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Wavy Soul
USA
779 Posts |
 Posted - 10/12/2009 : 00:49:58
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Has anyone looked at the news reports of a new discovery that a virus (also present in prostate cancer) is present in 98% of chronic fatigue sufferers (and very few people without the syndrome).
http://www.itwire.com/content/view/28412/1066/
I found myself having mixed reactions. It's the kind of news that I used to crave, after 30 years of severe CFS and FMS. Knowing about TMS has made me take the whole experience less seriously and it has seemingly alleviated somewhat. But not completely. And the thought that it might just be a damn virus really appeals to me today, feeling like crap, tired of thinking psychologically etc. etc.
Anyone else have any reactions to this news?
Love is the answer, whatever the question |
Edited by - Wavy Soul on 10/12/2009 00:50:46 |
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Scottydog
United Kingdom
330 Posts |
Posted - 10/12/2009 : 05:48:14
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I heard this discovery announced on the 6am BBC news here in the UK and thought to myself that we would be bombarded by 'Told you so' stories from sufferers who can't accept any psychological connection.
Instead there has been nothing. The announcement was never repeated. When you search online the only CF /virus stories are from 2008 and 2007 so maybe this type of discovery is one of many. |
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kilton
38 Posts |
Posted - 10/12/2009 : 06:00:41
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| Keep in mind that this study tells us nothing about cause and effect. Scientists tend to assume that the cause->effect arrow points in an intuitive direction (in this case, that the virus causes CFS), but it could just as easily be the opposite: that CFS effects the immune system in such a way that makes infection by this virus more likely. |
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flutterby
United Kingdom
79 Posts |
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Erata
63 Posts |
Posted - 10/12/2009 : 09:05:36
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Hi Wavy,
I can imagine that reading about that virus could present a fly in the TMS ointment, but I’d be skeptical--wasn’t it earlier thought, and then dismissed, that the Epstein Barr virus caused CFS?
(I’m not very experienced in reading analysis of scientific studies and my eyes tend to glaze over, but didn’t the study state that the virus was found in 67% of the CFS patients who were studied?)
And isn’t prostate cancer the most common form of cancer? That could mean that the virus is also fairly common. I think at least two other interesting questions that could be asked are: how many people diagnosed with prostate cancer also have CFS and how many men with CFS also have prostate cancer (at least you don’t have to worry about that!) Maybe future studies will show its presence in more of the general ‘healthy’ population.
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hundreth
USA
12 Posts |
Posted - 10/12/2009 : 14:01:39
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| Very interested to see what will come of this. Also interested in hearing what others think about it, like Hillbilly and la_kevin. |
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HilaryN
United Kingdom
879 Posts |
Posted - 10/12/2009 : 15:31:18
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I'm an ex-chronic fatigue sufferer - I got better (over a few years) by taking vitamin supplements. That was long before I knew about Sarno, though. Now I think it was TMS.
Check out my post in this thread:
http://www.tmshelp.com/forum/topic.asp?TOPIC_ID=4869
I definitely had a "structural" cause of my illness and I felt like crap. But the antibiotics didn't work and the TMS approach got me better.
Just because something has a structural cause doesn't mean it's not psychological, as my example above shows. One of the many things Dr Sarno's book taught me is that there is no dividing line between the mind and the body: hence his use of the term mindbody. Not mind-body.
It does sound like you need a break, though, Wavy. Maybe you should just cosset yourself for a while!
Hilary N |
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SarnoFan
USA
72 Posts |
Posted - 10/13/2009 : 11:20:06
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The opening paragraph states it has not been proven. They are looking at possible links. Depression has a strong link to cancer/disease/CFS/FMS, as does lifestyle, diet and environment.
If you look for something, you can find some correlation. However, it doesn't necessarily prove cause and effect as mentioned here already.
If we stop worrying, our stress and depression/anxiety/pain/fatigue go down. This makes us healthier. Our bodies like that environment. Viruses cause problems when we are weak and run down. Not the other way around...in my opinion (and experience).
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Edited by - SarnoFan on 10/13/2009 11:24:54 |
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ammuni
10 Posts |
Posted - 12/05/2009 : 09:06:22
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Hi Wavy Soul,
This is a very confusing article about the study. On the one hand they state that about 68 of the 101 patients they studied with CFS (about 67.3%), tested positive for XMRV genes. If this is the case, how is it that 32.7 % of CFS patients in the study did not have XMRV? Were they misdiagnosed with having CFS? 32.7% is a large number of people experiencing CFS but not having the XMRV gene. Also, about 4% of the general healthy population do have the XMRV gene but do not have CFS. If the gene is correlated with CFS, why do these healthy people not have CFS? Does it really lie dormant within them until a life stressor hits them or are they just less susceptible to TMS? In other words, could people who have the gene and develop CFS be more susceptible to TMS and therefore develop symptoms?
But then the study adds that "using additional tests, the scientists determined that more than 95% of the patients in the study are either infected with live virus or are making antibodies that show their immune systems mounted an attack against XMRV and now had the virus under control.”
I think one needs to read the original study directly to understand what they mean by 95% of patients. Was it that 95% of the 68 CFS patients in the study that had XMRV either had a live virus or antibodies?
