Recent FAQs about the clinic at the WPI

1. How can I be seen at the WPI?
There is already a long wait list. Patients will be contacted on a first come, first serve basis to be scheduled for the doctor of their choice. If you would like to be added to the wait list, please email, rather than call, your request to the WPI office:

2. Do I have to be XMRV positive to be seen?
No. Our physicians will treat ME/CFS and related neuroimmune illnesses, without respect to the results of any particular test.

3. What treatments will be offered? Will antiretrovirals be prescribed?
Each physician will treat their own patients. There will be no set protocol. Our physicians will be practicing in an environment that supports openness to all options. All decisions will be made within the context of a physician patient relationship at a particular moment, as always. Antiretrovirals are not promised, nor will they be forbidden. Off-label use of drugs is the usual and customary practice of medicine. We see ourselves as working within the context of a public health crisis. We believe that ME/CFS patients with severe disease should have the right to compassionate use of unproven drugs.

4. What will be different than the care I’ve had in the past?
The group nature will encourage a deeper insight into the illnesses at hand, and provide each physician with exposure to the treatment approaches most likely to be effective. Daily interaction between physicians and scientists will cross-fertilize the thinking of both, impacting patient care directly. Our doctors will be part of an international consortium of practitioners sharing experiences in our Physician Working Group. Records will become part of our database, which, with time, will grow to include a very large number of patients treated by a group of doctors, enabling us to look at outcomes in a broader way than is possible for a single doctor. Adverse outcomes will be reviewed and discussed within the group.

5. Will there be clinical trials?
As all of us know too well, there is no slam dunk, quick and easy trial to do. Tenofovir is probably worthy of study, but until we have a way to monitor, the clinical response is too incomplete and too slow for a short, simple study, given that any study we do now must be possible with extremely limited funds. Dr. Snyderman is interested in studying lenalidomide and we are looking at that. We are open to all options, but unfortunately, pharmaceutical options for study are limited at this time.

6. Is it going to be an alternative medicine clinic?
It will be a “conventional” medical facility, located on a medical school campus, with physicians who are CAM, complementary and alternative medicine, aware.

7. Will insurance be accepted?
No. A superbill will be provided for submission to insurance. Current Medicare and Medicaid reimbursement rates make it impossible for us to accept insurance and provide patients with the time consuming care necessary to impact the illness.

8. Can I see you or be supervised by you in Reno?
No. I’m not licensed in Nevada and getting a new license there with a “practice gap” will take some time. My duties in Reno are administrative. I have started a private practice on the Big Island, where I am licensed. Each physician in Reno will be responsible for seeing and following their own patients.

The enormity of the need feels a lot like charging hell with a bucket of water, considering our limited resources, but we’re going to do it anyway, as we start seeing patients one case at a time.

New Beginnings

As the battle is waged on the scientific front, it is with great joy that I am able to announce that we will begin to see patients at the WPI on August 1. It will close the circle necessary to be a true translational research center with synergy between disciplines.

Dr. Chitra Bhakta is a Family Practitioner with a private practice in Orange County where she treats ME/CFS and autism. She brings medical insight, scientific literacy and compassion for the patients. Dr. Bhakta will continue to be available to her Orange County patients during this transition.

Dr. Robert Fredericks is an Endocrinologist in private practice in Reno. His special interests include the endocrinology of neuroimmune illnesses and he is an expert in bone metabolism. He has decided to join us and is in the process of moving his practice into the clinic, thus providing us with our first specialist.

There are a very large number of patients asking to be seen. We will only be able to accommodate a few in the beginning. We have other interested doctors, but Nevada’s licensure process for new physicians coming into the state is long and can be convoluted. Dr. Bhakta has had a Nevada license since her residency at the University of Nevada, allowing her to begin without a delay. Our goal is to create a group of like-minded physicians. I tried active recruiting hoping to accommodate the volume of patients at the outset, but it will have to happen more organically, as we find the right doctors with passion for the project.

It’s a start.  The need is enormous. We will get our systems in place, fill in the gaps with respect to pathophysiology, and approach treatment with the benefit of the perspective of our scientists. The seeds are sown. We will water and care for this unique garden, growing our knowledge for the day when we can harvest in the form of clinical results.

A journey of a thousand miles begins with a single step.
~ Lao-tzu


Where large sums of money are concerned, it is advisable to trust nobody. ~ Agatha Christie

Thank you to Kristin Loomis, for contributing her comment and for the additional information she provided privately. I have a better understanding of the HHV-6 Foundation’s policies and interests. I understand that retroviruses really aren’t on the foundation’s radar these days. I apologize for any inaccuracies, this time, and anytime; I do my best to fact check before publishing, and to limit any criticism that is directed at an individual to what can be verified on the internet, not gossip. I write each blog with the information at hand at that moment, intending to stimulate discussion. It is personal opinion, reaction to the events, public and private, not investigative journalism, though I wish a good investigative journalist would take it on. I’m getting mail suggesting that I interview people before posting blogs, but I have a day job again:). In any case, the information circulating that HHV-6 Foundation funded Knox et al is apparently incorrect. I invite anyone who feels they have been criticized unfairly to join us. Everyone needs to know the truth.

