judy mikovits

Discussion in 'Fibromyalgia Main Forum' started by consuegra, Sep 25, 2009.

  1. consuegra

    consuegra New Member

    Experimental Pathology Seminar Series
    Judy Mikovits, PhD

    Research Director

    Whittemore Peterson Institute

    "Detection and Immune correlates of Infectious XMRV in the blood of
    patients with Neuroimmune Disease and Cancer."


    Mitovitz gives this talk on November 6th.

    Chris
  2. skeptik2

    skeptik2 Member

    At the WPI?

    Do you know if a paper has been published about this?

    Can anyone find out?

    Thanks,
    skeptik2
  3. ulala

    ulala New Member

    http://jvi.asm.org/cgi/content/abstract/82/20/9964

    this is about this virus in relation to prostrate cancer but in the footnotes of cittions is:

    Knouf, E. C., Metzger, M. J., Mitchell, P. S., Arroyo, J. D., Chevillet, J. R., Tewari, M., Miller, A. D. (2009). Multiple Integrated Copies and High-Level Production of the Human Retrovirus XMRV (Xenotropic Murine Leukemia Virus-Related Virus) from 22Rv1 Prostate Carcinoma Cells. J. Virol. 83: 7353-7356 [Abstract] [Full Text]


    This is in the last paragraph of the second article:

    DeRisi and Ganem said they are planning studies to explore whether XMRV is restricted to prostate cancers or whether it is more widespread in the body and in other segments of the human population. To answer such questions, the researchers are developing a blood test that can be used in epidemiological studies.




    Journal of Virology, October 2008, p. 9964-9977, Vol. 82, No. 20
    0022-538X/08/$08.00+0 doi:10.1128/JVI.01299-08
    Copyright © 2008, American Society for Microbiology. All Rights Reserved.


    Integration Site Preference of Xenotropic Murine Leukemia Virus-Related Virus, a New Human Retrovirus Associated with Prostate Cancer
    Sanggu Kim,1 Namshin Kim,3, Beihua Dong,5 David Boren,2 Serena A. Lee,2 Jaydip Das Gupta,5 Christina Gaughan,5 Eric A. Klein,6 Christopher Lee,3 Robert H. Silverman,5 and Samson A. Chow1,2,3,4*
    Biomedical Engineering Interdepartmental Program,1 Department of Molecular and Medical Pharmacology,2 Molecular Biology Institute,3 UCLA AIDS Institute, UCLA School of Medicine, Los Angeles, California 90095,4 Department of Cancer Biology, Lerner Research Institute,5 Glickman Urological and Kidney Institute, Cleveland Clinic, Cleveland, Ohio 441956

    Received 22 June 2008/ Accepted 3 August 2008

    Xenotropic murine leukemia virus-related virus (XMRV) is a new human gammaretrovirus identified in prostate cancer tissue from patients homozygous for a reduced-activity variant of the antiviral enzyme RNase L. Neither a casual relationship between XMRV infection and prostate cancer nor a mechanism of tumorigenesis has been established. To determine the integration site preferences of XMRV and the potential risk of proviral insertional mutagenesis, we carried out a genome-wide analysis of viral integration sites in the prostate cell line DU145 after an acute XMRV infection and compared the integration site pattern of XMRV with those found for murine leukemia virus and two human retroviruses, human immunodeficiency virus type 1 and human T-cell leukemia virus type 1. Among all retroviruses analyzed, XMRV has the strongest preference for transcription start sites, CpG islands, DNase-hypersensitive sites, and gene-dense regions; all are features frequently associated with structurally open transcription regulatory regions of a chromosome. Analyses of XMRV integration sites in tissues from prostate cancer patients found a similar preference for the aforementioned chromosomal features. Additionally, XMRV integration sites in cancer tissues were associated with cancer breakpoints, common fragile sites, microRNA, and cancer-related genes, suggesting a selection process that favors certain chromosomal integration sites. In both acutely infected cells and cancer tissues, no common integration site was detected within or near proto-oncogenes or tumor suppressor genes. These results are consistent with a model in which XMRV may contribute to tumorigenicity via a paracrine mechanism.



    --------------------------------------------------------------------------------
    * Corresponding author. Mailing address: 23-133 CHS, UCLA School of Medicine, Los Angeles, CA 90095. Phone: (310) 825-9600. Fax: (310) 825-6267. E-mail: schow@mednet.ucla.edu

    Published ahead of print on 6 August 2008.