95% is a large number. If this is the case that 95% of all CFS patients have XMRV as a live virus or have the antibodies, it is possible that they have indeed found a viral cause of CFS or that XMRV correlates with CFS but that something else causes the XMRV. (This could also mean that 5% of those with CFS are misdiagnosed.)
95% is the percentage being flagged on all news media about CFS (Dr. Oz just featured this on his show).
If anyone could locate the original article, I'd be interested in reading it.
Ammuni |
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ammuni
10 Posts |
Posted - 12/05/2009 : 10:14:34
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O.K. I found the the entire original study. Here it is below. If someone with a science background could explain to me how they came up with the figure that 95% of all CFS patients have the retrovirus or the antibodies to it, I'd appreciate your assistance in explaining this from the study.
Thanks,
Ammuni
Reports
Detection of an Infectious Retrovirus, XMRV, in Blood Cells of Patients with Chronic Fatigue Syndrome
Vincent C. Lombardi,1,* Francis W. Ruscetti,2,* Jaydip Das Gupta,3 Max A. Pfost,1 Kathryn S. Hagen,1 Daniel L. Peterson,1 Sandra K. Ruscetti,4 Rachel K. Bagni,5 Cari Petrow-Sadowski,6 Bert Gold,2 Michael Dean,2 Robert H. Silverman,3 Judy A. Mikovits1,{dagger}
Chronic fatigue syndrome (CFS) is a debilitating disease of unknown etiology that is estimated to affect 17 million people worldwide. Studying peripheral blood mononuclear cells (PBMCs) from CFS patients, we identified DNA from a human gammaretrovirus, xenotropic murine leukemia virus–related virus (XMRV), in 68 of 101 patients (67%) as compared to 8 of 218 (3.7%) healthy controls. Cell culture experiments revealed that patient-derived XMRV is infectious and that both cell-associated and cell-free transmission of the virus are possible. Secondary viral infections were established in uninfected primary lymphocytes and indicator cell lines after their exposure to activated PBMCs, B cells, T cells, or plasma derived from CFS patients. These findings raise the possibility that XMRV may be a contributing factor in the pathogenesis of CFS.
1 Whittemore Peterson Institute, Reno, NV 89557, USA.
2 Laboratory of Experimental Immunology, National Cancer Institute–Frederick, Frederick, MD 21701, USA.
3 Department of Cancer Biology, The Lerner Research Institute, The Cleveland Clinic Foundation, Cleveland, OH 44195, USA.
4 Laboratory of Cancer Prevention, National Cancer Institute–Frederick, Frederick, MD 21701, USA.
5 Advanced Technology Program, National Cancer Institute–Frederick, Frederick, MD 21701, USA.
6 Basic Research Program, Scientific Applications International Corporation, National Cancer Institute–Frederick, Frederick, MD 21701, USA.
* These authors contributed equally to this work. Back
{dagger} To whom correspondence should be addressed. E-mail: judym@wpinstitute.org
Chronic fatigue syndrome (CFS) is a disorder of unknown etiology that affects multiple organ systems in the body. Patients with CFS display abnormalities in immune system function, often including chronic activation of the innate immune system and a deficiency in natural killer cell activity (1, 2). A number of viruses, including ubiquitous herpesviruses and enteroviruses, have been implicated as possible environmental triggers of CFS (1). Patients with CFS often have active #946; herpesvirus infections, suggesting an underlying immune deficiency.
The recent discovery of a gammaretrovirus, xenotropic murine leukemia virus–related virus (XMRV), in the tumor tissue of a subset of prostate cancer patients prompted us to test whether XMRV might be associated with CFS. Both of these disorders, XMRV-positive prostate cancer and CFS, have been linked to alterations in the antiviral enzyme RNase L (3–5). Using the Whittemore Peterson Institute’s (WPI’s) national tissue repository, which contains samples from well-characterized cohorts of CFS patients, 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 XMRV env [352 nucleotides (nt)] and gag (736 nt) in CFS PBMC DNA (Fig. 1A) (6). 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 for both env and gag, only one sample was positive for gag and none for env (Fig. 1B). In all positive cases, the XMRV gag and env sequences were more than 99% similar to those previously reported for prostate tumor–associated strains of XMRV (VP62, VP35, and VP42) (fig. S1) (5).
Figure 1
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Fig. 1. XMRV sequences in PBMC DNA from CFS patients. Single-round PCR results for gag, env, and gapdh sequences in PBMCs of (A) CFS patients and (B) healthy controls are shown. The positions of the amplicons are indicated and DNA markers (ladder) are shown. These are representative results from one group of 20 patients.
Sequences of full-length XMRV genomes from two CFS patients and a partial genome from a third patient were generated (table S1). CFS XMRV strains 1106 and 1178 each differed by 6 nt from the reference prostate cancer strain XMRV VP62 (EF185282 [GenBank] ), and with the exception of 1 nt, the variant nucleotides mapped to different locations within the XMRV genome, suggesting independent infections. In comparison, prostate cancer–derived XMRV strains VP35 and VP42 differed from VP62 by 13 and 10 nt, respectively. Thus, the complete XMRV genomes in these CFS patients were >99% identical in sequence to those detected in patients with prostate cancer. To exclude the possibility that we were detecting a murine leukemia virus (MLV) laboratory contaminant, we determined the phylogenetic relationship among endogenous (non-ecotropic) MLV sequences, XMRV sequences, and sequences from CFS patients 1104, 1106, and 1178 (fig. S2). XMRV sequences from the CFS patients clustered with the XMRV sequences from prostate cancer cases and formed a branch distinct from non-ecotropic MLVs common in inbred mouse strains. Thus, the virus detected in the CFS patients’ blood samples is unlikely to be a contaminant.