In your comment, Kristin, you said that you believe that Abbott funded Knox et al. I guess it’s logical to conclude that if Abbott appears on a paper, there is money involved, either because they funded the study and/or there is a patent and potential lucrative test involved. This raises a number of questions. I hope that anyone with information to answer these questions will contribute to the discussion as you did. I have never thought that there is a conspiracy in the sense that Peterson, Knox, Coffin, Stoye, Vernon, McCleary, the editors at Science, et al are having conference calls plotting our destruction. Each individual has their own reasons for doing and saying the things they have.

In my opinion, whoever funded their study, Knox et al have some pretty unsavory stuff to explain to the patient community. If I put the best spin on it possible, then the patients have been harmed by misguided acts. The publication of their shoddy work was unethical and immoral, in my opinion. The collection of the specimens in the first place for this purpose is inexplicable to me. Even if Peterson woke up one morning and said OMG, XMRV is all a big mistake, it is inconceivable to me that he no longer believes it is a retrovirus. So his desire to bury XMRV has to be about being right, ego and revenge, or money. Roche funding Valcyte? Hemispherx funding Ampligen? As I’ve said, he is welcome to respond. I will be happy to post anything he’d care to share. I would like to point out here that although I’ve had a lot of questions about Dr. Peterson for a long time, and have heard many stories, from protagonists and patients (always my most important source), I didn’t mention his name on this blog until the publication of Knox et al, which I took as a declaration of war on the patient community.

Abbott turns up all over the place, e.g. link; see Industry Relationships at the bottom of the page. They are clearly interested in XMRV. Their employees appeared as co-authors on negative and positive papers in Belgium, the positive paper being about a test for XMRV in prostate cancer tissue, not blood. When someone does a study, they know what they want to find; then they blind it to make it convincing, keep it honest. It makes no sense to do a study knowing at the outset that your test detects nothing, unless that is what you were trying to show in the first place.

From where I sit, there are many unanswered questions. It would be lovely to have no need of considering anything but the unfolding science, answering all of our questions in logical sequence, so everyone could take the high road; but that isn’t what happened. Thus my questions of the moment. Why and when did Abbott approach Konstance Knox to do a study on XMRV, when she had never published on anything but HHV-6 and owns a commercial lab dedicated to it’s detection? Why is Abbott’s funding of Knox et al not disclosed? Why would Abbott want to publish a negative detection study? Who is Graham Simmons and what is his stake, as he appears on negative, equivocal and positive papers? He works for a business entity involved in transfusion science and has a teaching appointment at UCSF, as does Jay Levy. Where do Roche, manufacturer of Valcyte, and Hemispherx, manufacturer of Ampligen, fit in to all this, since it seems likely they are a piece of the puzzle as well? What else do these people/companies have waiting in the wings? Intellectual property laws support a unique patent. Who put pressure on Science to rush Knox and their EEC to press when they did? When did Dr. Peterson collect the specimens for Knox, and what was his relationship to the WPI at the time? Did he inform everyone of what he was doing? You can’t get into anyone’s head. In the end, only the Shadow knows. But facts, actions, dates can be verified.

Nobody wants to have anything to do with CFS, except the WPI (and the CAA, with their peculiar spin). It’s common to hear that this or that researcher is sorry they got involved in CFS, because the advocacy community is becoming so strident. I’m not sure what the answer is. Polite hasn’t gotten us anywhere, as witnessed by the useless money that’s been spent on the CAA over the years in their pitiful attempt to validate the illness scientifically. If that had worked we wouldn’t be confronted with the psychiatric community wanting to label us with “CSSD”. The CAA too is free to respond in any way they like; the comments on this blog aren’t moderated.

ME/CFS is of retroviral origin, as is ASD, in my opinion. Read the HIV and animal retrovirology literature, much of which is referenced in previous blogs. It’s all there, plus the methylation defect and mitochondrial issues, covered to a large degree in the HIV literature, that were making up the bulk of my reading until the recent salvo was fired. The parallels are obvious. Nothing we’ve ever had to work with as physicians comes even close as a workable model to provide us with an approach to treatment, with a chance of healing the patients, forgetting about whether XMRV is the major player or not. For an individual to take any action at this time which has the effect of shutting down research into the retroviral origin of the disease is a crime against humanity.

Nobody is saying that the associated, opportunistic infections seen in ME/CFS aren’t important, anymore than Pneumocystis is unimportant in AIDS. It is exactly analogous. In this case, there may be interaction between viruses. Activation of latent viruses may benefit the underlying retroviral process, turn it on if you will. Another possibility is that any persistent infection causes downstream inflammatory changes that favor activation of provirus. The research into how retroviral etiology explains CFS pathophysiology needs to proceed, even before everything is sequenced and proven, even while XMRV’s defendants are being raked over the coals. Everyone involved knows it’s much bigger than whether individuals get discredited or laughed at. Scientists and doctors are much the same when it comes to fear of ridicule restricting their abilities to fulfill their prime directives.