    Present address: Korean Bioinformation Center, Korean Research Institute of Bioscience and Technology, Daejeon 305-806, South Korea.



    --------------------------------------------------------------------------------
    Journal of Virology, October 2008, p. 9964-9977, Vol. 82, No. 20
    0022-538X/08/$08.00+0 doi:10.1128/JVI.01299-08
    Copyright © 2008, American Society for Microbiology. All Rights Reserved.




    This article has been cited by other articles:


    Schlaberg, R., Choe, D. J., Brown, K. R., Thaker, H. M., Singh, I. R. (2009). XMRV is present in malignant prostatic epithelium and is associated with prostate cancer, especially high-grade tumors. Proc. Natl. Acad. Sci. USA 106: 16351-16356 [Abstract] [Full Text]
    Hong, S., Klein, E. A., Das Gupta, J., Hanke, K., Weight, C. J., Nguyen, C., Gaughan, C., Kim, K.-A., Bannert, N., Kirchhoff, F., Munch, J., Silverman, R. H. (2009). Fibrils of Prostatic Acid Phosphatase Fragments Boost Infections with XMRV (Xenotropic Murine Leukemia Virus-Related Virus), a Human Retrovirus Associated with Prostate Cancer. J. Virol. 83: 6995-7003 [Abstract] [Full Text]
    Knouf, E. C., Metzger, M. J., Mitchell, P. S., Arroyo, J. D., Chevillet, J. R., Tewari, M., Miller, A. D. (2009). Multiple Integrated Copies and High-Level Production of the Human Retrovirus XMRV (Xenotropic Murine Leukemia Virus-Related Virus) from 22Rv1 Prostate Carcinoma Cells. J. Virol. 83: 7353-7356 [Abstract] [Full Text]
    Vatakis, D. N., Kim, S., Kim, N., Chow, S. A., Zack, J. A. (2009). Human Immunodeficiency Virus Integration Efficiency and Site Selection in Quiescent CD4+ T Cells. J. Virol. 83: 6222-6233 [Abstract] [Full Text]


    New human retrovirus - Xenotropic MuLV-related virus (XMRV)
    Apr 1, 2006, 19:27, Reviewed by: Dr. Priya Saxena


    When the researchers isolated and sequenced the genome of the virus, they found that it was a xenotropic virus – one that can only grow in foreign cells other than mouse cells. Thus, they named the virus, Xenotropic MuLV-related virus, or XMRV.



    By Howard Hughes Medical Institute, Howard Hughes Medical Institute researchers and their colleagues have discovered a new retrovirus in humans that is closely related to a cancer-causing virus found in mice. Their findings describe the first documented cases of human infection with a retrovirus that is native to rodents.

    The researchers discovered the virus in patients with a rare type of prostate cancer. The patients in the study have a genetic mutation that compromised some of their natural defenses against viral infection. Thus, the researchers said their discovery raises the possibility that increased susceptibility to viral infection may play a role in development of some cancers. However, they emphasized that their findings by no means implicate the virus, dubbed XMRV, in causing prostate cancer. The virus may well have flourished as a result of the failure of the defense mechanism; and other factors such as chronic inflammation may play a more direct role in the cancer.

    The discovery of the new virus was made by an interdisciplinary research team led by Robert Silverman of Cleveland Clinic and HHMI investigators Joseph DeRisi and Don Ganem, both at the University of California at San Francisco. A paper describing the findings was published on March 31, 2006, in the journal, Public Library of Science Pathogens.

    The search for the new virus began when Silverman and his colleagues provided samples of a rare familial prostate cancer in which the viral-defense gene, RNASEL, had been mutated in a specific way. This mutation compromised the function of the enzyme produced by RNASEL, which normally shreds viral genetic material. Infected cells carrying the shredded viral genetic material are usually targeted for destruction by the immune system. While some scientists believe that such vulnerability to viral infection is connected to prostate cancer in these rare cases, others have presented evidence contesting that theory.

    To screen for viruses in the prostate tissue samples, DeRisi and Ganem used the Virochip, which was invented by DeRisi and his colleagues. The Virochip consists of a microarray of some 20,000 characteristic gene sequences -- called oligonucleotides -- representing a vast array of known viruses. The oligonucleotides are deposited as tiny spots on a small glass chip.

