“Does XMRV cause CFS? While the presence of XMRV in 67% of CFS samples seems impressive, it could be misleading. For example, the samples could be from regions where XMRV infection is common. Alternatively, patients with CFS could be more susceptible to infection. This is why more extensive epidemiological studies must be done.”

Neither the WPI study nor any other scientific or medical orgaization is suggesting that we can know XMRV causes CFS. We can't know that, and it may well not. We don't even know for sure if XMRV causes any symptoms. All we know is that we sometimes find it significantly more often in certain patient populations and sometimes don't find it associated with any disease. Nobody should be using anti-retroviral drugs for CFS unless it can be shown through proper, controlled clinical trials to be helpful. But right now we don't even know enough to run clinical trials. Anti-retroviral drugs aren't safe to experiment with. You can try Omega-3 or tricyclic antidepressants (they can help with pain and sleep even if comorbid depression isn't an issue) or things of that sort without clinical trials, but this isn't a good idea with anti-retrovirals. What doctor do they have rx-ing this?

As a PWC, I understand the urgency of needing an effective treatment, but we have to be patient a little while longer. Treatment for our disease will come. I actually think the cardiovascular theories will provide a useful treatment soonest. Several other theories will hopefully add treatments in time.

“It will take time to answer the many questions raised by the discovery of XMRV. The good news is that some of the anti-retroviral drugs licensed for treating AIDS can be immediately tested for their efficacy against CFS.”

http://www.forums.aboutmecfs.org/showthread.php…
http://www.forums.aboutmecfs.org/showthread.php…

I have Fibromyalgia and was dx 1 year ago. My daughter tested paoitive for Epstein Barr. My mother has Lukemia, as did my grandmother and my great great grandmother. Is there some sort of DNA hereditary issue here?

http://www3.interscience.wiley.com/journal/1121…
Of mice, cats, and men: Is human breast cancer a Zoonosis?
Keywords
mouse mammary tumor virus (MMTV) • betaretroviridae • feline • breast cancer

Information regarding commercially available XMRV tests your doctor could order are not widely available as there is no standard at this time. However the Whittemore-Peterson Institute is temporarily allowing Viral Immune Pathology Diagnostics (VIP Dx) in Reno NV to offer the same test they used for their breakthrough study. More information is available at http://www.vipdx.com

Please keep in mind however, that no matter how much potential the XMRV study regarding patients with the neuroimmune disease CFS may have, there is currently no specific evidence that XMRV causes any disease in humans. Association is not causation.

Virology 2009 Dec 1.

http://www.ncbi.nlm.nih.gov/sites/entrez

Xenotropic murine leukemia
virus-related virus is susceptible
to AZT.

Sakuma R, Sakuma T, Ohmine S, Silverman
RH, Ikeda Y.

Department of Molecular Medicine, Mayo Clinic, 200
First Street SW, Rochester, MN 55906, USA.

The xenotropic murine leukemia virus-related virus
(XMRV) is a human retrovirus, recently isolated from
tissues of prostate cancer patients with impaired
RNase L activity.

In this study, we evaluated 10 licensed anti-HIV-1
compounds for their activity against XMRV, including
protease inhibitors (PI), nucleoside reverse
transcriptase (RT) inhibitors (NRTI), non-nucleoside
RT inhibitors (NNRTI) and an integrase inhibitor.

No PI affected XMRV production; even high
concentrations of Ritonavir failed to inhibit the
maturation of XMRV Gag polyproteins.

Among the NRTI, NNRTI and integrase inhibitors
used in this study, only AZT blocked XMRV infection
and replication through inhibition of viral reverse
transcription.

This sensitivity of XMRV to AZT may be explained by
the modest homology in the motif D sequences of
HIV-1 and XMRV reverse transcriptases.

If XMRV becomes established as an etiological agent
for prostate cancer or other diseases, AZT may be
useful for preventing or treating XMRV infections in
humans.

PMID: 19959199 [PubMed - as supplied by publisher]

As a scientist on another list has noted about AZT:

“…For information, the following is a quotation of the FDA-required black box
warning in the 2008 edition of the Physician's Desk Reference, page 1560,
under Retrovir (zidovudine) [also known as AZT]:

“WARNING

RETROVIR (ZIDOVUDINE) HAS BEEN ASSOCIATED WITH HEMATOLOGIC TOXICITY
INCLUDING NEUTROPENIA AND SEVERE ANEMIA PARTICULARLY IN PATIENTS WITH
ADVANCED HUMAN IMMUNODEFICIENCY VIRUS (HIV) DISEASE.