To determine whether XMRV proteins were expressed in PBMCs from CFS patients, we developed intracellular flow cytometry (IFC) and Western blot assays, using antibodies (Abs) with novel viral specificities. These antibodies included, among others, (i) rat monoclonal antibody (mAb) to the spleen focus-forming virus (SFFV) envelope (Env), which reacts with all polytropic and xenotropic MLVs (7); (ii) goat antisera to whole mouse NZB xenotropic MLV; and (iii) a rat mAb to MLV p30 Gag (8). All of these Abs detected the human VP62 XMRV strain grown in human Raji, LNCaP, and Sup-T1 cells (fig. S3) (5). IFC of activated lymphocytes (6, 9) revealed that 19 of 30 PBMC samples from CFS patients reacted with the mAb to MLV p30 Gag (Fig. 2A). The majority of the 19 positive samples also reacted with antisera to other purified MLV proteins (fig. S4A). In contrast, 16 healthy control PBMC cultures tested negative (Fig. 2A and fig. S4A). These results were confirmed by Western blots (Fig. 2, B and C) (6) using Abs to SFFV Env, mouse xenotropic MLV, and MLV p30 Gag. Samples from five healthy donors exhibited no expression of XMRV proteins (Fig. 2C). The frequencies of CFS cases versus healthy controls that were positive and negative for XMRV sequences were used to calculate a Pearson {chi}2 value of 154 (two-tailed P value of 8.1 x 10–35). These data yield an odds ratio of 54.1 (a 95% confidence interval of 23.8 to 122), suggesting a nonrandom association with XMRV and CFS patients.
Figure 2
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Fig. 2. Expression of XMRV proteins in PBMCs from CFS patients. (A) PBMCs were activated with phytohemagglutinin and interleukin-2, reacted with a mAb to MLV p30 Gag, and analyzed by IFC. (B) Lysates of activated PBMCs from CFS patients (lanes 1 to 5) were analyzed by Western blots with rat mAb to SFFV Env (top panel), goat antiserum to xenotropic MLV (middle panel), or goat antiserum to MLV p30 Gag (bottom panel). Lane 7, lysate from SFFV-infected HCD-57 cells. Molecular weight markers in kilodaltons are at left. (C) Lysates of activated PBMCs from healthy donors (lanes 1, 2, 4, 5, and 7) or from CFS patients (lanes 3 and 6) were analyzed by Western blots using rat mAb to SFFV Env (top panel) or goat antiserum to MLV p30 Gag (bottom panel). Lane 8, SFFV-infected HCD-57 cells. Molecular weight (MW) markers in kilodaltons are at left. (D) CD4+ T cells (left) or CD19+ B cells (right) were purified, activated, and examined by flow cytometry for XMRV Gag with a mAb to MLV p30 Gag.
To determine which types of lymphocytes in blood express XMRV, we isolated B and T cells from one patient’s PBMCs (6). Using mAb to MLV p30 Gag and IFC, we found that both activated T and B cells were infected with XMRV (Fig. 2D and fig. S4A). Furthermore, using mAb to SFFV Env, we found that >95% of the cells in a B cell line developed from another patient were positive for XMRV Env (fig. S4B). XMRV protein expression in CFS patient–derived activated T and B cells grown for 42 days in culture was confirmed by Western blots (fig. S4C) using Abs to SFFV Env and xenotropic MLV.
We next investigated whether the viral proteins detected in PBMCs from CFS patients represent infectious XMRV. Activated lymphocytes (6) were cocultured with LNCaP, a prostate cancer cell line with defects in both the JAK-STAT and RNase L pathways (10, 11) that was previously shown to be permissive for XMRV infection (12). After coculture with activated PBMCs from CFS patients, LNCaP cells expressed XMRV Env and multiple XMRV Gag proteins when analyzed by Western blot (Fig. 3A) and IFC (fig. S5A). Transmission electron microscopy (EM) of the infected LNCaP cells (Fig. 3B), as well as virus preparations from these cells (Fig. 3C), revealed 90- to 100-nm-diameter budding particles consistent with a gamma (type C) retrovirus (13).
Figure 3
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Fig. 3. Infectious XMRV in PBMCs from CFS patients. (A) Lysates of LNCaP cells cocultured with PBMCs from CFS patients (lanes 1, 3, and 5) or healthy donors (lanes 2 and 4) were analyzed by Western blots with rat mAb to SFFV Env (top panel) or goat antiserum to xenotropic MLV (bottom panel). Lane 6, uninfected LNCaP; lane 7, SFFV-infected HCD-57 cells. MW markers in kilodaltons are at left. (B) Transmission electron micrograph of a budding viral particle from LNCaP cells infected by incubation with an activated T cell culture from a CFS patient. (C) Transmission electron micrograph of virus particles released by infected LNCaP cells.