    To detect viruses from tissue samples, the researchers isolated genetic material from each sample and tagged the genetic material with a fluorescent tracer. They then applied the fluorescently tagged genetic material to the microarray chip. Since genes tended to adhere to those with a complementary genetic sequence, any viral gene sequences in the sample would attach themselves to corresponding viral sequences on the chip. The telltale fluorescence on spots on the chip signaled the presence of viral genetic material in the sample.

    Although the Virochip contains only sequences from known viruses, DeRisi said it can also detect new viruses because they invariably contain sequences that have been conserved in their evolution from related viruses.

    The initial screen of the RNASEL-mutant prostate cancers revealed the presence of a genetic sequence that closely resembled that of a mouse virus called murine leukemia virus (MuLV). Murine leukemia virus is known as an endogenous virus because it normally exists as an integrated part of the mouse genome, rather than as independent, infective particle. MuLV is also a retrovirus, meaning its genetic material is in the form of RNA. The RNA is then reverse transcribed into DNA that is integrated into the DNA of the host cell the virus is infecting.

    When the researchers isolated and sequenced the genome of the virus, they found that it was a xenotropic virus – one that can only grow in foreign cells other than mouse cells. Thus, they named the virus, Xenotropic MuLV-related virus, or XMRV.

    "This finding was a big surprise because most of these endogenous viral genomes have undergone such mutation and deletion that they are incapable of giving rise to viruses any more," said Ganem. "And while some of these viruses had been induced to grow in human cells in culture, the major question is whether such infection could ever happen in nature.

    "So, one of the things that is important about our study from a virologic point of view, is that this is the first really solid example of an authentic xenotropic retroviral infection in a human being," said Ganem.

    According to DeRisi, the Virochip made it possible to analyze these samples without preconceived biases about what viruses might be present. "Since the chip represents every known virus in one assay, it is agnostic as to what might be found," he said. "We would never have looked for this class of virus if it wasn't for the virus chip."

    Importantly, the researchers found that prostate cancers in which both copies of the RNASEL gene were crippled by mutation showed much more frequent XMRV infection than did those cancers that still had one normal copy of the RNASEL gene.

    "This link between the virus and RNASEL is the second finding that is important and is firmly established in this study," noted Ganem. "We don't see the infection in people who don't have the RNASEL mutation, which suggests strongly RNASEL is an important part of the defense against retroviral infection. This is the first evidence in humans of findings that were previously made only in vitro."

    DeRisi pointed out that detailed comparison of samples of the virus between people found that – although all were XMRV – they showed tiny genetic variations. "So, while it is the same virus in each patient, the viruses are different enough to say that they are most likely independently acquired and are not the result of some contamination of the samples," he said.

    Ganem cautioned that any link between XMRV and prostate cancer is tenuous at best. "First, the genetic variant we studied occurs in familial clusters that constitute only a very small sliver of prostate cancers," he said. "And secondly, there are many reasons to believe that the virus might not relate to prostate cancer."

    For example, he pointed out, analysis of prostate tissue by Silverman and his colleagues indicated that the virus appears only in a small percentage of connective tissue cells, called stromal cells, rather than in the tumors themselves. "So, one interpretation could be that the infection is entirely incidental to prostate cancer," said Ganem. "The patients with RNASEL mutations may be more likely to get the infection or perhaps less likely to clear it. Clearly XMRV is not a classic oncogenic virus."

    Nevertheless, said Ganem, an indirect link to cancer cannot be ruled out, since "in cancer research these days, there is a lot of interest in the stroma as the soil in which cancer arises." He added that the chronic inflammation from infection of stromal tissues may play a role in triggering such cancers.

    DeRisi observed that "it may be that men who are so-called RNASEL-mutant are just more susceptible to viruses in general, and this susceptibility has little to do with their cancer. Nevertheless, the fact that this virus is found in tumor tissue and that it is a new virus and the first of its kind ever documented in humans is an intriguing finding that demands to be followed up. This initial finding raises many questions. For example, what is the route of transmission? How is the virus passed from person to person? And are people the natural reservoir of this virus, or is it some other organism?"

    DeRisi and Ganem said they are planning studies to explore whether XMRV is restricted to prostate cancers or whether it is more widespread in the body and in other segments of the human population. To answer such questions, the researchers are developing a blood test that can be used in epidemiological studies.


