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Mikovits responds to Singh Study

Cort

Phoenix Rising Founder
Agreed, retraction seems a bit extreme. There are plenty of papers published on scientific theories that don't work out. Almost none of them are retracted. Thats how science works, people publish and others try the same (or in this case similar) experiments and theories are confirmed or not. There is no need for a retraction... sheez these people are worked up. I wish they'd just focus on figuring out what causes CFS, whatever that may end up being.

.

I agree it does seem extreme... I looked up retractions...they do occur from time to time - but why not just let the story play itself out?
 

Cort

Phoenix Rising Founder
if WPI played it alot safer, they (whoever gives out research grants) could have rolled her alot easier like Defreitus.

But, but heapsreal -- the WPI hasn't gotten any XMRV grants; something is not working..Actually there haven't been alot of XMRV grants anyway - that's true...just a handful I think; most researchers have found money somewhere. THe NCI, for instance, has dumped a boatload of money on XMRV without disbursing any or many grants.
 

alex3619

Senior Member
Messages
13,810
Location
Logan, Queensland, Australia
Hi Cort, the immune abnormalities paper is part funded by NIH, so the WPI got at least some money. Check the acknowledgements:

National Institutes of Health,
Grant RO1A1078234, and private funding by the Whittemore
Family Foundation supported these studies.

Bye
Alex
 

Cort

Phoenix Rising Founder
Actually that grant was for immune abnormalities in CFS and not for XMRV. It does however mention 'novel viral infections in CFS' which certainly can apply to XMRV. It started in 2009 - they may have applied for it well before XMRV showed up...Its supposed to go through 2014...so we should be hearing more over time.


DESCRIPTION (provided by applicant): Chronic Fatigue Syndrome (CFS) is a complex disease estimated to affect between 0.5%-2% of the population in the Western world. Its pathogenesis is thought to involve both inherited and environmental (including viral) components, as with other chronic inflammatory diseases such as, multiple sclerosis, rheumatoid arthritis, and atherosclerosis. Consistent with this chronic inflammatory context, CFS patients are known to have a shortened life-span and are at risk for developing lymphoma. We hypothesize that chronic inflammatory stimulation from active and recurrent infections of multiple viruses on a susceptible host genetic background leads to the pathogenesis characterized by CFS. The overall goal of this research project is to define these viral and host parameters in European and American cohorts of CFS patients that correlate with distinct disease phenotypes, including the development of mantle cell lymphoma (MCL) in a subgroup of the American cohort.

In Aim 1) we will identify and confirm novel viral infections in European and American CFS patient cohorts. 1.1) we will use two complementary methods for detection of novel virus mRNA: massive parallel signature sequencing (MPSS) and a custom DNA microarray. 1.2) Quantitative polymerase chain reaction Q-PCR will be used for confirmation of virus gene expression. 1.3) immortalized cell lines will be developed to isolate virus and elucidate links between virus and host cell gene expression.

In Aim 2), we will elucidate genetic factors of susceptibility and the dysregulation of the host defense system. Specifically, we will determine: 2.1) PBMC gene expression of 88 human genes previously confirmed as being differentially expressed in CFS 2.2) serum chemokine and cytokine profiles using multiplex suspension antibody arrays on a Luminex platform 2.3) HLA, KIR genotypes and whole genome SNP profiles 2.4) Defects in the type I Interferon signaling pathway. In each subaim both cohorts will be compared to normal and disease controls using specimens of serum and PBMC taken at multiple time-points from individual patients and taken from our unique and extensive sample repository.

This study will provide information necessary for development of treatment and diagnostic strategies for distinct subgroups of CFS patients, and may identify novel virus associations, genetic signatures and biomarkers, which can predict the development of MCL, thus enabling use of preventive therapeutics.

PUBLIC HEALTH RELEVANCE: The proposed research will provide significant insight into the disease mechanisms of Chronic Fatigue Syndrome so accurate testing and specific treatments can be developed with a goal of curing the disease and preventing life-threatening complications.
 

Cort

Phoenix Rising Founder
Actually that grant was for immune abnormalities in CFS and not for XMRV. It does however mention 'novel viral infections in CFS' which certainly can apply to XMRV. It started in 2009 - they may have applied for it well before XMRV showed up...Its supposed to go through 2014...so we should be hearing more over time.


DESCRIPTION (provided by applicant): Chronic Fatigue Syndrome (CFS) is a complex disease estimated to affect between 0.5%-2% of the population in the Western world. Its pathogenesis is thought to involve both inherited and environmental (including viral) components, as with other chronic inflammatory diseases such as, multiple sclerosis, rheumatoid arthritis, and atherosclerosis. Consistent with this chronic inflammatory context, CFS patients are known to have a shortened life-span and are at risk for developing lymphoma. We hypothesize that chronic inflammatory stimulation from active and recurrent infections of multiple viruses on a susceptible host genetic background leads to the pathogenesis characterized by CFS. The overall goal of this research project is to define these viral and host parameters in European and American cohorts of CFS patients that correlate with distinct disease phenotypes, including the development of mantle cell lymphoma (MCL) in a subgroup of the American cohort.

In Aim 1) we will identify and confirm novel viral infections in European and American CFS patient cohorts. 1.1) we will use two complementary methods for detection of novel virus mRNA: massive parallel signature sequencing (MPSS) and a custom DNA microarray. 1.2) Quantitative polymerase chain reaction Q-PCR will be used for confirmation of virus gene expression. 1.3) immortalized cell lines will be developed to isolate virus and elucidate links between virus and host cell gene expression.

In Aim 2), we will elucidate genetic factors of susceptibility and the dysregulation of the host defense system. Specifically, we will determine: 2.1) PBMC gene expression of 88 human genes previously confirmed as being differentially expressed in CFS 2.2) serum chemokine and cytokine profiles using multiplex suspension antibody arrays on a Luminex platform 2.3) HLA, KIR genotypes and whole genome SNP profiles 2.4) Defects in the type I Interferon signaling pathway. In each subaim both cohorts will be compared to normal and disease controls using specimens of serum and PBMC taken at multiple time-points from individual patients and taken from our unique and extensive sample repository.

This study will provide information necessary for development of treatment and diagnostic strategies for distinct subgroups of CFS patients, and may identify novel virus associations, genetic signatures and biomarkers, which can predict the development of MCL, thus enabling use of preventive therapeutics.

PUBLIC HEALTH RELEVANCE: The proposed research will provide significant insight into the disease mechanisms of Chronic Fatigue Syndrome so accurate testing and specific treatments can be developed with a goal of curing the disease and preventing life-threatening complications.