When Can Patients Expect Approved Therapies?

The availability of effective therapies for ME/CFS, FMS, and Gulf War Syndrome is still quite a ways off. Pharmaceutical companies have expressed a great interest in screening currently available HIV therapies, and compounds that did not pan out for treating HIV.  Likely it will be four years before the FDA approves any existing drug for treating XAND disorders - By next summer a number of drug candidates that work against XMRV will be selected for Phase II clinical trials (A Phase I trial is not necessary for a new indication), followed by a larger scale Phase III trial, which will likely not be completed well into 2012, with approval in 2013!  For new chemical entities, it will be even longer - at least that long for protease inhibitors (purifying the protein, doing X-ray crystallography studies, and finding small-molecule inhibitor candidates), then starting from scratch with phase I studies - what is going to turn out to be about a 10 year process, and likely the FDA won't grant accelerated review.

It's not to say that when results from ongoing studies begin to surface, that doctors won't begin the label of practicing current HIV drugs off-label to XAND patients.  However, such patients will have to shoulder the cost of treatment themselves, as insurers will be very reluctant to cover a drug which is not indicated for a particular disorder by the FDA.  High drug costs in the United States, which has been decried as criminal by AIDS activitists, will present a formidable barrier to most people.  In some countries with publicly funded health care systems, these drugs will be even harder to obtain: HIV patients have programs where drugs are given free of charge at clinics, and are not available in community pharmacies.  In some jurisdictions like British Columbia, which has a publicly funded drug plan, despite being approved for use by the federal government, the drug plan will do time-consuming studies which last on the order of 2 or more years, further delaying availability of treatment - so much for universal health care!

Norwegian Study Offers Clues

An experimental ME/CFS treatment in Norway involves some tantalizing clues: B cell depletion with Rituximab.  The study was initiated after a patient with CFS had unexpected, marked recovery of CFS symptoms following cytotoxic chemotherapy for Hodgkins's disease.  A following study was initiated recruiting patients, for B-Cell depletion therapy, all patients in the study demonstrated substantial improvement after the first infusion, followed by a relapse, improvement following the second infusion, and an even more marked  improvement after the third infusion.  This treatment will not likely gain a mainstay in ME/CFS treatment, as it poses a high degree of risk, costs over $10,000 a treatment, and would require infusions on an ongoing basis.

Nevertheless, it shows that B-Cells beyond a reasonable doubt play a major role in the pathogenesis of ME/CFS.  By depleting XMRV infected B cells, it can be seen that healthy B cells develop from progenitor stem cells, but soon succumb to infection - indicating that XMRV infects other classes of lymphocytes.  It leaves room to infer that antiretroviral therapy would have an even more profound and lasting effect: Most T-cells, with the exception of memory cells have an average lifespan of about 8 weeks. After a couple month course of antiretroviral therapy, it would not be unreasonable to see the vast majority of lymphocytes replaced by healthy cells

Fluge and Mella BMC Neurology 2009 9:28   doi:10.1186/1471-2377-9-28

The Modus Operandi: Part II

In my previous post, I gave my theory explaining the female predominance of ME/CFS and fibromyalgia, in this post I will explain my theory behind the neurological symptoms of ME/CFS, FM, and Autism.  My theory centers around the SYG1 membrane protein, which has been identified as a synaptic guidepost, directing neurons to connect to each other.  The SYG1 protein is in the immunoglobulin superfamily, with an extracellular domain, a single transmembrane segment, and an intracellular loop.  SYG1 binds to its receptor SYG2, which is also a member of the immunoglobulin superfamily.  Ironically, SYG1 is most heavily expressed during fetal development and early childhood, and its expression greatly diminishes thereafter.  In adulthood, it continues to be expressed in the limic region (which includes the hypothalamus), at neuromuscular junctions in skeletal muscle, and in arterial walls.  When it is activated, it initiates selective synapse elination through the SCF-Ubiquitin ligase complex - when it works properly, SYG1 binds to SKR, inhibiting formation of the SCF complex (Skp1-cullin-F-Box complex), protecting nearby synapses.