In the end, science will tell us who is right, irrespective of personalities, unless the work isn’t done at all. Although I look forward to the results of Dr. Lipkin’s study, and from what I have read and heard, he is worthy of the respect he has been proferred by being put in charge of such crucial work, it seems wrong to me that it all rests on one man’s conclusions, or the ability of a couple of scientists to flawlessly reproduce their work, though they will certainly try. Maldarelli, Lipkin, XMRV Blood Working Group. That’s not much for a million sick people. When John Coffin declared XMRV dead, he said it could be another retrovirus. Is he looking for it? Why is the federal government going to let this go another year, waiting for a ruling on one virus, before considering the bigger questions? It needs to be studied as an enormous health crisis, whatever the outcome of the work on XMRV. If it were anything other than a kangaroo court in session on a federal level, the work would be a priority, with our Center for Disease Control finally trying to do some controlling of our disease.

Once more unto the breach, dear friends

From Shakespeare’s King Henry V, Act III, Scene I

King Henry V:
Once more unto the breach, dear friends, once more;
Or close the wall up with our English dead.
In peace there’s nothing so becomes a man
As modest stillness and humility:
But when the blast of war blows in our ears,
Then imitate the action of the tiger;

Responding to the flurry of concern for my feelings and irritation from readers about negative comments left by angry Anonymous people, personally, I welcome the discussion, even if expressed without courtesy. There is much to be learned by considering the things the opposition is thinking. Their need for anonymity is amusing and speaks for itself. Don’t let them get you down. Keep your friends close and your enemies closer. It’s all grist for the mill.

As far as I know, the WPI, which is a non-profit, has no conflict of interest. The mission is clear and the people dedicated to the cause. The individuals at the WPI have waived their IP (intellectual property) rights in favor of the institute. Should VIP Dx ever make a profit, it all goes to the institute also. I challenge the other characters in this story to say the same.

As for everyone using their inside voices until the science runs it’s proper course, that’s just naive. That’s like saying that our newspaper reporters are only reporting the truth. People are people. They ask the questions they want answered, and they frame those questions in such a way that the answers will spin it the way they like. That’s why blinding is necessary for the scientific method.

I received an email this morning from Michael Snyderman that I am copying here with his permission:

There is a conflict interest here. A major player is a very wealthy woman by the name of Kristin Loomis who with Annette Whittemore founded the HHV-6 Foundation. Loomis is a great believer that Herpes 6 causes CFS and a lot of other disease. Both women had children with CFS.

Whittemore later set up the WPI with Daniel Peterson who gave the WPI its original CFS samples. Initially the WPI was going to further the cause of Herpes 6. They had a scientist, Konnie Knox and Peterson who were from the HHV-6 Foundation and continued to get money from the HHV-6 Foundation. Knox was fired from the WPI. About this time Lombardi et al. found XMRV (arguably a poor name). Peterson was disturbed because he was a believer in Herpes 6. He left soon after the Lombardi et al. report came out. The position of the HHV-6 Foundation is that Herpes 6 is the cause of CFS and not XMRV and indeed that XMRV does not exist. Peterson then gave Knox the samples from his patients that she reported as negative in the new Science article. She did not declare any conflict of interest over her funds from the HHV-6 Foundation or the fact that she had been fired from the WPI.

There is more. The other article in Science is by John Coffin from Tufts. He first reported that XMRV was a contaminant in 2010. His colleague at Tufts is Brigitte Huber and she was a coauthor on this paper.

On the Tufts website Huber is listed as getting a grant from the HHV-6 Foundation:
Huber, Brigitte HHV-6, EBV and Endogenous Retrovirus in Patients with CFS HHV-
6 Foundation 11/1/09 – 4/30/10

This grant was received right after the Lombardi et al. Science report in 2009. Coffin also did not declare any conflict of interest in his Science article although he had collaborated closely with Huber and was a colleague with her at Tufts.

The bottom line is that drug companies will not develop drugs that will help us if they believe that XMRV and related MLRVs do not exist. Lives could be saved with just one type of drug, a protease inhibitor – the one for HIV doesn’t work for XMRV and is a key category of drug for treatment of MLRV-related disorders as proteins such as env are not countered by raltegravir and the RT inhibitors.

Michael Snyderman, MD

Also from my morning mail:

My dr. and I have mostly contact by email because I am bedbound and cannot get to the office as much as I should. This morning I received an email from him … he made the remark that it is very interesting to him that WPI was asked to retreat their paper. Than he proceeded to tell me that he ran some test in his office and that WPI was mistaken to tell me I am XMRV positive because his test came out negative from the other…

How can that be? I feel like the ground has been pulled from under me. The hope I had to finding a solution for my 30 years of suffering is gone! How is it possible that a regular physician who specializes in ME/CFS and Fibromyalgia can do a test like this? I’m gobsmacked and feel myself tunneling in a deep depression. Everything I believed in he took away from me with just one sentence, I just can not stop crying and am so upset.

WPI tested me positive and I have been holding on to that, because I didn’t have much hope elsewhere. I don’t know what to do now. There isn’t any hope left for me. 

