The Emperor Has No Clothes

So now the Emperor walked under his high canopy in the midst of the procession, through the streets of his capital; and all the people standing by, and those at the windows, cried out, “Oh! How beautiful are our Emperor’s new clothes! What a magnificent train there is to the mantle; and how gracefully the scarf hangs!” in short, no one would allow that he could not see these much-admired clothes; because, in doing so, he would have declared himself either a simpleton or unfit for his office.

~ Hans Christian Andersen

The moment of clarity has passed. Science isn’t going to save us. No cavalry coming over the hill any time soon. Back to business as usual. Even as the public display of insanity continues in Reno, the discussion of the WPI’s “bad patch” is dying down. New science into a possible viral etiology for ME/CFS has all but died down, awaiting the results of the Lipkin study. It’s hard to expect much when it seems likely they aren’t looking for the right thing, but nevertheless, I still hope against hope they will find something of significance. The backlash has already started, with recent papers about reward deficiency states and perception of pain. The most innovative scientific minds willing to think about us at all are applying their attention to the genetic piece, a factor for sure, but not the root cause, still a downstream effect.

In the midst of losing the interest of the scientific community, the run for Rituxan is on. As a bit of a stalker magnet for the more extreme elements of the ME/CFS community, I got slammed after my last blog by some who like this approach. It is ironic that my opinion about this particular choice is interpreted by some as my wanting to limit access to treatment, given that I was a guinea pig for the last round of uncontrolled human drug trials. And before that, antibiotics for chronic Lyme. This option seems like the most dangerous by far to me over the long haul: hurling bazookas at the immune system will cause increasing dysfunction over time. Though the risk from the infusion itself goes down with repeated administrations, the infectious disease doctors will continue to be busy mopping up the mess caused by this approach to the disease. We are not talking a round of chemo here, but treatment that will presumably be needed for life.

Even so, no one can judge the degree of suffering of another, or what may or may not be the best course of action for anyone else at a given moment. It seems just like Lyme Disease to me. Any disagreement with their doctors’ approach is unacceptable, because those doctors are at least validating the illness. Thank God someone is willing to prescribe the big guns for our disease, no matter how misguided. An approved major pharmaceutical intervention means we have a real disease, instead of an ill-defined syndrome. I agree, it’s better; I just don’t like the risks associated with this treatment.

Big Pharma, an Emperor with no clothes if there ever was one, has waged a war on human disease that is an obviously failed experiment. The newspapers are reporting that more people die of adverse reactions to drugs than automobile fatalities. Our government’s complicity with the devil has left the entire medical establishment in an unsustainable position. You can’t run a society where everyone expects to be maintained on expensive drugs for life. The whole concept is misguided anyway. Take statins for example, which come up in my practice, because even completely unsuitable patients are subjected to the statin knee jerk reflex, though it seems particularly inadvisable in a group of patients already suffering from chronic myalgias. How did the statin brainstorm happen?  Twenty five or so years back, somebody got the bright idea that since people who live to very old age sometimes have low cholesterol, we should give everyone who wants to live a long time these drugs to lower their cholesterol to some artificially predetermined number to prevent heart disease. A logical fallacy if there ever was one. It’s taken all this time for doctors to realize that maybe it wasn’t such a good idea after all. They knew it could cause Polymyalgia rheumatica way back when, so essentially healthy people wound up on steroids long term from this particular experiment. Now it turns out statins increase the risk of diabetes.  And they cause cognitive decline in the elderly. Brilliant. Would you hire these critical thinkers to make an important decision for you with respect to your long term health and well being? In the meantime, Lipitor has made more money than any drug in history. Over 12 billion dollars. No evidence that it prevents primary cardiovascular disease. No improvement in quality of life. Lots of maimed people. An aside: although red rice yeast lowers cholesterol with fewer side effects than statin drugs, it contains naturally occurring lovastatin and can cause the same side effects as the drugs, though it is less likely to do so.