It is my opinion that SYG1 dysregulation is directly correlated to symptoms noted in all three conditions: ME/CFS, FMS, and Autism.  If you disrupt proper synapse formation in early childhood development, you almost certainly will end up with a developmental disability.  It leads me to theorize as some have that XMRV is passed from mother to child through saliva, body fluids, breast milk, and quite possibly placental transmission.  Likely the process of autism begins well before the first symptoms appear, and with XMRV screening could be reversed by early use of antiretrovirals, either by treating an infected mother, or the child.  There has been some mention by Dr. Mikovits that vaccines could create the immune insult setting off autism, however I believe the risk is far, far smaller than the immune insult from getting sick - as you are only exposed to an antigen at a point in time, as opposed to receiving a continuous onslaught of viral antigen while the immune system clears the virus.

Another interesting point is that SYG1 is primarily expressed in slow sodium fibers in the peripheral nervous system at neuromuscular junctions- nerve fibers responsible for transmission of pain signals - leading to an amplified pain response.  Substance P opens slow sodium channels, and closes potassium channels - and if you've got uncontrolled synapse formation, it may very well explain some of the observations made in FMS.

Vactruth strikes again - with even more defamatory information!

It is a site with slick graphics, designed to get you to believe their propaganda.  This week, Vactruth takes another stab at vaccines claiming that Chronic Fatigue is the result of a mouse virus contaminating vaccine reagents.  How can anybody invent this kind of psychotic diatribe "Well heres where the 'oops' comes in.  Every HIV-1 lab in the country uses TZM-bi cells for something.  All from the same stock from the NIH reagent bank.  Turns out this stock has been contaminated with another retrovirus - murine leukemia virus."
Whoever runs this site, thank you for your continued foolishness, dangerously misinforming the public - when you can't even spell here's properly, do you deserve to be believed?  They even make accusations against Glaxo Smith Kline for producing a deadly vaccine - three adverse reactions among 170,000 doses is not a lot - at least 250 people would have died from influenza complications had they not been vaccinated.  Far more people will get Guillian-Barre syndrome from contracting the flu, than getting the vaccine.

A site like Vactruth sickens me - and they hide their domain registration information and contact information - telling me a lot about their credibility.  If anybody knows who runs this site, please let me know, as I would like to have a few kind words with them about the defamatory libel they falsely and maliciously spread, in hopes you will not get vaccinated, and infect someone else.

The Modus Operandi of XMRV: Pt1

In a 2 part series I will explain the mechanisms by which XMRV enters human cells, and possible consequences.  The cell surface receptors for XMRV have been identified as XPR1 and SYG1: XPR1 is G-protein coupled receptor suspected as a putative progesterone receptor.  The first part I will deal with deals with XPR1.

XPR1 is a membrane protein which acts as a signal transducer: it crosses the plasma membrane 7 times.  Recently, the structures of a handful of G-protein coupled receptors has been elucidated: Rhodopsin - a visual protein, Beta-adregenic receptor - adrenaline receptor and target for beta blockers, and the A2A adenosine receptor - the receptor our favorite wake up drug caffeine binds to.  XPR1 is found in a fairly diverse array of tissues: lymphocytes, hepatocytes, as well as cells in the brain, pancreas, kidney, prostate, and muscle.  This is a very important finding indeed.

It is of note that progesterone tends to shift the immune balance towards Th2, and that progesterone levels rise to as much as 10 to 15 times normal during the third trimester.  So, as a molecular biologist, it leaves me to theorize that if this virus can mimic progesterone, it can create a state that allows the immune system to ignore the virus, very much like it ignores a developing fetus - scary isn't it?  It is also worth noting that mutations in XPR1 bear a strong association with miscarriage, and that such women often bear masculine-like features.  Observations reveal that high rates of estrogen, or high rates of testosterone in the absence of progesterone tend to favor the growth of XMRV - progesterone inhibits the formation of DHT.  It seems to indicate that succeptibility to ME/CFS is strongly hormone driven, and why ME/CFS and FM are strongly female prevalent.