One of the many sad things happening is that the only testing available may not yet be sensitive enough. Or it may be sensitive enough, but some of us have different viruses that cause clinically indistinguishable disease from the XMRV positive patients. The current VIP Dx serology is aimed at xenotropic and polytropic MLV’s and is not positive in everyone one would expect if the test picks up every infected patient or if XMRV was the only cause of CFS. VIP Dx has a test. It comes out positive or negative. But like many tests, it’s not that black and white. Like all lab tests, it must be interpreted by a doctor within the context of a complete clinical picture, and an understanding of the state of the testing with respect to a particular disease. At this point in time, it’s that test or nothing. Nothing is a valid choice. It is a personal matter. But why the invective? Nobody has to use VIP Dx that doesn’t want to.

As I’ve said before. I could be wrong about anything. Like everyone, I interpret what comes my way from my own perspective. I am not a retrovirologist or even a scientist. I’m a doctor who is fluent with the literature. I also have the disease and my daughter has the disease. Why does my sharing my opinions and experiences make some people so angry, when the vast majority seem to benefit from hearing my thoughts? I challenge any of the people I’ve criticized to come forward as themselves and tell us what happened from your perspective. My mind can change. I’d love to think that everyone involved has integrity and is motivated by the right things, but human beings being what they are, that isn’t likely. As I keep saying, I am wedded to nothing but the truth. And time is of the essence.

This abstract by Prosperi et al may be of importance and I look forward to the paper. It seems confirmation in concept of what I suspect, that 22Rv1 isn’t the one in a trillion recombination event described in Paprotka et al. Interestingly the et al includes William Switzer who published a 0/0 study with Satterfield, as discussed in a previous blog here.
Murine leukemia viruses (MuLV) and Xenotropic MuLV-related viruses exhibit inter-tropic complex recombination patterns. Prosperi/Salemi

Given the evidence of inter-tropic recombination in MuLV, detection and classification of recombination in XMRV using different MuLV tropism prototypes should be interpreted with caution. Despite using a small dataset, a strong phylogenetic signal in the alignments and highly resolved phylogenies inferred both by full-length and sliding-window approaches, different recombination programs reported conflicting results. These results suggest that identification of parental strains of the potential recombinants is difficult and that recombination in the highly genetically related MuLV have been occurring for some time.

The hysteria in the media about the thousands of patients taking AIDS drugs is a joke. If that had happened, we’d have learned a lot, but they shut it down pretty effectively. I still don’t understand the inordinate fear of these particular drugs. All drugs have side effects. Every prescription has a potential cost/benefit ratio that has to be considered by the doctor and the patient at a particular moment. All options should be considered for a disease with no cure that produces such tremendous suffering. This was a prohibition from the beginning, such that taking antiretrovirals feels almost like a form of civil disobedience. As I said at the beginning, what if it works? Why does the scientific community not want to know, irrespective of the detection problems and their horror at skipping beyond their deductive reasoning process, clutched to their breasts like a religious totem? I know of about 50 patients taking arv’s, one to three drugs, for varying lengths of time. All have been sick for a long time. About a third feel they are improved. The rate of change is slow. I don’t know of anyone who has been seriously harmed, other than self-limited adverse reactions in the very early part of treatment. Some people who haven’t done well have gone off. As far as I know, everyone is getting proper monitoring. The interference in the physician patient relationship, happening on a grand scale with respect to restricting this particular treatment, is a travesty.

I have gone from sofa bound to very high functioning in 15 months, while taking antiretrovirals. It was not a good experiment however, nor have I ever claimed otherwise. I am more of an atypical MS picture than classic ME/CFS (like Ali), and I was already on an upswing since quitting lots of Lyme and symptom based treatment six months prior, but still very sick and essentially non-functional. I have also started other medication since, Deplin and Actos. I feel safe in saying that arv’s haven’t hurt me, including a year of AZT. In no way am I suggesting that anyone should do what I did, but everyone should have the right to consider it. The scariest potential risk is renal failure from tenofovir, a very rare event in the HIV world, seen primarily in people with preexisting renal problems. There are some long term consequences of AZT that need consideration. Proper monitoring is necessary.

I’ve returned to practice on the Big Island in Hawaii, because that’s where my active license is, and because I love it there. I trained in Honolulu, after medical school in the Bronx, and had my first job there. I’ve been licensed since 1980, always hoping to return. My family has recently grown to include my eldest daughter (who is adopted and very healthy) and my two small grandchildren. My son has a year of high school to go in Santa Fe. Moving everybody right now is out of the question. And I’m still traveling to Reno also. My husband and I are adapting to the fact that we will be spending a lot of time apart, after 23 years of marriage without separation. I am profoundly grateful to be able to contribute again. When I was practicing in Great Barrington, I was at 90% and it was all about the 10%. Now 90% feels like 110%. When pain goes away, it’s better than if you’d never experienced pain in your life. So round 3 for me. The comeback kid. Who better to treat it? I know the enemy intimately.