PROLONGED USE OF RETROVIR HAS BEEN ASSOCIATED WITH SYMPTOMATIC MYOPATHY.

LACTIC ACIDOSIS AND SEVERE HEPATOMEGALY WITH STEATOSIS, INCLUDING FATAL
CASES, HAVE BEEN REPORTED WITH THE USE OF NUCLEOSIDE ANALOGUES ALONE OR IN
COMBINATION, INCLUDING RETROVIR AND OTHER ANTIRETROVIRALS.”

As in if it don't kill ya it may cure ya.

Also, do you know of any prescription medication for the latent form of the
EBV (Epstein Barr Virus), which as I understand is present in a significant
portion of the population, and may also be realated to CFS in some
individuals.

Thank You,
Adam.

Could anyone address the question about heredity? Is it possible that I may have passed this along to my children? They were born about ten years after my symptoms began occurring.

Thank you all for your very valuable information.

Here is a magnificent opportunity for data to be rapidly collected and analyzed. DHHS might even consider directly paying for these tests as part of a large clinical evaluation and save everyone from having to appeal this to their manifold insurance carriers one by one.

What makes it unique in the case of patients with CFS, is that it is post-exertional fatigue unrelieved by rest and lasting at least 24-hours. Post-exertional malaise and/or fatigue of inappropriate severity can temporarily immobilize the patient and worsen her/his symptoms following normal physical or mental activity. It takes the patient an inordinate amount of time to recover – 24 hours or more. De Becker et al assessed 2073 consecutive patients with major complaints of prolonged fatigue. Of the 1578 patients that met the (1994) Fukuda criteria, 97.3% had post-exertional malaise with a severity of 2.7 out of three. Of the 951 who met the Holmes criteria, 98.8% had post-exertional malaise with a severity of 2.8 out of 3. (It should be noted that the original 1988 Holmes definition contained many symptoms and signs common to viral illness.)

It could be argued that changing the definition doesn't change the disease, it simply confounds research results.

As De Becker et al, and many others, have shown, how fatigue is defined (severity and duration are always key in a differential diagnosis) makes a substantial difference in not only diagnostic value, but in what patients are actually being studied.

And, as Dr. Nancy Klimas stated in a March 24, 2009 interview with the Miami Herald regarding symptoms of CFS, “The big one would be post-exertional relapse. There aren’t many illnesses that get worse when you exercise…”

A postexertional relapse connection to the mind? Sorry, I couldn't find any research to support that hypothesis. Perhaps someone else knows of some.

Brain fog is also colloquialism that can also mean many things to many people. In CFS patients, perhaps not surprisingly, cognitive processing becomes more impaired in response to challenging physical exertion according to LaManca et al. The most common cognitive problems in CFS have been shown to be slowed processing speed, deficits in working memory and in some patients very high alpha amplitudes in their occipital and temporal regions per Harvard neurologist Frank H. Duffy in unpublished data. Duffy notes that these clinical findings are also consistent with head injury, extreme sleep deprivation, and encephalopathy. The findings were distinct from sleepy or depressed controls.

The question then might be what viruses or combination of activated viruses in CFS patients are neurotropic and what might their role be?

De Becker P, McGregor N, De Meirleir K. A definition-based analysis of symptoms in a large cohort of patients with chronic fatigue syndrome. J Intern Med 2001;250:234-240

La Manca JJ, Sisto SA, DeLuca J, Johnson SK, Lange G, Pareja J, Cook S, Natelson BH. Influence of exhaustive treadmill exercise on cognitive functioning in chronic fatigue syndrome. Am J Med 1998 Sept 28;105(3A):59S-65S.

Lange G, Steffener J, Cook DB, Bly BM, Christodoulou C, Liu WC, Deluca J, Natelson BH. Objective evidence of cognitive complaints in Chronic Fatigue Syndrome: a BOLD fMRI study of verbal working memory. Neuroimage. 2005 Jun;26(2):513-24. Epub 2005 Apr 7.