J. Battini, J.E. Rasko, D. Miller. (1998).  A human cell-surface receptor for xenotropic and polytropic murine leukemia viruses: Possible role in G protein-coupled signal transduction.  Proceedings of the National Academy of Sciences:

Scientific Consensus is Building Towards XMRV as Causal Agent of ME/CFS

I had the opportunity to speak with one of the researchers who attended the  Cleveland Clinic conference a short while back.  Since the landmark study appeared in Science last month, several groups have been in a race to replicate the findings of Dr. Judy Mikovits - preliminary results are beginning to come in, while other researchers are waiting for their virus samples to arrive.  There is now reasonable certainty that XMRV is the causal agent of CFS/ME, as opposed to probable grounds at the time of publication.  It is hoped that by the middle of next year XMRV will beyond a reasonable doubt be shown to be the causal agent of ME/CFS.

XMRV seems to follow Koch's postualtes, except for the first one: "The microorganism must be found in abundance in all organisms suffering from the disease, but should not be found in healthy animals."  The third "The cultured microorganism should cause disease when introduced into a healthy organism", and fourth "The microorganism must be reisolated from the inoculated, diseased experimental host and identified as being identical to the original specified causal agent." has yet to be shown.  However, the main criticism of Koch's postulates is that it does not account for asymptomatic infections.

It is worth noting that there was considerable attention paid to possible therapeutic agents for ME/CFS.  This is still very much of a gray area at this time - and it will be several months before it is known which existing HIV drugs will work against XMRV - only a couple Reverse Transcriptase inhibitors, and Raltegravir have shown early promising results.  This in itself has already led to a few doctors prescribing AZT off-label to ME/CFS patients outside of clinical trials, in addition to a handful of individuals purchasing the drug online from internet pharmacies - however AZT IS NOT a drug that should be taken without medical supervision under any circumstance.

Raltegravir is likely effective against XMRV

Raltegravir (Trade name Isentress), is a drug that inhibits retroviral integrases.  In the article Beck et. al "Early onset of autoimmune disease by the retroviral integrase inhibitor raltegravir", the author states in Proceedings of The National Academy of Science that "the activity profile of raltegravir on the replication or murine leukemia virus is similar to that for HIV, and that the drug specifically affects autoimmune disease in mice, in which endogenous retroelements are suspected to play a role."  Both parts of this statement are highly significant.

The inhibition of Murine Leukemia Virus Integrase, which is almost identical to XMRV integrase, is not that surprising after all.  The catalytic sites of retroviral sequences have a series of conserved residues which are essential for activity, meaning that this enzyme is probably the best therapeutic target for XMRV.  Integrase inhibitors alone could work very well as monotherapy, and Dr. Mikovits stated that HAART is probably not necessary.  Because XMRV is a slow replicating virus, the chances of the virus becoming refractory to inhibitors of retroviral integrase are slim, as compared to HIV.  The drug raltegravir has a much, much better safety profile than NNRT's, which inhibit reverse transcriptase - which have side effects such as lipodystrophy, and the possibility of liver damage.  The downside is: Isentress is very expensive, costing about $1100 a month, something insurers definitely will frown upon - which may lead to some of them requiring a trial course of an NNRT before covering an integrase inhibitor.

The second part, where raltegravir induced lupus in genetically succeptible mice also could have a very profound effect in treating autoimmune diseases in the future.   What is significant is that Lupus favors one arm of the immune system, while Rheumatoid Arthritis, Psoriasis, Ankylosing Spondylitis, Crohn's disease favor the opposite arm.  This is significant, in that XMRV could induce the translation of endogenous retroelements - of which there are over 7,000 on the human genome -which human cells do not have the machinery to transform them into proteins (no human promoter can activate them), leading to the expression of foreign proteins on the surface of human cells, which makes the immune system recognize these cells as foreign.  It also lends credibility to the fact that Fibromyalgia is often co-morbid with disorders such as Rheumatoid Arthritis.  It also lends credence that Lupus is the polar opposite of RA, AS, Psoriasis - leading me to theorize that an antiretroviral could bring about a clinical remission in AS, RA, PsA patients - the same groups that currently benefit from anti-TNF therapy, but could exacerbate lupus.  So Lupus might be a true autoimmune disease, while on the opposite side a viral mediated quasi-autoimmune state exists.