    New human retrovirus - Xenotropic MuLV-related virus (XMRV)
    Apr 1, 2006, 19:27, Reviewed by: Dr. Priya Saxena


    When the researchers isolated and sequenced the genome of the virus, they found that it was a xenotropic virus – one that can only grow in foreign cells other than mouse cells. Thus, they named the virus, Xenotropic MuLV-related virus, or XMRV.



    By Howard Hughes Medical Institute, Howard Hughes Medical Institute researchers and their colleagues have discovered a new retrovirus in humans that is closely related to a cancer-causing virus found in mice. Their findings describe the first documented cases of human infection with a retrovirus that is native to rodents.

    The researchers discovered the virus in patients with a rare type of prostate cancer. The patients in the study have a genetic mutation that compromised some of their natural defenses against viral infection. Thus, the researchers said their discovery raises the possibility that increased susceptibility to viral infection may play a role in development of some cancers. However, they emphasized that their findings by no means implicate the virus, dubbed XMRV, in causing prostate cancer. The virus may well have flourished as a result of the failure of the defense mechanism; and other factors such as chronic inflammation may play a more direct role in the cancer.

    The discovery of the new virus was made by an interdisciplinary research team led by Robert Silverman of Cleveland Clinic and HHMI investigators Joseph DeRisi and Don Ganem, both at the University of California at San Francisco. A paper describing the findings was published on March 31, 2006, in the journal, Public Library of Science Pathogens.

    The search for the new virus began when Silverman and his colleagues provided samples of a rare familial prostate cancer in which the viral-defense gene, RNASEL, had been mutated in a specific way. This mutation compromised the function of the enzyme produced by RNASEL, which normally shreds viral genetic material. Infected cells carrying the shredded viral genetic material are usually targeted for destruction by the immune system. While some scientists believe that such vulnerability to viral infection is connected to prostate cancer in these rare cases, others have presented evidence contesting that theory.

    To screen for viruses in the prostate tissue samples, DeRisi and Ganem used the Virochip, which was invented by DeRisi and his colleagues. The Virochip consists of a microarray of some 20,000 characteristic gene sequences -- called oligonucleotides -- representing a vast array of known viruses. The oligonucleotides are deposited as tiny spots on a small glass chip.

    To detect viruses from tissue samples, the researchers isolated genetic material from each sample and tagged the genetic material with a fluorescent tracer. They then applied the fluorescently tagged genetic material to the microarray chip. Since genes tended to adhere to those with a complementary genetic sequence, any viral gene sequences in the sample would attach themselves to corresponding viral sequences on the chip. The telltale fluorescence on spots on the chip signaled the presence of viral genetic material in the sample.

    Although the Virochip contains only sequences from known viruses, DeRisi said it can also detect new viruses because they invariably contain sequences that have been conserved in their evolution from related viruses.

    The initial screen of the RNASEL-mutant prostate cancers revealed the presence of a genetic sequence that closely resembled that of a mouse virus called murine leukemia virus (MuLV). Murine leukemia virus is known as an endogenous virus because it normally exists as an integrated part of the mouse genome, rather than as independent, infective particle. MuLV is also a retrovirus, meaning its genetic material is in the form of RNA. The RNA is then reverse transcribed into DNA that is integrated into the DNA of the host cell the virus is infecting.

    When the researchers isolated and sequenced the genome of the virus, they found that it was a xenotropic virus – one that can only grow in foreign cells other than mouse cells. Thus, they named the virus, Xenotropic MuLV-related virus, or XMRV.

    "This finding was a big surprise because most of these endogenous viral genomes have undergone such mutation and deletion that they are incapable of giving rise to viruses any more," said Ganem. "And while some of these viruses had been induced to grow in human cells in culture, the major question is whether such infection could ever happen in nature.

    "So, one of the things that is important about our study from a virologic point of view, is that this is the first really solid example of an authentic xenotropic retroviral infection in a human being," said Ganem.

    According to DeRisi, the Virochip made it possible to analyze these samples without preconceived biases about what viruses might be present. "Since the chip represents every known virus in one assay, it is agnostic as to what might be found," he said. "We would never have looked for this class of virus if it wasn't for the virus chip."

    Importantly, the researchers found that prostate cancers in which both copies of the RNASEL gene were crippled by mutation showed much more frequent XMRV infection than did those cancers that still had one normal copy of the RNASEL gene.