Nobody hopes more than I do that somebody pulls some existing drug that didn’t make it to market for something else off the shelf for us, or fast tracks an orphan drug, in the next few years, but I don’t see it happening. No one cares. No one cared enough to test the already existing possibilities for us when it made sense to do so, at one particular point in time. The round of experiments in vivo that did happen, and the very few of us still taking antiretrovirals, should have been enough to raise the question of why they may be useful for neuroimmune illnesses, but apparently, it wasn’t to be. The question is dead as far as the scientific community is concerned. All conveniently chalked up to the failings of one scientist, per Dr. Racaniello’s final analysis, which he figured out with the assistance of his good buddies Trine Tsouderos and ERV (you’d think he’d be ashamed to admit that publicly, but I guess not).

When does it stop being the human genome and become a rescuable virus that can make other people sick? How many deletions do you have to put back to call it retrovirology instead of genomics? Take the next step. What are the most likely sources of animal viruses and pieces of viruses (not just murine) that could be rescuing defective remnants of past infections long quelled by the sands of time, causing some people to spit out enough viral product to cause disease, and others, exogenous virus that can infect other people? Because it isn’t simple, in the sense that it doesn’t fit the one virus, one disease paradigm, it, or much more likely they, have been missed for decades. Also it was assumed that exogenous retroviruses known to be present in tissue culture, and known to be able to infect human cells in the lab, weren’t a problem for people, even parenterally introduced, since most human cells have retroviral restriction factors. I am not a virologist, but I can read, and retrovirology is an extension of genomics, and visa versa, meeting in the middle of each field.

Here is a paper from 1987. The Four Classes of Endogenous Murine Leukemia Virus: Structural Relationships and Potential for Recombination. The authors, John Coffin and Jonathan Stoye, went after Dr. Mikovits very publicly on multiple occasions. Coffin said publicly that she would be “burned at the stake”. I’m sure that’s what he wanted. After all, when this all comes clear, he will have to admit that almost the entire human race is infected with retroviruses that he chose not to worry about. Not surprisingly, he doesn’t want to think about that possibility now. Max Planck said science changes one funeral at a time. Highlights from this paper:

The modified polytropic proviruses can serve as env donors in some recombinants. Two viruses derived by recombination with the Friend strain of MLV have been sequenced and appear to have acquired env genes from different proviral classes.

It thus appears that  different ecotropic viruses can recombine with different endogenous sequences. It is possible that viral sequences themselves directly determine whether recombination can take place… Endogenous sequences expressed in a differentiation specific fashion would thus provide distinct opportunities for recombination to occur.

In light of this relationship it seems reasonable to speculate that evolution of the ecotropic virus endogenous to inbred strains of mice might have involved a recombination between a nonecotropic virus of the type present in the mouse genome with another virus which has not been fixed in laboratory strains of mice. Thus, the recombinations which occur in highly leukemic strains of mice might in fact be reciprocal to an event that occurred many years ago.

Dr. Michael Snyderman, who has CLL (chronic lymphocytic leukemia) and CFS, and for whom we have the only hard data showing a response to antiretrovirals, was culture negative for XMRV, but had positive serology. Here is a link to Dr. Snyderman’s last guest post. We don’t know if MMTV-like virus infection can cross react with a serology test that picks up MLVs. Andrew Mason believes he has isolated a beta retrovirus associated with primary biliary cirrhosis and an anti-mitochondrial antibody. I have presented his work and lots of other evidence on this blog in the past that supports a retroviral etiology for certain neuroimmune diseases, as well as case reports of responses to antiretrovirals.

Since gamma retroviruses (and other simple animal retroviruses) replicate mostly by mitosis, unlike HIV, in hindsight, we shouldn’t have expected anything other than slow improvement, since stopping viral replication doesn’t fix the problem (n.b. there was one rapid complete response, anecdotally, in a young patient who hadn’t been sick for long). Infected cells need to be replaced by apoptosis, which the virus tries to prevent, hence the clonality that Dr. Snyderman is studying.