**It is also noted that Echinacea extracts have been reported to produce lupus flares.

G.B. Beck-Engeser, D. Eilat, T. Harrer, H.-M. Jack, M. Wabl (2009). Early onset of autoimmune disease by the retroviral integrase inhibitor raltegravir Proceedings of the National Academy of Sciences : 10.1073/pnas.0908074106

Will Ampligen Ever See The Light of Day?

For many ME/CFS patients, Ampligen offered a glimmer of hope for an effective treatment.  New developments which I've been monitoring however pour some cold water on the flame of hope that was burning for ME/CFS sufferers.  In an unexpected turn, the FDA has demanded additional data from Hemispherx Biopharma regarding safety data, and to perform additional clinical trials regarding its efficacy.  This did not bode well for the securities regulators, and shareholders, who filed suit claiming that it's CEO Bill Carter provided misleading information regarding Ampligen's regulatory status.

Something of this magnitude is by no means unheard of in the pharmaceutical company - Supergen's CEO Jon Rubinfeld was involved in a similar controversy with the drug Orathecin to treat pancreatic cancer.  It certainly will have a profound impact on the approval process for Ampligen.  Given the current situation, an approval for the drug should not be expected until  Q3 2010 at the very least.  Given the litany of lawsuits Hemispherx potentially faces, it could very well derail the Ampligen approval process, and bankrupt the company.  Hopefully, if this is the case, one of the pharmaceutical giants picks up Ampligen, and does the proper filings.

Chicoric Acid - A Natural Integrase Inhibitor.

Over the weekend, I pored over numerous scientific journals, and came across something particularly interesting when searching for inhibitors of XMRV Integrase - Chicoric Acid.  I found numerous studies done, showing that it inhibits not only HIV-1 integrase, but a broad spectrum of integrase enzymes.  This holds some potential as a low cost treatment, however its efficacy remains to be seen.  Chicoric Acid is one of the active principles in extracts of purple coneflower (echinacea).  For pharmaceutical companies, there is little interest in the compound, as it cannot be patented, however in the not-too-distant future we may see it appear on shelves of health food stores.

I for one, cannot guarantee its efficacy.  No pharmacokinetic studies have been done on it.  Normally, a lot of phytochemicals that show a lot of promise in vitro, have little to absolutely no effect in vivo.  This is because everything that is absorbed through the intestine is taken to the liver through the hepatic portal vein, where it undergoes first-pass metabolism, usually through the Cytochrome P450 enzyme system, followed by glucoronidation where it is eliminated through bile.  However, pharmaceutical chemists have devised clever ways to thwart the P450 system, by identifying key parts of the molecule that are vulnerable to attack, and replacing functional groups with Chlorine or Fluorine atoms, giving them a much longer half-life in the body.  Some of these analogs are already being studied as candidate compounds for HIV - for example it has been found that the carboxyl groups of caffeic acids are not necessary to inhibit integrase.

Vactruth.com's Allegations of Vaccines Containing XMRV Laughable.

While doing some research, I came across a site called Vactruth.com, which makes claims that vaccines that are developed to protect us are contaminated with retroviruses.  The author of this website is unknown, as all domain information has been registered privately - but the article is signed by this Dawn Crim.  I could see why she? would not want her information known - some of the information contained in her blog is just laughable!  The allegations sound like this person blames vaccines for allergies, ADHD, Anxiety, Depression, Lyme Disease, and her very own problems with fatigue.