    "This link between the virus and RNASEL is the second finding that is important and is firmly established in this study," noted Ganem. "We don't see the infection in people who don't have the RNASEL mutation, which suggests strongly RNASEL is an important part of the defense against retroviral infection. This is the first evidence in humans of findings that were previously made only in vitro."

    DeRisi pointed out that detailed comparison of samples of the virus between people found that – although all were XMRV – they showed tiny genetic variations. "So, while it is the same virus in each patient, the viruses are different enough to say that they are most likely independently acquired and are not the result of some contamination of the samples," he said.

    Ganem cautioned that any link between XMRV and prostate cancer is tenuous at best. "First, the genetic variant we studied occurs in familial clusters that constitute only a very small sliver of prostate cancers," he said. "And secondly, there are many reasons to believe that the virus might not relate to prostate cancer."

    For example, he pointed out, analysis of prostate tissue by Silverman and his colleagues indicated that the virus appears only in a small percentage of connective tissue cells, called stromal cells, rather than in the tumors themselves. "So, one interpretation could be that the infection is entirely incidental to prostate cancer," said Ganem. "The patients with RNASEL mutations may be more likely to get the infection or perhaps less likely to clear it. Clearly XMRV is not a classic oncogenic virus."

    Nevertheless, said Ganem, an indirect link to cancer cannot be ruled out, since "in cancer research these days, there is a lot of interest in the stroma as the soil in which cancer arises." He added that the chronic inflammation from infection of stromal tissues may play a role in triggering such cancers.

    DeRisi observed that "it may be that men who are so-called RNASEL-mutant are just more susceptible to viruses in general, and this susceptibility has little to do with their cancer. Nevertheless, the fact that this virus is found in tumor tissue and that it is a new virus and the first of its kind ever documented in humans is an intriguing finding that demands to be followed up. This initial finding raises many questions. For example, what is the route of transmission? How is the virus passed from person to person? And are people the natural reservoir of this virus, or is it some other organism?"

    DeRisi and Ganem said they are planning studies to explore whether XMRV is restricted to prostate cancers or whether it is more widespread in the body and in other segments of the human population. To answer such questions, the researchers are developing a blood test that can be used in epidemiological studies.


    New human retrovirus - Xenotropic MuLV-related virus (XMRV)
    Apr 1, 2006, 19:27, Reviewed by: Dr. Priya Saxena


    When the researchers isolated and sequenced the genome of the virus, they found that it was a xenotropic virus – one that can only grow in foreign cells other than mouse cells. Thus, they named the virus, Xenotropic MuLV-related virus, or XMRV.



    By Howard Hughes Medical Institute, Howard Hughes Medical Institute researchers and their colleagues have discovered a new retrovirus in humans that is closely related to a cancer-causing virus found in mice. Their findings describe the first documented cases of human infection with a retrovirus that is native to rodents.

    The researchers discovered the virus in patients with a rare type of prostate cancer. The patients in the study have a genetic mutation that compromised some of their natural defenses against viral infection. Thus, the researchers said their discovery raises the possibility that increased susceptibility to viral infection may play a role in development of some cancers. However, they emphasized that their findings by no means implicate the virus, dubbed XMRV, in causing prostate cancer. The virus may well have flourished as a result of the failure of the defense mechanism; and other factors such as chronic inflammation may play a more direct role in the cancer.

    The discovery of the new virus was made by an interdisciplinary research team led by Robert Silverman of Cleveland Clinic and HHMI investigators Joseph DeRisi and Don Ganem, both at the University of California at San Francisco. A paper describing the findings was published on March 31, 2006, in the journal, Public Library of Science Pathogens.

    The search for the new virus began when Silverman and his colleagues provided samples of a rare familial prostate cancer in which the viral-defense gene, RNASEL, had been mutated in a specific way. This mutation compromised the function of the enzyme produced by RNASEL, which normally shreds viral genetic material. Infected cells carrying the shredded viral genetic material are usually targeted for destruction by the immune system. While some scientists believe that such vulnerability to viral infection is connected to prostate cancer in these rare cases, others have presented evidence contesting that theory.

    To screen for viruses in the prostate tissue samples, DeRisi and Ganem used the Virochip, which was invented by DeRisi and his colleagues. The Virochip consists of a microarray of some 20,000 characteristic gene sequences -- called oligonucleotides -- representing a vast array of known viruses. The oligonucleotides are deposited as tiny spots on a small glass chip.