I wish it were Ali and not me that was better enough to reenter. I have tremendous survivor’s guilt writing this. My impression is that the second generation is sicker. Simple retroviruses can endogenize or maybe it’s just worst to get it before your immune system is developed. I have heard of very small children who sound like they have full-blown CFS (Beethoven’s 9th symphony?), 4 being the youngest. Not autistic. ME/CFS. 3rd generation.

The Fire Smolders

Here are more abstracts about XMRV from Belgium which strongly suggest that it is more than a contaminant:

Restricted infection of xenotropic murine leukemia virus-related virus in human lymphoid tissue
Marta Curriu, Jorge Carrillo, Marta Massanella, Elisabet Garcia, Bonaventura Clotet, Julian Blanco, Cecilia Cabrera

Heme oxygenase-1 activation inhibits XMRV pathogenesis and carcinogenesis in prostate cancer cells
Subhash Dhawan

A prototype RT-PCR assay for detection of XMRV in multiple human sample types
Ning Tang, Andrea Frank, Robert Kowal, Gregor Leckie, John Hackett Jr, Graham Simmons, Michael Busch and Klara Abravaya

Dr. De Meirleir’s presentation was listed in the Poster Section of the agenda and was called “Serological evidence of XMRV in CFS and blood donors in Belgium”. I don’t believe it’s available online, but certainly look forward to his report.

The take home message from this conference and the recent publications from the point of view of what does it all mean to a patient? If you have prostate cancer, you may be allowed to have it, but if you have CFS, you aren’t. But there are a few fighting for us, Mikovits, Russcetti, Lombardi, Hanson, Snyderman, Bell and co-authors.

If you look at the conflicting papers of which Graham Simmons is a co-author, assuming that you believe that Knox et al is worthy of consideration in light of the various potential conflicts of interest of its authors, the combined findings suggest that blood isn’t the best place to look for XMRV by PCR. The Tang et al paper referenced above is co-authored by more people who work for Abbott. The author’s of the paper looking for XMRV in blood donors (#3 last blog) also work for Abbott; they concluded the positives were due to cross-reactivity with HTLV sequences.

Simmons and Busch work for Blood Systems Research Institute, an institute dedicated to transfusion safety, primarily funded by NIH grants according to their website, apparently a for profit organization; they are also part of the Blood XMRV Scientific Research Working Group, whose abstract (#4 last blog) states they found enough going on with Phase II to keep going, even though it was inconclusive. More evidence that something’s going on, but we don’t know how to look for it yet. The clinical evidence and the first paper above, suggest that lymphoid tissue would be a good place to look. Gut is another likely reservoir, not too difficult to get tissue. The Tang paper looked at paraffin embedded tissue. There’s lots of that to go around, some small intestine of mine in paraffin at the hospital down the street.

#6, 7 and 8 in the last blog represent the kind of work we need to be seeing, to begin to figure out the nuts and bolts. Fascinating how they are going about producing a mouse that expresses XPR1 receptors in prostate tissue. Exploring receptor physiology, and tissue tropism.

Pointing out the connections between various authors and potential conflicts is not coming from some kind of inside information. Everything I’ve noted is readily available on the internet. I don’t claim to know exactly what’s at the bottom of it. Only that it doesn’t add up, the Knox paper being especially suspect, and the people involved suspect by association. The work isn’t going as well or as quickly as it should be, as we need it to, and there seem to be certain entities and individuals coming up with studies which seem designed to fail. There are an awful lot of people parroting negative studies without looking at the totality of the evidence. People attached to HHV-6 as The Cause come up a lot. People attached to it not being a retrovirus. Different individuals have different stakes I’m sure. There’s too much at stake not to bring out the worst in human nature.

If anybody feels the need to write in the comments that I am biased, don’t bother. I am biased. I believe that ME/CFS and related neuroimmune disorders are caused by retroviruses, of which XMRV is likely only one. The other organisms that turn up with regularity are opportunists and copathogens. There are patients that are both culture and serology positive. Contaminant and cross-reacting antibodies with HTLV? My working hypothesis is that we are infected with simple retroviruses that jumped from mice, probably naturally, but then assisted tremendously by the use of animal cells and gene manipulation in tissue culture and nude mice, for various purposes including vaccine production. That starting point for considering my illness has gotten me very far from where I was when I didn’t have that understanding.

At the bottom of this blog are links and excerpts from the NIH online project reporter that are of interest to us. Sandra Ruscetti giving us clues as to why VIP Dx is getting different serology results than those using tests derived from infected monkeys.

Also Ila Singh’s contention that it is present not only in prostate cancer tumors, but in 6% of controls. And she didn’t wonder why she couldn’t find it in anybody’s blood in her new study, including controls? And that didn’t bother her because? It makes me shake my head in disbelief every time I think of it. Scientists like Singh, Knox and Coffin telling people they don’t have the right to treatment based on such flimsy evidence and faulty logic? It’s disgusting.

Maribeth Eiden is an expert in GALV, the only other gammaretrovirus found in a primate. “In addition to being a horizontally transmitted infectious agent, xmrv is a threat to the human genome.”