First of all, any pharmaceutical company would do their due diligence, as they have their reputations to protect.  Second, the possibility of secondary retrovirus contamination nowadays is extremely remote - even with live attenuated vaccines, as they use multi-stage molecular sieves to screen out any contaminants, and most vaccines only contain parts of the virus - usually highly purified antigenic peptides.  Third, the claim that Squalene is carcinogenic is absolute hogwash!  Squalene is a natural oil-like substance that is found in copious amounts in shark liver oil, olives, wheat germ, rice bran, and amaranth seed - things that are found in abundance at your local health food store!  And on other ingredients in vaccines - would you drink water if someone told you it was toxic, Mrs. Crim?  The fact is everything is toxic in large enough amounts - just like the amount of mercury contained in a vaccine preparation is less than what is found in a tuna sandwich.  And no pharmaceutical company would conspire to deliberately mass poison a population through a vaccine - someone would blow the whistle, and company executives would face decades long prison terms, and the whistleblower would get millions for doing the right thing!

It sounds like the author of this article can add one more affliction to problems faced by herself and her family: Paranoid Schizophrenia.  Vactruth.com sounds more like a collaboration of patients in a state mental hospital working on a project to pass the time.  I hear it gets awfully boring and lonely in the Loonie Bin.

Google Robots Identifying My Blog As Spam?

I just couldn't believe it - Google's robots have flagged my blog as spam!  How ridiculous.  Some people can't see my new posts until some real humans read my blog and decide it is not spam.  I don't know how their robots work, but I am certainly not advertising any goods or services for sale on my blog, and I will only recommend products which have research behind them.

Should You Get Tested For XMRV Now?

The XMRV test offered by VIP Diagnostics is basically a second generation test - the one where the Whittemore Peterson Institute announced that almost all ME/CFS patients were positive for XMRV, compared to the test at press time where only 67% tested positive.  The test is by no means perfect, and it is not yet clinically validated.  For persons who have severe disability, it's better than what they had before.  It's pretty impressive to go from 67% accuracy to 97% in such a short period of time - it is more accurate than current tests for lyme disease.

It takes a considerable amount of research to refine testing methods, some of which involves making DNA primers with higher stringency.  It also involves standardizing the test amoung several research institutions.  Blood banks will usually want a clinically validated test.  If you get tested today, there is still a small chance the test may not detect anything.  If you are willing to part with you money, it may provide some answers, however it might be better to wait until a clinically validated test is available.

CFS - History of an Old Disease With Many Aliases

Chronic Fatigue-like illnesses have been described in medical literature for over a century-and-a-half.  The disease has went through many different name changes since then:

• In 1751, Manningham described a syndrome of low-grade fever, weariness throughout the body, and pains.
• 1760 - Dr. Snow described a new illness in West Otago, New Zealand as Tapanui flu.
• 1816 - Fibromyalgia was first described by Dr. William Balfour as rheumatism.
• In 1860, Dr. George Beard identified a syndrome with similarities to CFS that he called Neurasthenia.
• In 1861, Florence Nightingale became ill with CFS symptoms.
• 1884 - Sigmund Freud advocated cocaine use to alleviate chronic fatigue.
• 1904 - William Weichardt described that CFS had an etiological agent.
• In 1936, an outbreak occurred in a Wisconsin Convent.  The name Encephalitis was given to the condition.
• 1937 - An outbreak occurred in two Swiss towns, that were described as abortive poliomyelitis..
• In 1938 Dr. Alexander Gillam described an outbreak that occurred in 1934 at Los Angeles County hospital affecting all or most of its nurses and doctors resembling symptoms of today's description of Chronic Fatigue Syndrom.  Dr. Alexander Gillam gave the syndrome the name of atypical poliomyelitis.
• 1915 - The AMA Journal referred to neurasthenia as an adrenal disorder.
• 1939 - 73 Swiss soliders were given the diagnosis of abortive poliomyelitis.
• 1948 - Outbreak at Akureyri Iceland.
• In 1949-1951 over 800 people in Adelaide, Australia became ill with symptoms resembling the atypical poliomyelitis described by Dr. Alexander Gillam.
• 1955 - An outbreak at the Royal Free Hospital in England, the first reference made to a neuroimmune condition with a proposed name of Royal Free Disease.
• 1964 - A theory arose that CFS was chronic brucellosis.
• In 1970, McEvedy and Beard proposed the name benign myalgic encephalomyelitis and mass hysteria.
• 1982 - Lake Tahoe Outbreak - A large number of persons fell ill, with a mystery illness, and many never recovered.  Hippocrates Magazine proposed the name "Raggedy Ann Syndrome".
• 1983 - The term Chronic Eppstein-Barr virus was used
• 1986 - The Term Yuppie Flu was coined
• 1988 - The term Chronic Fatigue Syndrome became widely accepted.
• 1989 - 1990 - Edmonton Outbreak - Over 600 people reported symptoms resembling CFS, beginning in the fall of 1989.  Several cases were traced back to two student residences at the University of Alberta which began with a flu like illness at the beginning of the fall semester, where some blood abnormalities were noted.
• 1990 - Researchers announced they found DNA sequences of a retrovirus in CFS patients, and presented their findings in Kyoto.
• 1996 - CFS was described as a neuropsychiatric disorder.  
• 2003 - A Canadian panel developed diagnostic criteria for CFS.
• In 2006, the CDC recognized CFS as a serious illness
• 2007 - Monterrey Outbreak - Several Catholic nuns fell ill with CFS in Monterrey, Mexico.  The CDC was enlisted to analyze the blood by Mexican health officials, but they declined.  Researchers at Guadalajara University noted abnormalities in the RNASE-L pathway.