    To detect viruses from tissue samples, the researchers isolated genetic material from each sample and tagged the genetic material with a fluorescent tracer. They then applied the fluorescently tagged genetic material to the microarray chip. Since genes tended to adhere to those with a complementary genetic sequence, any viral gene sequences in the sample would attach themselves to corresponding viral sequences on the chip. The telltale fluorescence on spots on the chip signaled the presence of viral genetic material in the sample.

    Although the Virochip contains only sequences from known viruses, DeRisi said it can also detect new viruses because they invariably contain sequences that have been conserved in their evolution from related viruses.

    The initial screen of the RNASEL-mutant prostate cancers revealed the presence of a genetic sequence that closely resembled that of a mouse virus called murine leukemia virus (MuLV). Murine leukemia virus is known as an endogenous virus because it normally exists as an integrated part of the mouse genome, rather than as independent, infective particle. MuLV is also a retrovirus, meaning its genetic material is in the form of RNA. The RNA is then reverse transcribed into DNA that is integrated into the DNA of the host cell the virus is infecting.

    When the researchers isolated and sequenced the genome of the virus, they found that it was a xenotropic virus – one that can only grow in foreign cells other than mouse cells. Thus, they named the virus, Xenotropic MuLV-related virus, or XMRV.

    "This finding was a big surprise because most of these endogenous viral genomes have undergone such mutation and deletion that they are incapable of giving rise to viruses any more," said Ganem. "And while some of these viruses had been induced to grow in human cells in culture, the major question is whether such infection could ever happen in nature.

    "So, one of the things that is important about our study from a virologic point of view, is that this is the first really solid example of an authentic xenotropic retroviral infection in a human being," said Ganem.

    According to DeRisi, the Virochip made it possible to analyze these samples without preconceived biases about what viruses might be present. "Since the chip represents every known virus in one assay, it is agnostic as to what might be found," he said. "We would never have looked for this class of virus if it wasn't for the virus chip."

    Importantly, the researchers found that prostate cancers in which both copies of the RNASEL gene were crippled by mutation showed much more frequent XMRV infection than did those cancers that still had one normal copy of the RNASEL gene.

    "This link between the virus and RNASEL is the second finding that is important and is firmly established in this study," noted Ganem. "We don't see the infection in people who don't have the RNASEL mutation, which suggests strongly RNASEL is an important part of the defense against retroviral infection. This is the first evidence in humans of findings that were previously made only in vitro."

    DeRisi pointed out that detailed comparison of samples of the virus between people found that – although all were XMRV – they showed tiny genetic variations. "So, while it is the same virus in each patient, the viruses are different enough to say that they are most likely independently acquired and are not the result of some contamination of the samples," he said.

    Ganem cautioned that any link between XMRV and prostate cancer is tenuous at best. "First, the genetic variant we studied occurs in familial clusters that constitute only a very small sliver of prostate cancers," he said. "And secondly, there are many reasons to believe that the virus might not relate to prostate cancer."

    For example, he pointed out, analysis of prostate tissue by Silverman and his colleagues indicated that the virus appears only in a small percentage of connective tissue cells, called stromal cells, rather than in the tumors themselves. "So, one interpretation could be that the infection is entirely incidental to prostate cancer," said Ganem. "The patients with RNASEL mutations may be more likely to get the infection or perhaps less likely to clear it. Clearly XMRV is not a classic oncogenic virus."

    Nevertheless, said Ganem, an indirect link to cancer cannot be ruled out, since "in cancer research these days, there is a lot of interest in the stroma as the soil in which cancer arises." He added that the chronic inflammation from infection of stromal tissues may play a role in triggering such cancers.

    DeRisi observed that "it may be that men who are so-called RNASEL-mutant are just more susceptible to viruses in general, and this susceptibility has little to do with their cancer. Nevertheless, the fact that this virus is found in tumor tissue and that it is a new virus and the first of its kind ever documented in humans is an intriguing finding that demands to be followed up. This initial finding raises many questions. For example, what is the route of transmission? How is the virus passed from person to person? And are people the natural reservoir of this virus, or is it some other organism?"

    DeRisi and Ganem said they are planning studies to explore whether XMRV is restricted to prostate cancers or whether it is more widespread in the body and in other segments of the human population. To answer such questions, the researchers are developing a blood test that can be used in epidemiological studies.

    - March 31, 2006, in the journal, Public Library of Science Pathogens.