A clinical trial of IV saline for POTS found its way into my inbox today: It’s fascinating that doctors in an academic setting taking care of a condition that used to be very rare, but now isn’t, haven’t noticed that it occurs mostly in ME/CFS patients, and seem unaware of XMRV as even a possibility. In any case this approach has had some success anecdotally for keeping ME/CFS patients on their feet, but isn’t practical for most, and like everything, it doesn’t help everyone, including me. It helps Ali a little, but, in general, not enough for the stick, and she doesn’t have enough veins for daily access, nor does she tolerate indwelling lines or FB’s of any kind.

The infusions so far seem very helpful to Ali: more energy, less reactive. I had an adverse reaction to the first one, generalized over-activation, sleep disruption, PVC’s, GI hypermotility, etc. The only thing in the infusion I haven’t had before was Leukovorin, and too much Deplin can cause a similar, though less severe, reaction. It took almost 5 days to resolve and was yet another reminder that sometimes it’s best to leave well enough alone. I did an infusion of glutathione alone about 10 days after the first one and didn’t notice anything. I haven’t been too excited about sticking myself again, since I’m doing amazingly well (knock on wood).

The mild hyperbaric treatments are wonderful for me. I feel great in the chamber, a little slowed after, then really good later on. Ali continues to be sensitive to odors and has stayed away from the chamber because of the new plastic smell. However, the fire burning in Arizona has made the air quality very poor here (in Santa Fe). The horizon is obscured by smoke and there is ash on the ground, though the fire is hundreds of miles away. It burns your eyes, nose and lungs. Yesterday she became short of breath and decided to use the concentrator with a well aired non-rebreather mask at 10L/min. After 20 minutes she felt much better. She repeated that treatment again last night before bed and slept much better than usual, something I notice after each treatment (I’m going in about 3 times/week). Since she tolerates the mask, she can wear it in the chamber and will be protected from any other smells inside the chamber itself. We are both grateful for something so safe that helps in such an immediate way.

Ongoing NIH projects:

Sandra Ruscetti
In collaboration with the laboratories of Judy Mikovits and Frank Ruscetti, we were able to use antibodies developed against the envelope protein of SFFV to detect infectious xmrv in the blood cells and plasma of patients suffering from the neuroimmune disease chronic fatigue syndrome (CFS). We were further able to develop a seroconversion assay using cells expressing the SFFV envelope protein to detect antibodies against the virus in the plasma of CFS patients. We now plan to apply our knowledge of the pathogenesis of mouse retroviruses that cause cancer and neurological disease in rodents to study the molecular basis for similar diseases associated with xmrv. We are in the process of developing rodent models for determining the biological effects of xmrv in vivo, which if successful will provide a small animal model for preclinical testing of potential anti-xmrv drugs. In addition, we are testing both in vitro and in vivo the biological effects of the envelope protein of xmrv, which like its related SFFV counterpart may be responsible for the pathogenicity of xmrv.

Ila Singh
Narrative: xmrv is a new retrovirus that was recently identified from human prostate cancers. This study will attempt to understand the replication of this virus in vitro and its association with cancer. We will explore mechanisms of oncogenesis in cells, in tumors, as well as in animal models, and carry out epidemiological studies to estimate prevalence of viral infection in the general population.

Maribeth Eiden
Our lab is recognized for our research on a similar gammaretrovirus isolated from nonhuman primates, gibbon ape leukemia virus (GALV). GALV is the only gammaretrovirus other than xmrv found in primates. In collaboration with Frank Ruscetti at the NCI, Bill Switzer at the CDC and Suzan Winfield and Jessica Siegal-Willcot at the National Zoo, we are investigating the source animal for xmrv, and screening gibbon apes in US zoos for the presence of GALV and xmrv. We have obtained samples from the CDC and the Biological Research Steering Committee that provide us with materials permitting us to determine that many gibbon apes at various zoos have been infected with an xmrv-like virus. We have determined the cell tropism of xmrv using an engineered biologically active xmrv virus with a GFP reporter gene and are identifying cellular factors that restrict xmrv infection of receptor bearing cells. These factors that can restrict xmrv infection will be used as a means of developing xmrv antiviral drugs. In addition to being a horizontally transmitted infectious agent, xmrv is a threat to the human genome. We are in the process of isolating rat germ line cells and exposing these cells to engineered biologically active xmrv virus with a GFP reporter. Sperm obtained from these cells are being assessed. Positive results of sperm expressing GFP indicate that xmrv can be transmitted from infected individuals horizontally (i.e., to offspring as a mendelian trait) as well as vertically through the more traditionally route of viral infection. We used cysteine scanning mutagenesis (SCAM) methods to assess the topology of the GALV receptor and intend to identify extracellular domains of the xmrv receptor using similar methods. These studies will lead to the identification of the xmrv-binding domain. Finally the spread of most retroviruses is mediated not by direct virus infection but by cell-cell transmission from an infected cell to an uninfected cell. We have developed a model system to assess blocks to cell-cell virus transmission using spinning-disc confocal microscopy to visualized individual budding of fluorescently labeled virus particles into adjacent cells in three dimensional space over time.