Gulf War Syndrome - Evidence For An Insect Vector of XMRV?

Considering how similar Gulf War Syndrome is to CFS, it leads me to postulate that time will reveal they are the same illness - different identity.  How do I come up with this hypothesis - a large number of soldiers who served in Iraq during Desert Storm have been diagnosed and treated for Leishmaniasis - a sandfly borne disease.  The tagline in the movie Casablanca reads "Round Up The Usual Suspects" - Mosquitoes and Ticks are not endemic in the desert - so what is left - Sandflies!  Maybe even Leishmania is a vector for XMRV?

Battle fatigued soldiers are often immunocompromised from stress - and then a bite from an infected sandfly - you've got the perfect storm to set XMRV related disease in motion.  Out the window goes the hypothesis of spent uranium, exposure to toxins, and prophylactic use of Pyridostigmine Bromide as an antidote.  Most chemical warfare agents are Organophosphates, which also include common pesticides such as Diazinon, Malathion, Guthion - the effects of poisoning which do not resemble CFS symptoms at all, and Pyridostigmine Bromide is used as a treatment for Myastenia Gravis and to treat orthostatic hypertension - a complaint of CFS patients!

Is it time for CFS/FM/Gulf War Syndrome patients to wage a legal battle?

The cat is out of the bag: it can be said with reasonable certainty that XMRV is the single agent that sets the wheel in motion for the immune disturbances associated with XMRV.  According to a CDC insider which I have spoken to, the CDC long knew back in the late 1980's that a single viral agent would be capable of causing the perturberences seen in ME/CFS.  I've also heard from a patient in Toronto, Ontario who developed CFS 3 months after receiving a blood transfusion after a motor vehicle accident in 1994 - it's more than a co-incidence.  More information keeps surfacing each and every day about the CDC hanky-panky.

For patients, there is enough there to start looking at litigation against the CDC and other parties.  This would not come at a small price - going against the CDC would require hiring a law firm that specializes in high stakes litigation.  The CDC would not be the only defendant - the Social Security Administration and the American Red Cross likely share some liability.  How much is at stake - Billions.  Each CFS/ME/FM/Gulf War Syndrome patient costs $35,000 a year in lost productivity - that's $595 Billion!  It's also $595 Billion that the Social Security Administration does not have to pay out in disability costs, HMO's and PPO's don't have to pay in drug treatments, and that pension plans don't have to pay out!