We have no marker of disease. When I started antiretrovirals, I naively expected to have viral load measures in a year or so, to benefit from all the work that had already been done for HIV disease. But now there is nothing to follow but patient report. Instead of going back to the drawing board to figure out what it is, everybody went home, since XMRV was created in a lab. However, that lab contaminant spreads through a clean lab in a few days, infecting human cells. It also establishes a persistent infection in macaques. Dr. Snyderman has real trackable numbers. His CFS symptoms have waxed and waned with his remissions and relapses. He will try to publish as a clinical case study in a medical journal, but no one will notice. Just like the occasional case reports that have shown antiretrovirals to be effective for MS and Sjogren’s Syndrome (both of which show up frequently in the families of CFS patients).

In what follows, any time you read “XMRV”, think instead, “similar simple animal retrovirus”…

Silverman abstract, XMRV infection induces 30 host genes that regulate inflammation and cellular physiology, published only as a supplement: XMRV Infection Induces Host Genes that Regulate Inflammation and Cellular Physiology – Source: The Journal of Urology, Apr 2011 Supplement (#280) and Integration Site Preference of Xenotropic Murine Leukemia Virus-Related Virus, a New Human Retrovirus Associated with Prostate Cancer

There are other known instances where virus is necessary, but not sufficient without the genetic piece. I have a Crohn’s diagnosis, along with many others that are almost right (most autoimmune diagnoses in ME/CFS patients are not full blown, symptoms and antibodies, but not the full picture). Virus-Plus-Susceptibility Gene Interaction Determines Crohn’s Disease Gene Atg16L1 Phenotypes in Intestine

Simple animal retroviruses have glucocorticoid (and hormone) response elements and anyone who knows anything about the disease knows how well this fits. It is one of the reasons why the patients look so crazy. The disease is definitely exacerbated by persistent stress in many people, in much too direct a way. Hormonal shifts, puberty, childbirth and menopause were also obvious triggers historically for many. Xenotropic Murine Leukemia Virus-Related Virus Establishes an Efficient Spreading Infection and Exhibits Enhanced Transcriptional Activity in Prostate Carcinoma Cells and Androgen Stimulates Transcription and Replication of Xenotropic Murine Leukemia Virus-Related Virus

Here is a paper from 1978 showing that murine and primate sequences can mix it up with each other and rescue defective endogenous sequences. Rescue of endogenous 30S retroviral sequences from mouse cells by baboon type C virus.

And from 1985: Maturation of murine leukemia virus env proteins in the absence of other viral proteins. “Cell surface gp70 was found alike in the mutant and wild type. However, cleavage of Pr15E to p15E did not occur in the mutant. This final cleavage step of AK 71 Prp15E could be made to occur by superinfecting cells containing the mutant with baboon endogenous virus.”

Here are three blogs I wrote when I was figuring out the vaccine/biotechnology piece. My understanding is deeper now, but I still think the basic thesis is correct. I’ve made some scientists angry (preferable to being ignored), but nobody has yet told me why my hypothesis is wrong, or offered a better explanation for the clinical observations; what else explains all of the observed phenomena? If you haven’t read them, there’s some interesting stuff  in these posts about the history of vaccinations that you may not know.

Now in the 21rst century we have “humanized” monoclonal antibodies produced from hybridomas, derived from antigenically stimulated B cells from sick mice that are known to be producing infectious virus; these B cells are then “fused” with immortalized human myeloma cells. We inject the antibodies produced, and the sludge?, into people, e.g. high risk babies to prevent RSV. Then there is xenotransplantation. And on and on. And what about the lab workers, since they are working with exogenous adventitious retroviruses that easily spread throughout the lab uncontrolled by the usual precautions?