We also found that XMRV could be transmitted from CFS patient plasma to LNCaP cells when we applied a virus centrifugation protocol to enhance infectivity (6, 14, 15). Both XMRV gp70 Env and p30 Gag were abundantly expressed in LNCaP cells incubated with plasma samples from 10 of 12 CFS patients, whereas no viral protein expression was detected in LNCaP cells incubated with plasma samples from 12 healthy donors (Fig. 4A). Likewise, LNCaP cells incubated with patient plasma tested positive for XMRV p30 Gag in IFC assays (fig. S5B). We also observed cell-free transmission of XMRV from the PBMCs of CFS patients to the T cell line SupT1 (Fig. 4B) and both primary and secondary transmission of cell-free virus from the activated T cells of CFS patients to normal T cell cultures (Fig. 4C). Together, these results suggest that both cell-associated and cell-free transmission of CFS-associated XMRV are possible.
Figure 4
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Fig. 4. Infectious XMRV and antibodies to XMRV in CFS patient plasma. (A) Plasma from CFS patients (lanes 1 to 6) were incubated with LNCaP cells and lysates were prepared after six passages. Viral protein expression was detected by Western blots with rat mAb to SFFV Env (top panel) or goat antiserum to MLV p30 Gag (bottom panel). Lane 7, uninfected LNCaP; lane 8, SFFV-infected HCD-57 cells. MW markers in kilodaltons are at left. (B) Cell-free transmission of XMRV to the SupT1 cell line was demonstrated using transwell coculture with patient PBMCs, followed by nested gag PCR. Lane 1, MW marker. Lane 2, SupT1 cocultured with Raji. Lanes 3 to 7, SupT1 cocultured with CFS patient PBMCs. Lane 8, no template control (NTC). (C) Normal T cells were exposed to cell-free supernatants obtained from T cells (lanes 1, 5, and 6) or B cells (lane 4) from CFS patients. Lanes 7 and 8 are secondary infections of normal activated T cells. Initially, uninfected primary T cells were exposed to supernatants from PBMCs of patients WPI-1220 (lane 7) and WPI-1221 (lane 8). Lanes 2 and 3, uninfected T cells; lane 9, SFFV-infected HCD-57 cells. Viral protein expression was detected by Western blot with a rat mAb to SFFV Env. MW markers in kilodaltons are at left. (D) Plasma samples from a CFS patient or from a healthy control as well as SFFV Env mAb or control were reacted with BaF3ER cells (top) or BaF3ER cells expressing recombinant SFFV Env (bottom) and analyzed by flow cytometry. IgG, immunoglobulin G.
We next investigated whether XMRV stimulates an immune response in CFS patients. For this purpose, we developed a flow cytometry assay that allowed us to detect Abs to XMRV Env by exploiting its close homology to SFFV Env (16). Plasma from 9 out of 18 CFS patients infected with XMRV reacted with a mouse B cell line expressing recombinant SFFV Env (BaF3ER-SFFV-Env) but not to SFFV Env negative control cells (BaF3ER), analogous to the binding of the SFFV Env mAb to these cells (Fig. 4D and S6A). In contrast, plasma from seven healthy donors did not react (Fig. 4D and fig. S6A). Furthermore, all nine positive plasma samples from CFS patients but none of the plasma samples from healthy donors blocked the binding of the SFFV Env mAb to SFFV Env on the cell surface (fig. S6B). These results are consistent with the hypothesis that CFS patients mount a specific immune response to XMRV.
Neurological maladies and immune dysfunction with inflammatory cytokine and chemokine up-regulation are some of the most commonly reported features associated with CFS. Several retroviruses, including the MLVs and the primate retroviruses HIV and HTLV-1, are associated with neurological diseases as well as cancer (17). Studies of retrovirus-induced neurodegeneration in rodent models have indicated that vascular and inflammatory changes mediated by cytokines and chemokines precede the neurological pathology (18, 19). The presence of infectious XMRV in lymphocytes may account for some of these observations of altered immune responsiveness and neurological function in CFS patients.
We have discovered a highly significant association between the XMRV retrovirus and CFS. This observation raises several important questions. Is XMRV infection a causal factor in the pathogenesis of CFS or a passenger virus in the immunosuppressed CFS patient population? What is the relationship between XMRV infection status and the presence or absence of other viruses that are often associated with CFS (e.g., herpesviruses)? Conceivably these viruses could be cofactors in pathogenesis, as is the case for HIV-mediated disease, in which co-infecting pathogens play an important role (20). Patients with CFS have an elevated incidence of cancer (21). Does XMRV infection alter the risk of cancer development in CFS? As noted above, XMRV has been detected in prostate tumors from patients expressing a specific genetic variant of the RNASEL gene (5). In contrast, in our study of this CFS cohort, we found that XMRV infection status does not correlate with the RNASEL genotype (6) (table S2).
Finally, it is worth noting that 3.7% of the healthy donors in our study tested positive for XMRV sequences. This suggests that several million Americans may be infected with a retrovirus of as yet unknown pathogenic potential.