Such a lawsuit is perhaps what is needed to "Stimulate" the CDC into recognizing that these disease have an infectious etiology, that they are not some idiopathic fire of unknown origin like they want us lemmings to believe.  They will be forced to admit that CFS/ME/FM/Gulf War Syndrome is another acquired immune deficiency syndrome, and that they've been covering up this silent pandemic for just too long.  Likely if a judgment was won, it would be an egg in the face of the CDC, but they would exhaust all appeals.  Likely other lawsuits would follow in other countries.  Perhaps even a movie by the name of Osler's Web, done with an A list director and Cast might embarrass the CDC enough to change  their ways.

Dr. William Reeves - Another Mark Whiteacre? Criminal Negligence Perhaps?

For those of you who don't know, Mark Whiteacre was a biochemist at Archer Daniels Midland, who is most famously remembered as one of the highest level corporate whistleblowers in the history of corporate America.  He got the inside scoop on a price fixing scandal on Lysine and other products, and got his bosses in trouble, while he himself had his own embezzlement scheme going on within the company.  A similar thing can be said about Dr. Reeves at the CDC - he blew the whistle on his bosses, and yet he continues to be hypocritical to the extreme by stating that the retroviral program at the CDC was taking the lead in an attempt to replicate the WPI XMRV results.

Reeves acted unethically by stating to the press that he did not expect the agency (CDC) to replicate the WPI findings of XMRV in ME/CFS patients.  He acted unethically in that he pre-judged someone else's findings, before doing any research of his own.  He put his credibility, and quite possibly his career on the line - and he will be watched very closely.  Falsifying data won't go over this time.

But why would the CDC engage in such sinister behavior?  Their mission is to protect the public from emerging infections, and in this case they've failed miserably.  The pharmaceutical companies rely on them to lay out their research roadmaps for the future - if they put out junk science, how is the pharmaceutical industry to develop new treatments?  And why would they want to intentionally try and deny scientific facts???

It's certainly not in the interest of the drug companies, CFS/ME/FM/Gulf War Syndrome patients.  It seems the CDC's motto is if it isn't a deadly disease, then feed them Thorazine, Zyprexa, and Amitriptylline, and keep them so sedated they can't think straight - something that's already difficult enough for these patients - now we'll turn them into living zombies!  For the drug companies this would only represent five or six dollars a day - so it wouldn't contribute much to their bottom lines - Amitryptilline and Thorazine are off patent and cheap.  But anti-retrovirals would be a potential goldmine for the pharmaceutical industry - rather than sell just to HIV patients, now they could quadruple their sales to CFS/ME/FM/Gulf War Syndrome patients.

So who would not want that?  The first that come to mind are HMO's PPO's, publicly funded health plans.  Having to pay $1000 or more for XMRV treatments for an indeterminate period of time is something they would not take sitting down.  The second that comes to mind is blood banks - now they've got to worry about tainted blood on an unprecedented scale - making HIV and Hep C look like child's play.  Then comes the issue of liablity and lawsuits - like in Canada after the Canadian Red Cross was found negligent.  If they can keep it as a neuropsychiatric illness, then they can keep putting off liability.  It's criminal negligence at it's finest - the CDC knew of a viral link for twenty years, and they failed to act on it, and thousands more people became ill!

Significance of Co-morbidity of FM CFS/ME and Autoimmune Diseases

The co-morbidity of Fibromyalgia and several autoimmune diseases is well documented in medical literature.  It was accepted for a time that FM CFS/ME were autoimmune disease as well.  It leads me to theorize that many autoimmune diseases are not autoimmune diseases, but rather a consequence of an XMRV-mediated immunodeficiency syndrome.  The finding that the human genome contains many endogenous viral genes that cannot be expressed under normal physiological mechanisms, but can be turned on by certain viruses like EBV, and most likely XMRV makes this a distinct possibility.  So how could this happen?

Many viral proteins are membrane proteins - they embed in the lipid membrane of the virion.  Conceivably, our cells could start expressing these proteins at their surfaces, triggering an immune response.  Many retroviruses contain transcriptional transactivators which there is a strong possibility could accomplish this very event.  It is also conceivable that herpesviruses could work in concert with XMRV to amplify this effect.  An XMRV ravaged immune system in theory can't mount an effective enough response to keep EBV, HHV-6 levels below the "Noise floor".