Frank Maldarelli
We have established useful collaborations with Drs. W. Marston Linehan and Peter Pinto (Urologic Oncology Branch, CCR) to study samples from patients with prostate cancer, and with Drs. Frank Ruscetti and Kathryn Jones (Laboratory of Experimental Immunology, CCR) and Dr. Judy Mikovits (Whittemore Peterson Institute) to study patients with severe CFS. As immune deficiency may contribute to infection by xmrv, we have also established collaborations with NIAID to obtain samples from study individuals with immune deficiency, including HIV-infected patients and patients with both HIV infection and prostate cancer. In addition, we are collaborating with Dr. Vinay Pathak (HIV Drug Resistance Program, CCR) in a study of xmrv pathogenesis and prostate cancer as part of a Bench to Bedside Award to Dr. Pathak. Reports of xmrv infection in individuals with chronic fatigue and in otherwise healthy individuals raised concerns regarding new health risks. Within a year of these reports, we have optimized a series of detection and analytical assays with excellent performance characteristics. In the next year, we will apply these approaches to shed new light on the potential role of mouse-related viruses in human disease.

Arthur Horowitz
In a related and collaborative project, we have joined Dr, Frank Ruscetti in his studies of the link between prostate cancer and xmrv, a recently-identified retrovirus associated with prostate cancer. Together, we are testing the hypothesis that inflammatory cells serve as a viral reservoir or infection route. We are characterizing the susceptibility of prostate-infiltrating myeloid cells (macrophages and dendritic cells) to xmrv infection. A long-term goal is to identify murine models to study the link between xmrv pathogenesis and prostate carcinogenesis.

Susan Swedo
D. Vargas et al (Johns Hopkins) demonstrated that individuals with autism and a history of neurodevelopmental regression had evidence of chronic brain neuroinflammation, as exemplified by activation of microglia and astroglia and the abnormal production of inflammatory cytokine and growth factors assayed in both tissue samples and CSF. The authors remarked that chronic microglia activation appeared to be responsible for a sustained neuroinflammatory response that facilitated the production of a number of neurotoxic mediators. Alternatively, neuroglial activation could occur in response to a secondary neurotoxic factor(s) and thus represent the result, rather than the cause, of the injury. Neuroglial activation requires the nuclear translocation of the pro-inflammatory transcription factor NF-kappaB. A small pilot study of minocycline, an antibiotic with known effects on NF-kappaB was undertaken in an effort to determine if the drug might have an effect on autistic behaviors or change patterns of distribution for the CSF or serum cytokines or chemokines. At the doses used in the pilot investigation, no clinically meaningful improvements were seen in behavior nor in the pattern of distribution of the CSF or serum cytokines or chemokines. Thus, no further investigations are planned for minocycline, but the search for novel therapeutic agents continues through the phenotyping study, where longitudinal assessments provide the opportunity to identify biomarkers of neuroinflammation in serial CSF and serum samples and to correlate the results of the assays with clinical symptomatology.

Christine Kozak
We are also interested in determining the extent to which virus resistance is mediated by polymorphisms of the cell surface receptor. We seek to analyze the XPR1 receptor for the xenotropic/polytropic gammaretroviruses and for xmrv, a xenotropic virus-like virus isolated from humans with prostate cancer or chronic fatigue syndrome.

Some interesting abstracts from the conference in Belgium about HTLV:

HERV’s and MS

Stem cells for HTLV

Raltegravir inhibitis HTLV


Arsenic trioxyde for ATLL

Ascorbic acid and HTLV

Risk of vertical transmission of HTLV correlates with maternal proviral load.

γδ T cell immunotherapy for HTLV ???

Estradiol and HTLV

XMRV-related abstracts from 15th International Conference on Human Retroviruses

For easier reading and sharing XMRV Global Action has compiled the XMRV related abstracts from the 15th International Conference on Human Retroviruses: HTLV and Related Viruses, Leuven and Gembloux, Belgium. 5-8 June 2011

1. XMRV replicates preferentially in mucosal sites in vivo: Relevance to XMRV transmission?

Francois Villinger1,2*, Jaydip Das Gupta3, Nattawat Onlamoon4, Ross Molinaro1,2, Suganthi Suppiah1,2, Prachi Sharma5, Kenneth Rogers5, Christina Gaughan3, Eric Klein3, Xiaoxing Qiu6, Gerald Schochetman6, John Hackett Jr6, Robert H Silverman3

“In fact, a single atraumatic mucosal exposure with a high dose of XMRV virus into the urethra resulted in infection of 1 out of 4 macaques providing proof of concept that such transmission is possible. However, additional work is needed to fully investigate potential modes of XMRV infection.”

2. Development of XMRV producing B Cell lines from lymphomas from patients with Chronic Fatigue Syndrome

Francis Ruscetti1*, Vincent C Lombardi2, Michael Snyderman3, Dan Bertolette4, Kathryn S Jones1, Judy A Mikovits1

“Therefore XMRV infection may accelerate the development of B cell malignancies by either indirect chronic stimulation of the immune system and/or by direct infection of the B-cell lineage . Since viral load in peripheral blood is low, these data suggest that B cells in tissues such as spleen and lymph nodes could be an in vivo reservoir for XMRV.”