MedScape is throwing out numbers like 20% of the population has a rheumatic disease (not to mention 1/88 children are autistic, 1/54 boys under 8, up 78% over a few years time, and it is probably already higher now). It is very difficult to absorb how serious it is and how much of it could have been prevented. I was taught, in medical school in the ’70s, to do a review of systems, so that I didn’t miss anything, expecting it to be negative for most people. Almost nobody it seems has a negative review of systems any more, even children. The mothers of ASD children know when their kids got sick, even if their doctors and the scientists studying the problem are too dumb to believe them. The state of the art can’t deal with the uncertainty involved in studying something that isn’t one thing. Why do you think more than 1/3 of Gulf War veterans have GWI or CFS or whatever you want to call it, (since they are clinically indistinguishable from ME), and their children have an unusually high rate of autism? It was, and is, in the vaccines, folks.  And there were chemical and infectious exposures involved in the Gulf also, creating a perfect storm.

Something is terribly wrong and this hypothesis covers it. It explains the increase in neuroimmune and autoimmune diseases, as well as cancer- increases, and the emergence of new diseases. The diseases in question didn’t exist or were very rare in the early 20th century. Very little common sense being applied to the situation. Upcoming meeting: 2ND INTERNATIONAL SYMPOSIUM ON VACCINES: 8th International Congress on Autoimmunity at the Palacio de Exposiciones y Congresos de Granada in Grenada, Spain on May 9th.

There are still readers coming to this blog from public and private institutions of higher learning. Not as many as when Dr. Mikovits was fired, sued and arrested, but quite a few still visit and new ones are finding it. There is no “translation” happening between the clinic and the lab. Sadly, the internet is all we’ve got. Anyone who knows something about the science in question, please tell me why I’m wrong. I want to be wrong. It’s difficult to find the energy to continue to think about the science in a vacuum, with little hope now that understanding the frontiers of the science will have clinical utility any time soon.


  1. Does the “normal” human genome contain murine sequences? Avian sequences?
  2. What processes other than retroviral replication might be impacted by a reverse transcriptase inhibitor?
  3. Do retroviral RTI’s have activity against other reverse transcriptase enzymes?  Do RTI’s inhibit telomerase reverse transcriptase? Here’s a paper that suggests the answer is yes: Persistent inhibition of telomerase reprograms adult T-cell leukemia to p53-dependent senescence.
  4. Do retroviral RTI’s inhibit transpositional behavior? Please read this very important paper: Inhibition of endogenous reverse transcriptase antagonizes human tumor growth

Meanwhile, Ali and I continue to do amazingly well. Not every minute, but we are having many wonderful minutes. Ali just finished her first semester at U Mass Lowell online and her first college grade was an A. She is planning to increase to a full program for the summer. She has friends and is currently in a relationship. She is starting to go out, just for fun, without any major MCS set backs. She has been making and going to her own health care appointments and dealing with the other odious tasks of life. She has been regularly cooking inspired meals for the family. She has begun to do calisthenics, without weights and walk a little, without significant PEM.

I was in Hawaii for two months, so Ali didn’t have any infusions during that time. She had an adverse reaction to a glutathione push early in the year that had soured me a bit on IV’s, and I didn’t use any for K (guest blog by her mom a few back), since we were getting good improvement without it, but Ali wanted one when I got home and she responded to her usual modified Meyer’s, no glut, with a burst of energy that has so far lasted a week.

I had a huge push to get home. I went to a big local party in North Kohala, spent the next day packing up the house so it would be together when I return, then took the red eye home. I hit the ground running and left four days later for a six day RV trip in Arizona, where my husband was entered in a mountain bike race. We went to some amazing places, Prescott, Sedona, Petrified Forest National Park. I hiked every day of the trip, including the hard part of a hike, described as “strenuous” by the park service.

Petrified Forest National Park May Day, 2012

I have been able to throw myself off the proverbial cliff and fly for a day or two for quite some time; all the while payback has been reducing in severity and duration, but this is the first time I’ve been able to keep it up. I’ve had a little PEM here and there, to let me know I was up against my limit, but at a hard half mile hike, with rock clambering, I am much beyond where I was six months ago when we went to New Orleans and I wasn’t up to walking around the Tulane campus, even though I really wanted to. The only things I’m doing consistently is taking Viread, using a little oxygen here and there, Cozaar, aspirin, hormones. I need to take my own advice and be more consistent with oxygen and do some neurofeedback. I’m on minimal supplements, D3, B12, Deplin, ubiquinone, others sporadically.