Ultimately, the significance could be that one viral gene could mean Rheumatoid Artthritis, another could mean Ankylosing Spondylitis, and another could mean Multiple Sclerosis.  This hypothesis could also help explain why what we call autoimmune diseases follow a relapsing-remitting pattern. It could also help prove/disprove the concept of molecular mimicry.

Possible Explanation for Pain Processing Abnormality in Fibromyalgia

Over the years, studies have revealed that a pain processing abnormality as an explanation for the pain fibromyalgia patients experience.  Several observations have been made, noting elevated Substance P in cerebrospinal fluid, and increased Glutamate activity.  These observations are not a cause, but rather a symptom of a much bigger picture.  Some morphological studies have been done showing ragged red fibers in skeletal muscles, in addition to atrophy of type II fibers.  Surprisingly few studies of this nature have been done, considering that performing a muscle biopsy with a special needle is relatively simple, and does not require any incision.

The pain processing abnormalities in Fibromyalgia are not unique.  It has become clearly established that Interleukin-1 Beta is an inducer of Cyclooxygenase-2 mediated inflammatory pain hypersensitivity, which in turn up-regulates substance P and Glutamate transport.  Muscle pain in influenza bears a striking similarity to Fibromyalgia pain, although it resolves itself once the virus is cleared from the body.  In Fibromyalgia, likely the XMRV virus plays a pivotal role.

A CFS/ME/FM Timeline - We Knew About A Retrovirus All Along!

The linkage of CFS/ME to a retrovirus is noting new and suspicion began to grow that it was the case in Fibromyalgia as well.  The first documented findings that a retrovirus might be responsible for CFS/ME surfaced around 1985. The timeline of findings begins in 1985.

• 1985 - Four out of 5 samples sent by Dr. Dan Peterson from the Lake Tahoe Outbreak tested positive for an HTLV-1 like virus.  Incredible disruptions were noted in flow cytometry of peripheral mononuclear cells producing grossly unbalanced CD4/CD8 ratios - showing CD8 cell depletion.  Scatter patterns were also noted in the flow cytometry which were previously only seen in HIV/AIDS infections.
• 1986 - Dr. Robert Gallo - the co-discoverer of the HIV virus remarked after analyzing blood samples from the Lake Tahoe outbreak the presence of HHV-6A, in a manner consistent with an opportunistic infection in HIV patients.
• 1988 - MRI brain scans showed abnormalities similar to HIV cases.
• 1991 - Dr. Elaine DeFreitas published her findings that genetic material of a virus similar to HTLV-I had been found in a similar proportion of patients to the current study at the Whittemore-Peterson Institute, though no virus had yet been isolated.
• 1992 - The CDC and Dr. James Gow would go on to state that the findings of Dr. Elaine DeFreitas could not be replicated.
• 1994 - The CDC dismissed further findings of immune disturbances such as high RNASE-L activity and CD8 depletion.
• 1995 - Research began to surface in CDC and NIH funded studies about pain processing abnormalities in Fibromyalgia - notably elevated substance P, and high Glutamate.  These studies would lead researchers to look for a neurological cause - leading to the theory that the "Volume control" is turned up too high in the brain's pain processing areas - something that certain cytokines are shown to do.
• 1997 - Up-regulation of the RNASE-L pathway is demonstrated in another study.
• 2001 - A study noted the shift in redox state in CFS patients just like in HIV.  The Redox shift leads to P450 decoupling from NADPH depletion, perhaps explaining the multiple drug and environmental sensitivities CFS/ME and Fibromyalgia patients experience.  Of note is the Cytochrome P450 enzymes are responsible for detoxifying drugs and environmental toxins.
• 2007 - The XMRV virus is discovered for the first time in humans in Prostrate Cancer patients who have a rare genetic mutation.
• 2009 - The Whittemore-Peterson publishes the discovery of XMRV as a likely cause of ME/CFS, showing the virus able to replicate and infect healthy blood cells.