What makes it unique in the case of patients with CFS, is that it is post-exertional fatigue unrelieved by rest and lasting at least 24-hours. Post-exertional malaise and/or fatigue of inappropriate severity can temporarily immobilize the patient and worsen her/his symptoms following normal physical or mental activity. It takes the patient an inordinate amount of time to recover – 24 hours or more. De Becker et al assessed 2073 consecutive patients with major complaints of prolonged fatigue. Of the 1578 patients that met the (1994) Fukuda criteria, 97.3% had post-exertional malaise with a severity of 2.7 out of three. Of the 951 who met the Holmes criteria, 98.8% had post-exertional malaise with a severity of 2.8 out of 3. (It should be noted that the original 1988 Holmes definition contained many symptoms and signs common to viral illness.)

It could be argued that changing the definition doesn't change the disease, it simply confounds research results.

As De Becker et al, and many others, have shown, how fatigue is defined (severity and duration are always key in a differential diagnosis) makes a substantial difference in not only diagnostic value, but in what patients are actually being studied.

And, as Dr. Nancy Klimas stated in a March 24, 2009 interview with the Miami Herald regarding symptoms of CFS, “The big one would be post-exertional relapse. There aren’t many illnesses that get worse when you exercise…”

A postexertional relapse connection to the mind? Sorry, I couldn't find any research to support that hypothesis. Perhaps someone else knows of some.

Brain fog is also colloquialism that can also mean many things to many people. In CFS patients, perhaps not surprisingly, cognitive processing becomes more impaired in response to challenging physical exertion according to LaManca et al. The most common cognitive problems in CFS have been shown to be slowed processing speed, deficits in working memory and in some patients very high alpha amplitudes in their occipital and temporal regions per Harvard neurologist Frank H. Duffy in unpublished data. Duffy notes that these clinical findings are also consistent with head injury, extreme sleep deprivation, and encephalopathy. The findings were distinct from sleepy or depressed controls.

The question then might be what viruses or combination of activated viruses in CFS patients are neurotropic and what might their role be?

De Becker P, McGregor N, De Meirleir K. A definition-based analysis of symptoms in a large cohort of patients with chronic fatigue syndrome. J Intern Med 2001;250:234-240

La Manca JJ, Sisto SA, DeLuca J, Johnson SK, Lange G, Pareja J, Cook S, Natelson BH. Influence of exhaustive treadmill exercise on cognitive functioning in chronic fatigue syndrome. Am J Med 1998 Sept 28;105(3A):59S-65S.

Lange G, Steffener J, Cook DB, Bly BM, Christodoulou C, Liu WC, Deluca J, Natelson BH. Objective evidence of cognitive complaints in Chronic Fatigue Syndrome: a BOLD fMRI study of verbal working memory. Neuroimage. 2005 Jun;26(2):513-24. Epub 2005 Apr 7.

Recap provided by Dr. David Bell whose patients were among those examined by the WPI team and who first indentified 60 children who contracted ME/CFS in a cluster outbreak in Western New York in 1985.

“XMRV DNA was found from 68 of 101 patients (67%), and this was in the Science paper. That leaves 33 patients with CFS who were negative. But on further testing 19 of these 33 are XMRV antibody positive, 30 of these 33 had transmissible virus in the plasma, and 10 of these 33 had protein expression. Overall 99 of the 101 patients show evidence of XMRV infection.
These results have interesting implications. The most important is that there is not a simple test now that will tell you if you have XMRV or if the virus is active in your system. And we need a good control study using all three measures to accurately know control presence of the virus. Right now, it is necessary to do several tests to know the XMRV status:
a) DNA by PCR
b) Viral infectivity
c) Detection of viral proteins
d) Antibody to the XMRV envelope…”

http://www.davidsbell.com/

Also in testimony: the NCI, in as yet unpublished findings, has replicated the XMRV findings in patients with ME/CFS. In a cohort entirely unrelated to the WPI cohort they found 9 of 15 ME/CFS patients positive by PCR and 13 of 15 were positive by culture technique.

XMRV was also found using at least one of the three techniques as follows:

Atypical MS: 3 out of 3 were positive.
Fibromyalgia: 12 out of 20 were positive.
Autism: 6 out of 15
GWI: not tested