However, not to paint too rosy a picture, I’ve had some progression of my radicular sensory neuropathies, upper and lower extremities. I had one episode of numbness in the distribution of an upper extremity dermatome, with very brief motor involvement, that threatened to push me over into an RRMS (relapsing remitting multiple sclerosis) diagnosis, to go with all my other almost diagnoses, but it hasn’t recurred, and I am unwilling to go another round with the experts to be told I don’t fit neatly into any of their diagnostic categories. I already know that they don’t know. Why subject myself to ridicule and uninformed care, for something they can’t do anything about anyway. Been there, done that.

The treatments we are using, and I am using in practice, all have global effects. They interact synergistically to tip the balance in favor of the patient instead of the disease, without doing further harm. Reverse transcriptase inhibitors may be in that class, even though they are unstudied in this context. Antibiotics used intelligently may have a place as well for some patients, though determining who and when to treat, and for how long, is tantamount to being a witch doctor casting the bones.

The point is no longer that we suffered. The point is that we aren’t suffering much now and others are, needlessly. I have almost died twice due to misunderstanding of my illness. I met David Bell in Aug 2010 and told him I was going back to work after being bed and couch bound for over 5 years; he told me he’d never seen it happen at that stage of the illness and it has happened. My reason for being now is to keep others from making the mistakes I made. And to move it along if at all possible. Suffering is inevitable, but unnecessary suffering is evil. There is ample evidence for an infectious etiology, at least in some families, if anyone would bother to look. We will try. Somehow we will complete our family survey, without funding. The technology exists to answer the question, but no one cares. The disease is treatable. More importantly, it is preventable! But it appears that it will remain invisible for now, until somebody has the patent for The Test, individual DNA sequencing, readily available from your local commercial lab, which will unravel each patient’s mystery, proving ME/CFS, chronic Lyme, ASD, PANDAS, GWI, RRMS are not one thing, but variations on a theme. Then, in a decade or two, some genius will look at the data and say Ah ha!


Today’s song: When In Rome by Nickel Creek

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26 thoughts on “The Emperor Has No Clothes

  1. Hi Jamie – what an amazingly detailed and informative blog – I will print off a copy to give to my GP. He might look back one day and remember it was through reading one of your blogs that he first became introduced to the idea of where our illness originated from. Fingers crossed it will be in the not too distant future:).
    Regarding your quote about the Lipkin study “it’s hard to expect much when it seems likely they aren’t looking for the right thing”. Could you please explain this/ expand on it. I thought they were looking not just for XMRV but HGRVs in general. What is it that you feel they should be looking for in particular?

    • @Maisie, the CDC has no test, they have never had a clinically validated assay. The Lo lab now uses the failed assay from the Lo paper, as they did in the blood study. All we have is Mikovits and Ruscetti and they found polytropic sequences.

      By the way the difference between xenotropic and polytropic is totally subjective. They shouldn’t be claiming they are different viruses.

      Prostate cancer patients are infected with the XMRVs. Urisman et al. said they were viruses.

      The Government is only picking on ME. There is no big (useless) NIH study on XMRV in prostate cancer.

      When it comes to the NIH study, commissioned by Fauci and Collins with golden boy Lipkin asked to put his name to it, there is no guarantee this is to be a replication study. They have still kept all the study details a secret to this day and will we even get the full details when it is published? I doubt it. Not unless we take this to court.

      And lets not forget how easy it is to mess up the clinically validated assays of Mikovits and Ruscetti. The first thing they have no control over is sample collection and processing. Then there is coding, blinding and patient/control selection.

      If the technicians are not briefed correctly the assays will fail. If the blood is frozen and thawed slowly the assays will fail. If no trizol is added, as occurred in the blood study, the assays will fail, if PCR inhibitors are used the assays will fail. It is a political study for politicians.