Supporting Online Material
www.sciencemag.org/cgi/content/full/1179052/DC1
Materials and Methods
Figs. S1 to S6
Tables S1 and S2
References
References and Notes
* 1. L. D. Devanur, J. R. Kerr, J. Clin. Virol. 37, 139 (2006). [CrossRef] [Web of Science] [Medline][UBC's eLink]
* 2. T. L. Whiteside, D. Friberg, Am. J. Med. 105, 27S (1998). [Medline][UBC's eLink]
* 3. R. J. Suhadolnik et al., J. Interferon Cytokine Res. 17, 377 (1997). [Web of Science] [Medline][UBC's eLink]
* 4. G. Casey et al., Nat. Genet. 32, 581 (2002). [CrossRef] [Medline][UBC's eLink]
* 5. A. Urisman et al., PLoS Pathog. 2, e25 (2006). [CrossRef] [Medline][UBC's eLink]
* 6. Materials and methods are available as supporting material on Science Online.
* 7. R. Wolff, S. Koller, J. Ruscetti, Virology 43, 472 (1982).[UBC's eLink]
* 8. B. Chesebro et al., Virology 127, 134 (1983). [CrossRef] [Web of Science] [Medline][UBC's eLink]
* 9. K. A. Smith, F. W. Ruscetti, Adv. Immunol. 31, 137 (1981). [Web of Science] [Medline][UBC's eLink]
* 10. G. Dunn, K. Sheehan, L. Old, R. Schreiber, Cancer Res. 65, 3447 (2005).[Abstract/Free Full Text]
* 11. Y. Xiang et al., Cancer Res. 63, 6795 (2003).[Abstract/Free Full Text]
* 12. B. Dong et al., Proc. Natl. Acad. Sci. U.S.A. 104, 1655 (2007). [Abstract/Free Full Text]
* 13. B. J. Poiesz et al., Proc. Natl. Acad. Sci. U.S.A. 77, 7415 (1980). [Abstract/Free Full Text]
* 14. G. R. Pietroboni, G. B. Harnett, M. R. Bucens, J. Virol. Methods 24, 85 (1989). [CrossRef] [Web of Science] [Medline][UBC's eLink]
* 15. S. M. Yoo et al., J. Virol. Methods 154, 160 (2008). [CrossRef] [Web of Science] [Medline][UBC's eLink]
* 16. L. Wolff, E. Scolnick, S. Ruscetti, Proc. Natl. Acad. Sci. U.S.A. 80, 4718 (1983). [Abstract/Free Full Text]
* 17. C. Power, Trends Neurosci. 24, 162 (2001). [CrossRef] [Web of Science] [Medline][UBC's eLink]
* 18. X. Li, C. Hanson, J. Cmarik, S. Ruscetti, J. Virol. 83, 4912 (2009). [Abstract/Free Full Text]
* 19. K. E. Peterson, B. Chesebro, Curr. Top. Microbiol. Immunol. 303, 67 (2006). [Web of Science] [Medline][UBC's eLink]
* 20. A. Lisco, C. Vanpouille, L. Margolis, Curr. HIV/AIDS Rep. 6, 5 (2009). [CrossRef] [Medline][UBC's eLink]
* 21. P. H. Levine et al., Cancer Res. 52, 5516s (1992).[Abstract/Free Full Text]
* 22. We thank D. Bertolette, Y. Huang, C. Hanson, and J. Troxler for technical assistance; K. Nagashima for EM; and C. Ware and K. Hunter for discussions. Funded by the Whittemore Peterson Institute and the Whittemore Family Foundation; the National Cancer Institute (NCI); NIH (under contract HHSN26120080001E); and grants to R.H.S. from NCI/NIH (CA104943), the U.S. DoD Prostate Cancer Research Program (W81XWH-07-1338), the V Foundation for Cancer Research, the Charlotte Geyer Foundation, and Mal and Lea Bank. The content of this publication does not reflect the views or policies of the U.S. DHHS, nor does mention of trade names, commercial products, or organizations imply endorsement by the U.S. government. R.H.S. may receive royalty payments in the future from Abbott Laboratories. GenBank accession numbers are as follows: WPI-1130, GQ483508 [GenBank] ; WPI-1138, GQ483509 [GenBank] ; WPI-1169, GQ483510 [GenBank] ; WPI-1178, GQ497343; WPI-1106, GQ497344; and WPI-1104, GQ497345.
Note added in proof: V.C.L. is operations manager of Viral Immune Pathologies Laboratory, which is in negotiations with the Whittemore Peterson Institute to offer a dianostic test for XMRV. |
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Wavy Soul
USA
779 Posts |
Posted - 12/06/2009 : 16:36:01
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Wow - thanks for reviving this thread and putting in these excellent responses and the article.
I have to say that for me it's a both/and thing. And I mean a both/and thing at the level of an impossible Zen koan, not just a "balance of this and that" thing.
In other words, I am pretty sure that the whole thing is both physical AND non-physical, as in:
1) there is some tendency in me and some series of cascading factors that prepped my body for CFS and FMS. Maybe the core, bottom-line tendency is the fact of being a "highly sensitive person," which has been discussed elsewhere as a factor in why some of us somatize our stuff, whereas others don't.
Although back problems may be experienced by the whole population, this is a lot simpler than X-Games TMS, i.e. the FMS (fibromyalgia syndrome) type, which I have been, who experiences an almost constant torrent of near-debilitating symptoms. I have been a therapist for 30 years, I feel my feelings, am aware of my thinking, do a lot of presence practice, inner child work up the kazoo... you name it.