  4. consuegra

    consuegra New Member

    I went back and looked at the Mikovits talk in London and she mentioned that her work on a novel virus not previously associated with CFS had been submitted to Science Magazine. My guess would be that this is going to be published in the next Science magazine in mid-October. I do not think she would be giving a presentation until it was published.

    Chris
  5. skeptik2

    skeptik2 Member

    ...for your extra efforts at looking at Mikovits talk in London and
    finding out it would be in Science in mid-October...just in time for
    it to expose the CDC's lack of scientific rigor!!!

    Right on!

    skeptik2
  6. simpsons

    simpsons Member

    http://www.wpinstitute.org/research/research_basic.html
    You can find judy's and other researchers profiles and history on this link too.

    WPI
    Current Research Program

    Study Title and Description Collaborators
    Role of Chronic Inflammatory and Immune Stimulation by Active Herpesvirus Infection in the Development of Immune Dysfunction in CFS
    Studies of immune abnormalities in this CFS cohort will involve phenotypic analysis of NK, DC, and T cell populations. States of activation and differentiation will be studied to determine whether the cells are immune activators or suppressors due to response to infection.


    The goal is to understand the imbalance in the immune system that leads to unregulated virus expression.

    Francis Ruscetti, PhD, NCI
    Dennis Taub, PhD, NIA
    (INIP Research Award)
    Novel Viruses/Co-infections in Subgroups of CFS
    A Virus DNA Microarray (Virochip) was used to screen a cohort of CFS with Immunological defects and increased incidence of Mantle cell lymphoma (MCL).

    Francis Ruscetti, PhD, Cancer Inflammation Program, NCI

    Role of the Interferon/RNaseL Antiviral Pathway in CFS
    The goal of this study is to characterize defects in the Interferon/RNaseL antiviral pathway which result in viral persistence.

    Robert Silverman, PhD, Cleveland Clinic

    Role of Inflammatory Cytokines and Chemokines in CFS
    The purpose of this study is to identify and develop the serum biomarker patterns of cytokine and chemokines, which correlate with clinical disease and can be used to monitor intervention. Dennis D. Taub, PhD, NIA

    Host Susceptibility in CFS
    The goal of this study is to elucidate genetic factors of susceptibility and the dysregulation of the host defense system in order to develop biomarkers for diagnostic development and thus predict response to immune modulating therapy and vaccines.

    Jonathan R. Kerr, MD, PhD, St. Georges University, London UK
    Mary Carrington, PhD, NCI
    Mike Dean, PhD, NCI
    Enumeration and Function of Natural Killer (NK) Cells in CFS
    The purpose of this project is to develop improved NK diagnostic tests for both the number and function of NK cells. Doug Redelman, PhD, UNR, Dept. of Microbiology & Immunology
    Epidemiologic Evaluation of Lymphoma and Cancer Incidence in Nevada CFS Cohort

    The goal of this study is to determine if a possible cancer cluster exists in the cohort of Nevada CFS patients.

    Paul Levine, MD, George Washington University

    Study of Clonal T Cell Receptor-gamma Rearrangements in Nevada CFS Cohort
    The purpose of this study is to determine the significance of clonal T cell receptor-gamma rearrangements in the pathogenesis of CFS.
    Dorothy Hudig, PhD, UNR, Dept. of Microbiology & Immunology

    Development of a Whole Genome Transcriptome Assay for HHV6
    The goal is to develop a whole genome transcriptome assay for HHV6 and a sub array for HHV6A specific detection to be used as a diagnostic tool or research tool to understand the viral life cycle in disease.
    Rachel Bagni, PhD, Applied Technology Program, NCI

    HHV6 Latency in CFS
    The goal of this study is to understand the role of HHV6A latency in bone marrow hematopoietic stem cells in the pathogenesis of CFS.

    Stephen St. Joer, PhD
    Marianna Bego, PhD, UNR, Dept. of Microbiology & Immunology
  7. simpsons

    simpsons Member

    being also at that conference you spoke of i heard judy say that there was a link with non hodgekinsons lymphoma. so this seems to fit in with that. i wonder how that fits in with prof k d m's research do you think. there is still viral load and perhaps this is the long term risks????

    good to seee johnathon kerr still in there he is a brilliant scientist also

    thanks for the information. i should think you are the best carer and advocate one could ask for, we appreciate you
    peace love and goodwill