      @Jamie, we shouldn’t give in. Lets fight them on this. They fear a patient backlash and we do have grounds to have officials investigate. Congress?

      Everyone of these articles involves damning evidence against contamination as an explanation. In fact what contamination theory? There is no evidence for it. They are naked. The first article here actually could bring the NCBI into disrepute. I would argue it does. You can’t switch one virus for another! Answers about what is taking place in the Genbank are critical to the health of millions. This is the evidence we need to launch hearings into the actions of certain groups.

      Is VP62 in fact PreXMRV-1? Virus swapping occurring in the Genbank!

      Missing env gene in the 22Rv1 virus, the consensus XMRV virus.

      Two PreXMRV-1 viruses

      PreXMRV-1 and -2 not shown integrated into nude mice.

      The scientists out there who are scared are more likely to go for it if thy see support from the patients. So don’t give in science is the only thing that can make a difference and we have to ensure it is allowed to happen. The HHS should not be interfering as they have done.

      • 2012 presidential orders officially declared congress “ceremonial only’ , and placed the UN (corporatocracy) in charge!

    • It is known that the CDC test cannot detect any kind of gammaretrovirus let alone the Mikovits/Ruscetti retrovirus.

      The Lo test cannot detect the Mikovits retroviruses and Lo used a test in the BWG that could not detect a MLV in people with ME either. So the only tests with a chance are the mikovits ruscetti tests.

      We all know that the Mikovits/Ruscetti gammaretroviruses are not related to the VP-62 sequence.

      What most people dont realise is how important sample preparation is. Heamolysis or not washing the buffy coats properly will leave lactoferratin in the sample and inhibit PCR. The resultant matrix effects disrupt antibody antigen avidity and affinity rendering the Mikovits and Ruscetti assays useless. In blood the concentration of MuLV is so low that even minor flaws in sample preparation will render them undetectable. They can however be detected using a simple throat swab as per Fischer et al.

  2. Thank you for this summary. It will really be helpful to many people.

    Re: “New science into a possible viral etiology for ME/CFS has all but died down, awaiting the results of the Lipkin study. It’s hard to expect much when it seems likely they aren’t looking for the right thing, but nevertheless, I still hope against hope they will find something of significance. ”

    Does this mean they are looking only for XMRV, which was proven to be a contaminant, or are they looking for retroviruses in general?

    • Maisie and Patricia,
      I was not commenting from a place of knowing any details of the study design, but thinking about it generally, because the purpose of the study was to replicate something that we already know, from the BWG, has problems. There was a lot of work done looking for XMRV in patients and nobody could find it. It therefore seems most likely that we have another closely related, or maybe not so closely related retrovirus, or retroviruses. I hope that they are looking for something broader than XMRV, but haven’t heard that they are.

      • XMRV has not been proven to be a contaminant. What evidence? They know VP62 is not a natural isolate, but that is all they are focusing on in the negative studies. They have been looking for the wrong virus and failing to ensure their tests can detect wild type viruses. A spiked sample is like looking for Saturn in the sky with your naked eye, a wild type virus is like trying to find a black hole with your naked eye. So what about VP42, or VP35 or the other variants found in prostate cancer patients and what about the polytropic sequences found by Mikovits and Ruscetti?

        There has also been nothing official posted about this being a replication study. That is wishful thinking.

        If they wanted replication results then the contamination researchers should have tried. What are they scared of?

  3. Also, it is interesting as Jamie says, that a so-called ‘lab contaminant’, XMRV, can infect rhesus macques – so if them, then why not us? And what disease/s would this infection cause in the long- term/or with the right trigger. The poor monkeys were ‘sacrificed’ so I guess we shall never know…

  4. Petrified Forest National Park (near WInslow, AZ) is likely my favorite location anywhere. If I were going to choose a place for someone with CFS to try aggressive hiking, that would be it. (The area near Prescott and Sedona is pretty good too.)