Something happened when I was about 28. I had been travelling on behalf of my then-Guru all over South America, and got a serious gut problem, undoubtedly some parasites or something, and from then on, I gradually got more and more stuff. There are CFS authors who describe it as a coming together of 5 factors or more that send the body into this kind of spiral. And I have to say it's a powerful spiral, and unless you experience it firsthand, you really can't say "Oh, that's just your emotions." Because I was working on my emotions all along.
2) And... Every time I reify (make real, make a thing of) the so-called illness, I nowadays feel a kind of heaviness because I have learned to stop doing that. How I relate to it creates its new manifestation (or non-manifestation, at least to some degree). I work with people on this and see how much attachment there is in proving that the illness is real, because THERE ARE FEELINGS THAT HAVE NEVER BEEN VALIDATED, and the illness then becomes a badge of our unacknowledged suffering. So when it is threatened with removal, the part of us that hasn't been seen and heard (or felt, or whatever) panics, and the cycle of illness is born, and after a while as we all know, it becomes a "reality," and a new identity that explains our inner fears. If we just concentrate on the symptoms, we can keep the nasty emptiness in our gut at bay.
Yet I cannot deny that I can absolutely believe that there is a virus involved, and that once that cycle gets started, it has something of its own momentum, no matter how much one tries to do the awakening work (Sarno and other). Invalidating this offends my core sense of truth, just like if you told me I was really a Martian. I know that I don't particularly have that much more wounding than my healthy friends and clients. The deep decision of my bodymind or perhaps my soul to act it out through drawing in a (possible, alleged) "virus" is a mystery.
Ah, there we have it, it's a mystery. But as we move towards it with the best we can do in the moment according to to what we understand, rather than according to unconscious habits, it seems to unravel. I seem to be getting better, or at least I'm doing better than you might expect at 58, babelicious and mostly radiant, considering the unbelievable amounts of stress in my life.
love to all
Love is the answer, whatever the question |
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ammuni
10 Posts |
Posted - 12/06/2009 : 20:06:05
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Hi Wavy Soul,
I like your Zen koan response. I do tend to think that some people are more susceptible to TMS, and as you say "more sensitive," i.e. that we experience our emotions through somatic pain or illness.
Were you diagnosed with both CFS and FMS? Is it common to have both? I had FMS for ten years throughout my twenties. It was so debilitating that I couldn't work and my daily activities were limited. I did completely heal from FMS using Dr. Sarno's method. That was just over twelve years ago.
If a new study would suddenly appear linking FMS to a viral infection, I don't know how I would react because Dr. Sarno's method did completely cure me of FMS.
I'm interested in CFS because I have recently (in the last 8 months) developed CFS symptoms. I'm going through a series of tests right now to get a diagnosis. My understanding is that CFS is a diagnosis of exclusion, so I am asking my family doctor to run the gamut of tests I need.
If I end up being diagnosed with CFS, I will certainly use Dr. Sarno's method. However, this whole correlation of a retrovirus with CFS has unsettled me. I still don't understand how this 95% figure is derived from the study.
Ammuni |
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Wavy Soul
USA
779 Posts |
Posted - 12/07/2009 : 11:53:47
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Hi Ammuni
I would say that if it really proves to be a virus, the healing approach for me will be to say, "Wow, that's incredible! I can get additional help with this, although of course I will also do the non-physical work."
I know there is sometimes a "rule" here that you have to stop treating the physical, but many of us have found that not to be totally true in our own experience. For me it kinda comes down to whether I believe in physical matter or not. Well, I do and I don't. In terms of science, it's an illusion. In terms of TMS, what seem to be "real" conditions turn out to be changeable.
Yet until I can put my hand through a wall, I'll continue to "both/and" it. I'll stretch and unravel my shoulder when it goes into one of its snits, even though the tension came about through emotional holding, and I also need to do the TMS work. Whatever anyone (sometimes scathingly) says, I'll honor my own truth and continue many of the things that I have found to be good for my body's ecology. I don't want plastic in the world's landfills and I don't want too many toxins in my liver.
All of which is to say that although the news or possible news about CFS is initially confusing, or was to me, I'm not going to make it another thing to stress about. It's all here as part of the friendly universe that is allowing me to heal. It's just my anxiety patterning that makes it a new problem.
love to you
Love is the answer, whatever the question |
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miche
Canada
283 Posts |
Posted - 12/08/2009 : 22:50:18
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Here is the latest I read on FM , no wonder we get confused!
NEW ANTIBODY DISCOVERED IN THE BLOOD OF MANY FIBROMYALGIA PATIENTS Reactivity on the APA Assay Correlates with Fibromyalgia Severity in Many Patients FOR IMMEDIATE RELEASE
NEW ORLEANS, February 10, 1999 - Autoimmune Technologies, LLC, a New Orleans
biotechnology company, today announced that scientists have discovered a new antibody in the blood
of many fibromyalgia patients. This research is described in an article entitled "Anti-Polymer
Antibody Reactivity in a Subset of Patients with Fibromyalgia Correlates with Severity," which
appears in the February 1999 issue of The Journal of Rheumatology, a prominent scientific journal. Using a patented blood test called the Anti-Polymer Antibody Assay, or APA Assay, researchers
found anti-polymer antibodies in approximately one-half of all patients who were diagnosed with
fibromyalgia and in more than 60% of the fibromyalgia patients with severe fibromyalgia symptoms.
