:110
Re;Retraction (Mariko Tomita, 19 January 2011)
Dr. Naoki Mori submitted this article for retraction without my agreement. Although I agree to retract our paper(Retrovirology 2006, 3:22), I have not agree to share responsibility with Dr. Mori. read full comment
Comment on: Tomita et al. Retrovirology, 8:1
Baysian knowledge is not Scientific knowledge (Gerwyn Morris, 13 January 2011)
A consideration of Hue et al, 2010
The paper states
"To consider the provenance of XMRV we sequenced XMRV from the cell line 22Rv1, which is infected with an MLV-X that is indistinguishable from patient derived XMRV."
The virus expressed by the 22Rv1 cell line has been sequenced and has the unique nucleotide sequences in the env and gag regions which identify it as XMRV 123, therefore it is the same virus. The cell line originates from a patient suffering from prostate cancer in 1993(4). Taking the evidence as a whole the explanation that the origin of XMRV expressed by these cells in that patient, in which case the difference in sequence was not derived from replication in an immortalised cell line but was representative of wild type XMRV in 1993 and... read full comment
Comment on: Hué et al. Retrovirology, 7:111
Sato et al missed a trick (Isabel Greenwood, 12 January 2011)
A number of retrovirologists have expressed a belief that the recent discovery of MLV related viruses in people with Myalgic Encephalomyelitis also called Chronic Fatigue Syndrome (ME/CFS) and Prostate Cancer Patients are in fact contaminants. Four studies were posted simultaneously in this journal in Dec 2010 where the authors offered their interpretation of their findings as evidence in support of their hypothesis. Others have argued that alternative explanations of their findings are readily available. They argue that even without other lines of evidence, not considered in these studies, an alternative interpretation argues against the advocates of contamination argument. This letter focuses on a critique of one of these papers namely the one authored by Sato and others (1). The... read full comment
Comment on: Sato et al. Retrovirology, 7:110
XMRV in CFS subjects? (A Dusty Miller, 29 December 2010)
After solving the contamination problem reported in this article, do you find any XMRV RNA in sera from chronic fatigue syndrome patients in Japan? read full comment
Comment on: Sato et al. Retrovirology, 7:110
is this really the final straw? (aidan walsh, 21 December 2010)
for the past year all efforts have been placed soley on xmrv! let us all hope that this paper puts a final end to this retrovirus infection theory! there are numerous other serious ongoing research with regards to the following... c.pneumonaie,dr.charles stratton vanderbilt university...drs. garth/nancy nicolson mycoplasma with 45% of the hiv virus envelope,institute for molecular medicine, california... ciguetera 'epitope' toxins university of hawaii with a link to low level radiation...also a prominent neuro surgeon in the u.s.a. found 300 consecutive cfs/fibro patients with chiari malformation and/or cervical spinal stenosis and last dr.a.martin lerner on herpes viral ebv,cmv and hhv-6 causing heart muscle problems and successfully treated with herpes antivirals...it is now time to put... read full comment
Comment on: Hué et al. Retrovirology, 7:111
The Lo/Alter team (FDA/NIH) have tested these samples (Tom Kindlon, 24 August 2010)
We now have more evidence suggesting the absence of positives in this study could be a cohort issue.
As I previously pointed out, I do not believe the samples in this study are representative of Chronic Fatigue Syndrome (CFS) patients as normally defined, particularly those that attend specialist clinics [1,2].
A paper has just been published by researchers from the FDA and NIH which found MLV-like virus gag gene sequences in 32 of 37 (86.5%) of their CFS patients compared with only 3 of 44 (6.8%) healthy volunteer blood donors[3].
In accompanying material[4], they mention the following:
"10. How are the differences between the CDC and FDA study results being evaluated?
Differences in the results could reflect differences in the... read full comment
Comment on: Switzer et al. Retrovirology, 7:57
Clarificaiton on Herpesviruses (Monica Tomaszewski, 26 July 2010)
Is there a particular reason why the authors choose to make a distinction between HCMV and HHV-5, as CMV is the 5th human herpesvirus? read full comment
Comment on: Banerjee et al. Retrovirology, 7:8
Methodological deficiencies in the study by Switzer et al (Gerwyn Morris, 23 July 2010)
A number of people here have already commented (quite eloquently) on the inappropriateness of using the Reeves 2005 criteria to diagnose people with ME/CFS. Indeed, using a selection criteria which has roughly the same chance of separating people with this illness from a generally fatigued population as tossing a coin is not the most auspicious of starts. That said however there are also some serious shortcomings with the methodology of the Switzer et al. paper which would make the detection of an in vivo virus highly unlikely, if present, in the people included in this study, regardless of the patient criteria used.
The terms analytical sensitivity and diagnostic sensitivity, although often used interchangeably, have entirely different meanings. Analytical... read full comment
Comment on: Switzer et al. Retrovirology, 7:57
What patient group are they studying? (Robin Durham, 23 July 2010)
I am a patient. I was given the diagnosis 15 years ago using the original Fukuda definition (which does include tender lymphadenopathy despite what the authors of the study say). I also meet the criteria for the Canadian Consensus definition. I would have been excluded from this study because I have some of the physical findings of the Canadian definition. If I don't have CDC defined CFS, what do I have? read full comment
Comment on: Switzer et al. Retrovirology, 7:57