    Lisa Petrison, Ph.D.

    lisapetrison at yahoo

  5. What an excellent and beautiful post; full of life, thought, and heart. I wonder how many people actually appreciate, intellectually and emotionally, what Jamie is doing for, essentially, humanity. Cynicism leads to nowhere accept itself. Science advances because scientists dare to ask, to admit they don’t know, and then to seek more concretely, what in fact ALREADY IS. Too bad most of the people in positions do something about it are too stupid, stubborn, selfish, or scared to do so. They would be wise to remember that nobody was helped by Semmelweis’ critics.

    The hermit will doubt whether behind every one of his caves, there is not – must not be – another deeper cave, a more comprehensive, richer, stranger world beneath the surface, an abysmally deep ground behind every ground, under every attempt to furnish “grounds.” – Nietzsche

  6. Two things, re: your episode of near RRMS. I don’t know nothing, but I have lived with this stuff since the ’70’s now. My impression is that whatever approach one takes that allows normal-appearing function, it will result in new leaks-new symptoms- in some other area. Its perverse.
    Second; unnecessary suffering. Yeah. There was a time when I thought about it that way a lot. But it is just how life is. One funeral at a time.
    It’s not just medicine or science. It is how we moderns live life. It is entirely messed up. Every way you look at it. Civilization is a bizarre spectacle, getting more so all the time. It is so unnatural! To me that is the essence of it: unnatural. But having said that, then what?
    I haven’t the slightest inkling where it will end. But I am not cynical.
    I am blessed to hold a religious perspective, so I know what my response is; first, do no harm; and second, be as useful and helpful as I can. Be honest. It’s all I can do.

  7. Brilliant post as always Jamie! Just one thought. You say:

    “Our government’s complicity with the devil has left the entire medical establishment in an unsustainable position.”

    Problem is the government *is* the devil. It takes what a billion dollars to run for president? So much for democracy. Its the corporations & the corrupt rich that run America. Also look at the trillions the US government spends on new ways to kill, maim & torture people. Not to mention the illegal invasion and occupation of other people’s countries. All in the name of money & power (& oil). Sadly the US Governments support for Pharma is the least of its evils. Thankfully people have the right to refuse dangerous drugs (like statins). Sadly people do not seem to have the right to refuse to be bombed, invaded, rendered (kidnapped), tortured, assassinated etc.

  8. A slow thaw time will also kill PBMCs and render the Mikovits/Ruscetti western blot methodology ineffective too, and if they rely on culture to increase titre this will obviously be ineffective as well.

    A delay in separating the components, or separating or storing at the wrong temperatures, will have the same effect. The people doing this stuff are rarely well qualified or well briefed as to the potential for ruining samples.

    Now why is Lipkin not running this test?

    Polymerase chain reaction was used to detect XMRV in 267 respiratory samples taken from German patients. One group comprised sputum and nasal swab specimens from 75 travelers from Asia who had respiratory tract infections. The second group consisted of 31 bronchoalveolar lavage samples from patients with chronic obstructive pulmonary disease, while samples from the third group were from 161 immunosuppressed patients with severe respiratory tract infections. The study included 62 healthy controls. It should be noted that none of the patients had been diagnosed with CFS.

    XMRV sequences were detected in 3 of 75 samples (2.3%) in group 1, 1 of 31 samples (3.2%) in group 2, and 16/161 (9.9%) in group 3. Six of the XMRV-positive samples in the second group also contained rhinovirus, adenovirus, or pathogenic fungi. The higher rate of detection of XMRV and other microbes in immunosuppressed individuals is not unexpected. The control group contained 2 of 62 samples (3.2%) positive for XMRV.

    Explain that finding with plasmid contamination.

    Why didn’t Lipkin use respiratory secretions?

  9. Brilliant.
    Yes, Pandora’s Box of Bioweapons.
    BPI corexit
    Designer pathogens
    Electrical Transmission Lines
    Tasers , Heart attack darts, ETC.