Patients with diseases frequently confused with fibromyalgia, including rheumatoid arthritis, systemic
lupus erythematosus, and systemic sclerosis/scleroderma, had a much lower incidence of these
antibodies than did the fibromyalgia patients. Fibromyalgia syndrome is a chronic pain disorder that affects millions of individuals, primarily
women, in many countries throughout the world. The cause or causes of fibromyalgia are currently
unknown, but researchers have suggested that trauma, infection, and exposure to environmental
factors may all participate in the development of this debilitating illness. Together with widespread
pain and tender points in various areas of the body, signs and symptoms include fatigue, sleep
disorder, morning stiffness, headache, cognitive problems, and other symptoms. In the United States,
some 3% to 5% of adult women meet the strict diagnostic criteria of the American College of
Rheumatology for fibromyalgia, but as many as 15% to 20% of adult women may have fibromyalgia-
like symptoms. Fibromyalgia syndrome is often difficult to diagnose, and typically a diagnosis is reached through the
time-consuming and expensive process of ruling out other illnesses that have similar symptoms. In
addition, many physicians consider fibromyalgia to be the result of aging and other normal body
processes and do not regard it as a distinct clinical disorder. The resulting reluctance on the part of
some physicians to attribute their patients' symptoms to a specific illness has added considerably to the
distress of many fibromyalgia patients. Until now, there has been no laboratory test to help identify
fibromyalgia. "Our results show that there is a unique immunological response in many fibromyalgia patients," said
Russell B. Wilson, Ph.D., president of Autoimmune Technologies and lead investigator of the
published study. "We hope that these findings will lead to a better understanding of the illness and to
the development of treatments for these patients." It is possible, Dr. Wilson pointed out, that anti-polymer antibodies are associated with one of the
several different causes of fibromyalgia, perhaps the cause that tends to produce the most severe - 2 - symptoms. The published data indicate that this may be the case, although more research will be
needed. In addition to serving as a marker for fibromyalgia, he noted, it is also possible that these
antibodies are directly involved in initiating or promoting fibromyalgia. The development of a laboratory test for fibromyalgia was welcomed by experts in the field. "The fibromyalgia syndrome is common in clinical medicine and in the general community. We also
have data on its cost," said I. Jon Russell, M.D., Ph.D., an internationally recognized fibromyalgia
investigator and clinician from the University of Texas Health Center at San Antonio. "The direct
medical costs of this disorder to the U.S. economy are over $16 billion annually. The findings of this
study raise the hopeful prospect that a new test will help us better understand fibromyalgia. Further
research is needed to confirm the clinical specificity of the test relative to other painful conditions. In
addition, it will be important to determine whether the antibody identified by this test in the blood of
people with fibromyalgia is related to the cause of the disorder or simply represents an interesting
epiphenomenon," Dr. Russell said. Associated factors appear in parallel in epiphenomena. If further research shows the production of
anti-polymer antibodies to be an epiphenomenon, the antibodies would serve as a laboratory marker
for fibromyalgia without playing a direct role in the disease process. Kristin Thorson is president of The Fibromyalgia Network, a patient self-help organization
headquartered in Tucson, Arizona, and president of The American Fibromyalgia Syndrome
Association, a charitable organization dedicated to funding research on fibromyalgia and chronic
fatigue syndrome. "In the past," Ms. Thorson said, "many health insurance companies and some
members of the medical community have argued that fibromyalgia is not real - all because no one had
developed a lab marker to indicate otherwise. Now that there is a blood marker that can be shown to
correlate with disease severity, there should be no more debate over the existence of fibromyalgia and
scientists should be encouraged to research effective therapies for this potentially disabling illness." Robert M. Bennett, M.D., a physician and scientist who is chairman of the Division of Arthritis and
Rheumatic Disease of Oregon Health Sciences University in Portland and a widely published and
internationally known expert on fibromyalgia syndrome, said "There are two major problems for most
physicians in accepting fibromyalgia. The first is the lack of an easily performed laboratory test. The
second is its recalcitrance to therapy. The promise of a potentially useful diagnostic marker is an
exciting development in this field. If the sensitivity and specificity of this test can be confirmed by
independent laboratories, it could open up an important new research avenue for a condition that
compromises the quality of life of five million to ten million U.S. women." Autoimmune Technologies expects during 1999 to apply to the U.S. Food and Drug Administration
for approval of a kit form of the Assay as a diagnostic test. "The reproducibility of the APA Assay has
already been independently demonstrated by the National Institute of Public Health and the
Environment, or RIVM, in The Netherlands," said Dr. Wilson. "The RIVM has found the APA Assay
to give reproducible results and to be useful for the evaluation of the presence of anti-polymer
antibodies in human serum. The other confirmatory studies discussed by Drs. Russell and Bennett are
already well under way. These studies, together with our research published in The Journal of
Rheumatology, will be included in our application to the FDA for approval of the Assay as an in vitro
diagnostic test to aid in the diagnosis of fibromyalgia." Other authors of the article in this month's issue of The Journal of Rheumatology include Dr. Oscar S.
Gluck and Dr. John R. P. Tesser of the Arizona Rheumatology Center in Phoenix, Dr. Janet C. Rice of
Tulane University School of Public Health and Tropical Medicine, and Dr. Alan J. Bridges of the
University of Wisconsin School of Medicine in Madison. - 3 - Anti-polymer antibodies were discovered by researchers at Tulane University Medical Center, where
the APA Assay was developed. Autoimmune Technologies has licensed the APA Assay from Tulane.
