NIH $1.6 Million award for ME/CFS Research for Drs. Mikovits & Kerr

XMRV Retrovirus Whittemore Peterson CFS study Media Round up: 13

WordPress Shortlink: http://wp.me/p5foE-2co

Media

Source: Prohealth

http://www.prohealth.com/library/showarticle.cfm?libid=14948

NIH Bets $1.6 Million on Continued ME/CFS Research by Drs. Mikovits & Kerr*

October 21, 2009

Dr. Judy Mikovits (principle investigator) and the Whittemore-Peterson Institute, with collaborator Dr. Jonathan Kerr, have been awarded a 5-year, $1.6 million grant from the NIH’s National Institute of Allergy and Infectious Diseases (NIAID) to support ongoing research into the disease mechanisms of chronic fatigue syndrome. Dr. Kerr is associated with St. George’s College in London.

The award was announced Sep 24 on the WPI website, before news of the CFS-associated XMRV retrovirus was published Oct 8 by the journal Science. A description of the project (# 1R01AI078234-01A2) is now included in the NIH’s Research Portfolio Online.

( http://projectreporter.nih.gov/reporter.cfm?CFID=7257406&CFTOKEN=97499939 )

Key Details from the NIH’s Project Description

• Title: “New Strategies to Decipher the Pathophysiology of Chronic Fatigue Syndrome.”

• Objective: “To 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.”

• Timing: start date Sep 28, 2009; projected end date, Aug 31, 2014.

• Funding: First fiscal year funding $335,600; total funding $1.6 million.

• Project Description provided by applicant: (excerpt formatted for greater legibility, as follows).

______________________________

“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.”….

 

[*Ed: Dr. Jonathan Kerr is a member of the Research Committee for the UK CFS Research Foundation; Dr Kerr is also a member of the MRC's CFS/ME Expert Group  which is chaired by Professor Stephen Holgate.  Professor Holgate is also a member of the CFS Research Foundation's Research Committee. ]

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Patient community websites, blogs, commentaries

Previous material in the XMRV series of Media updates has referred to “Koch’s postulates”

Jean Harrison, via Co-Cure, 22 October 2008:

From Wikipedia (admittedly not always the best source, but in this case pretty sound)

“1.The microorganism must be found in abundance in all organisms suffering from the disease, but should not be found in healthy animals.

2.The microorganism must be isolated from a diseased organism and grown in pure culture.

3.The cultured microorganism should cause disease when introduced into a healthy organism.

4.The microorganism must be reisolated from the inoculated, diseased experimental host and identified as being identical to the original specific causative agent.

Koch’s postulates were developed in the 19th century as general guidelines to identify pathogens that could be isolated with the techniques of the day.[3] Even in Koch’s time, it was recognized that some infectious agents were clearly responsible for disease even though they did not fulfill all of the postulates.[2][4] Attempts to rigidly apply Koch’s postulates to the diagnosis of viral diseases in the late 19th century, at a time when viruses could not be seen or isolated in culture, may have impeded the early development of the field of virology.[5][6] Currently, a number of infectious agents are accepted as the cause of disease despite their not fulfilling all of Koch’s postulates.[7] Therefore, while Koch’s postulates retain historical importance and continue to inform the approach to microbiologic diagnosis, fulfillment of all four postulates is not required to demonstrate causality.”

Source: http://en.wikipedia.org/wiki/Koch’s_postulates

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Previous ME agenda Media Round ups

Round up 13: NIH $1.6 Million award for ME/CFS Research for Drs. Mikovits & Kerr: http://wp.me/p5foE-2co (you are here)

Round up 12: XMRV Retrovirus Whittemore Peterson CFS study Media Round up 12: http://wp.me/p5foE-2c2

Round up 11: XMRV Retrovirus Whittemore Peterson CFS study Media Round up 11: http://wp.me/p5foE-2bB

Round up 10: Whittemore Peterson Institute XMRV retrovirus study link with CFS (Science journal):
http://wp.me/p5foE-2bk

Round up 9: Notice from Dr David Bell, Lyndonville News; Article by Paul R. Cheney MD, PhD:
http://wp.me/p5foE-2aQ

Round up 8: XMRV retrovirus study: Position statement from ME Association 14.10.09: http://wp.me/p5foE-2at

Round up 7: XMRV Retrovirus: Whittemore Peterson Institute: CFS: Media Round up 7: http://wp.me/p5foE-2aa

Round up 6: XMRV Retrovirus: Whittemore Peterson Institute Chronic Fatigue Syndrome study: Videos and audios: http://wp.me/p5foE-29L

Round up 5: Supporting Online Material for XMRV Chronic Fatigue Syndrome study: http://wp.me/p5foE-299

Round up 4: XMRV Retrovirus: Whittemore Peterson Institute Chronic Fatigue Syndrome study:
http://wp.me/p5foE-28F

Round up 3: Whittemore Peterson Institute (WPI) Chronic Fatigue Syndrome retrovirus XMRV in the media: http://wp.me/p5foE-280

Round up 2: Science 9 October 2009: Whittemore Peterson Institute (WPI) Chronic Fatigue Syndrome link to retrovirus: 08.10.09: http://wp.me/p5foE-27v

Round up 1: Whittemore Peterson Institute (WPI) Chronic Fatigue Syndrome link to retrovirus: 09.10.09: http://wp.me/p5foE-272

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