  10. Electromagnetic Microwave Radiation 24/7 from towers, antennas, gadgets

  11. 20 years ago Daniel Peterson had $10,000 worth of blood work done on me. I photographed the 50 tubes of blood taken in 1 draw.( A bona fide miracle for this one with a vein that many days can’t hold up for even a 1 tube ‘stick’. )

    Peterson’s summary letter for that testing lists several pathogens circulating in my bloodstream, including a “spuma-like retrovirus’. Also that only 50% of blood-oxygen reaches cellular metabolisms. T cells all screwed up. ETC.

    Physicians read all this and totally glaze over —-because they can’t treat a baby the devil is denying.

    Permanent damage of mitochondria caused by ME/cfs ever discussed here ?

    microwave radiation wireless gadgetries now 24/7 are permanently damaging the mitochondria , and breaking both strands of the DNA double helix = permanent deformity of the species is already birthing Frankensteins…\

    YOU HEARD IT HERE 1st. Thanks Jamie…

  12. Given that there could potentially be great problems with the current Lipkin study (i.e. many reasons the assays will fail to detect the retroviruses), can anyone confirm whether the Chronic Fatigue Initiative Pathogen study using Next Generation Sequencing will avoid these issues and give us a non-disputable result on whether or not we are infected with HGRVs? We need some clear proof that the powers that be cannot ignore!

  13. Two things (one on-topic, one not):

    1. I would think that Dr. Martin Lerner would have quite a bit of data to contribute on the effectiveness of ARV’s and ME.

    2. Re: Marfan Syndrome – Check out
    May 6 – How an engineer repaired his own heart

    • ARVs are not necessarily going to be affective because these viruses do not use reverse transcriptase to replicate. Does Martin Lerner also study fatigue patients?

      • From what I understand, Dr. Lerner has (or had) ME and has helped ME patients over many years.

      • I’m mistaken about Dr. Lerner using ARV’s. Lerner believes ME/CFS is caused by EBV, CMV, and HHV6 and treats with antivirals with some success.

        • How many patients has he cured? It is a not a hypothesis to say they all do it.

          • I spoke with a woman at my doctor’s office who claimed that Dr. Lerner cured himself of ME/CFS and cured her. She also said that Lerner has “helped many others”. That’s the extent of what she said.

      • where to see the facts on reverse transcriptase NOT part of reproduction of gamma retroviruses ?
        “The Sex Life of Gammaretroviruses”


  14. Very interesting and informative post as always.

    I am glad of the studies being done over in Norway by Drs. Malle and Fluge, not so much because of the Rituximab, but because of their learning and publicizing more about the way this disease works and the damage to the immune system. Also, the physical manifestations of the disease that can be objectively measured. This should help people world-wide with diagnoses, medical care, disability benefits, and understanding by society, friends, families and doctors.
    I am quite glad of all objective biomarkers as I think it will help people with the disease in many ways. Of course, as medical insurance, including government programs cut back in testing and treatment, things may be very rough anyway for people with many diseases, including this one.
    Also, I think another issue that needs much more study is the role of environmental toxins in causing cancer and so many other diseases. Thousands of chemicals are discovered every year, and nearly everything that’s around us contains many of them, unless we consciously try to keep a toxic-free environment. Many of these are not benign.
    As far as WPI, I don’t know why they’re now out of the doghouse. What are they doing exactly as far as research? Honestly, I’m still quite outraged that they used a quote by Anne Frank in their annual financial statement and fundraising brochure. It’s such crass opportunism. No one except Holocaust memorials should be using her name. So I will never trust them or respect them, on top of everything else that’s gone on in the past few years.
    With having had a day where I did errands within a few blocks of my house and thought I’d faint and had to sit down twice, it makes me more impatient than ever for research so that this disease is understood. At least the stigma and denial of concern and understanding could be alleviated for some people with CFIDS.

    • When is the Rituximab study to happen? They haven’t said they are ready to start yet and are having funding trouble aren’t they?

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