An APA Assay kit is not currently in commercial distribution in the U.S., although the Assay is being
performed by Autoimmune Technologies as a service to physicians and researchers for investigational
use only. A kit form of the APA Assay will be available in the near future in other countries. The APA Assay is covered by U.S. and European patents, and patents in other countries are pending. For further information, please visit www.autoimmune.com. |
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scd1833
USA
124 Posts |
Posted - 12/21/2009 : 23:58:55
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I'm no expert, but it sounds to me like another common virus that may be pervasive in humans.
i tend to think almost everything is TMS, but I have no proof. |
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catspine
USA
239 Posts |
Posted - 12/29/2009 : 07:00:18
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If it were not for Dr Sarno’s and some luck I would probably be still laying in bed or searching for a solution to get operated with a potentially hazardous outcome anyway not to mention that as it turns out none of it was necessary so I know now that his theory and diagnosis are producing positive results and I’m very grateful even if I learned more since then. I recovered successfully from TMS twice already but symptoms imperatives resurfaced over a year ago.
My actual condition includes symptoms very similar to CFS so I explored the subject as a possible reason to my latest problems.
What I found in my case is that it is not impossible for a virus to take advantage of the situation when TMS is at work so I sought medical advice first in a process of elimination without dropping the other options, after all the immune system must be kind of confused somehow especially when it comes to CFS as a symptom imperative of TMS.
According to J.Sarno the brain needs to create a diversion and it will choose the best option available to do so because it must succeed... What this means to me is that if the part of the brain making the decision can increase the efficiency of the distraction by joining a viral infection it will likely use this method first (That is if the virus is present before TMS starts of course) and I ‘m saying this because I’m right in the middle of it at this time and that‘s what seems to be happening. But if TMS is there first then it may weaken the immune system and allow a virus to invade the body. I had to figure this out on my own as I was told by my doctor that I may never know what causes my problems. I’m now making progress towards recovery using these observations and knowledge from personal experience. It may not work with anyone else but I thought it was worth sharing.
In addition to this the subconscious and the autonomic part of the brain know everything your conscious mind does thinks or plans to do so there is really nowhere to hide from it. That makes it very difficult to sort things out until you manage to see through it and deal with it as separate problems. Understanding comes with time and patience can wear out sometimes. After a lot of despair and ups and downs then the TMS part of it become more obvious once the doubts clear up and the problem can be addressed accordingly, the viral part can be left to the experts in the matter. Some of them are very good at what they do and can really help a lot too but I discovered that where I live health care is really basic and questionable and I was better off not to mention anything about TMS to them… Too confusing!
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kilton
38 Posts |
Posted - 01/06/2010 : 13:57:40
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Well, not surprisingly this study's results have not been able to be replicated. Here's a new one: http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0008519.
"Unlike the study of Lombardi et al., we have failed to detect XMRV or closely related MRV proviral DNA sequences in any sample from CFS cases... Based on our molecular data, we do not share the conviction that XMRV may be a contributory factor in the pathogenesis of CFS, at least in the U.K." |
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Dave
USA
1864 Posts |
Posted - 01/06/2010 : 14:54:57
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This was bound to happen, just like the H.plyori bacteria was found in some patients with stomach ulcers.
Even if it is true, the issue that these researchers fail to address is whether the chemistry is a cause or effect.
This finding, even if true, does not invalidate the fact that Fibromyalgia is TMS. Who is to say that the antibody is not produced by the brain as part of the mechanism to induce the symptoms? Or that the brain suppresses the immune system in such a way that makes the body more hospitable to this antibody?
Medical research loves to pound their chest when they find something under the microscope. They continue to miss the point. |
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catspine
USA
239 Posts |
Posted - 01/06/2010 : 20:48:45
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| I'm aware of the fact that TMS affects everyone differently but is there some kind of a pattern that emerges from the number of patients followed closely by physicians as to how often TMS can suppress the immune system? Thanks |
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miche
Canada
283 Posts |
Posted - 01/10/2010 : 12:51:24
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Good point Dave regarding the H.plyori bacteria , my confusion arises from the fact that autoimmune disorders are often triggered by stress combined with the already existing gene , rheumatoid arthritis for example , but once one has such an autoimmune didorder one cannot tms away rheumatoid or lupus for example , so if fibromyalgia is eventually proven to be autoimmune , what then , believe me I so want to think that it's all tms and anxiety , I just cannot get convinced so far , I do believe tms and anxiety are the souce of much chronic pain however .
Anything you have to add will be appreciated, there are times like lately when I feel despair from it all . |
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Dave
USA
1864 Posts |
Posted - 01/11/2010 : 07:04:51
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If you allow this research to derail your belief in TMS you are doing yourself a disservice.
Let's assume for a minute the research is 100% correct. What can you do about it? There is no treatment. There is no medicine. So, you're stuck with the virus or autoimmune disorder, right? Treating it as TMS has helped. Should why stop now?
I believe the immune system is a big target of TMS. The brain may manipulate the immune system in subtle ways to manipulate body chemistry in such a way to introduce symptoms. |
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Topic |
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chronic fatigue virus