3. Prevalence of XMRV in blood donors, HTLV and HIV cohorts

Xiaoxing Qiu1*, Priscilla Swanson1, Ning Tang2, Gregor W Leckie2, Sushil Devare1, Gerald Schochetman1, John Hackett Jr1

“XMRV seroprevalence ranged from 0 – 0.6% in US blood donors, HIV-1 infected and HTLV uninfected subjects. Notably, 4.1% of Japanese HTLV-I infected individuals were p15E reactive. Inspection of sequence homology between HTLV and XMRV revealed a high level of conservation within the immunodominant region of HTLV gp21 suggesting increased seroreactivity is due to cross-reactive antibodies.”

4. Multi-laboratory evaluations of XMRV nucleic acid detection assays

Graham Simmons1,2*, John M Coffin3,4, Indira K Hewlett5, Shyh-Ching Lo6, Judy A Mikovits7,8, William M Switzer9, Jeffrey M Linnen10, Francis Ruscetti11, Simone A Glynn12, Michael P Busch1,2

“The Blood XMRV Scientific Research Working Group was formed to facilitate collaborative studies into the impact of XMRV in blood donors. Studies will evaluate XMRV detection assays in terms of sensitivity, specificity and reproducibility; assess performance on specimens represented in existing blood donor repositories, and determine the prevalence of XMRV in donors.” Phase III results expected soon. Phase IV will test a blinded panel of 300 blood donor samples.

5. Immune correlates of XMRV infection

Vincent Lombardi1, Deborah Goetz2, Max Pfost1, Cassandra Puccinelli1, Judy Mikovits1*

“XMRV infection results in dysregulation of the immune response, either directly by infection of specific leukocyte subsets or indirectly through cytokine modulation.”

6. The effects of XMRV gene expression on the mouse prostate

Daniel Rauch, Sirosh Bokhari, John Harding, Lee Ratner*

“Breeding PRO-XMRV mice with PRO-XPR1 mice will allow us to test whether XMRV integration or gene expression can cause more advanced prostate pathology in vivo. With these XMRV mouse models we seek to address the question that remains unanswered to date as to whether XMRV is capable of causing prostate dysplasia or cancer in vivo.”

7. XMRV: usage of receptors and potential co-receptors

Mohan K H G Setty*, Krishnakumar Devadas, Ragupathy Viswanath, Veeraswamy Ravichandran, Shixing Tang, Owen Wood, Durga S Gaddam, Sherwin Lee, Indira K Hewlett

“XMRV replication was observed in GHOST cells that express CD4, and each of the chemokine receptors ranging from CCR1- CCR8 and Bob suggesting that infectivity in hematopoietic cells could be mediated by use of these receptors. Infection of Lung epithelial cell A549 lacking XPR1 expression clearly indicates usage of other receptors by XMRV for entry into susceptible cells.”

8. Cell line tropism and replication of XMRV

Krishnakumar Devadas, Mohan K H G Setty, Ragupathy Viswanath, Durga S Gaddam, Owen Wood, Shixing Tang, Jiangqin Zhao, Xue Wang, Veeraswamy Ravichandran, Sherwin Lee, Indira K Hewlett*

“Replication of XMRV could be observed in cervical and lung epithelial cells, T-cell lines Jurkat and H9, B-cell line HL60, U937 cells and in primary PBMC and monocyte-derived macrophages. The levels of XMRV transcripts were lower in primary monocytes compared to T-cell lines suggesting less efficient replication in these cells.”

9. Structure of the xenotropic murine leukaemia virus-related virus matrix protein

Michal Doležal1,2, Iva Pichová1, Tomáš Ruml2, Richard Hrabal3, Michaela Rumlová1*

“Although the protein sequence of the XMRV-MA is very similar to that of the murine leukaemia virus matrix protein (MLV-MA), it varies in several amino acid residues. We compared the structures of the XMRV-MA and MLV-MA and found that those changes are localized in a few domains, mostly on the surface of the protein.”

10. Serologic and PCR testing of persons with chronic fatigue syndrome in the United States shows no association with xenotropic or polytropic murine leukemia virus related virus.

William M Switzer1*, Hongwei Jia1, HaoQiang Zheng1, Shaohua Tang1, Rebecca A Garcia2, Brent C Satterfield2

“Our findings are consistent with previous negative reports and do not support an association of XMRV or MuLV in the majority of CFS cases across the US.”

11. Detection of MLV-like gag sequences in blood samples from a New York state CFS cohort

Maureen R Hanson1 , Li L Lee1, Lin Lin1, David E Bell2, David Ruppert3 and David S Bell4

“gag sequences could be amplified from genomic DNA from LNCaP cells of some subjects after 4 or 6 subcultures following incubation with certain subjects’ plasma, indicating the presence of infectious virus in blood. All gag sequences detected in this cohort were more similar to the MLV-like sequences reported by Lo et al. (2010) than to the XMRV sequences reported by Lombardi et al. (2009). Detection of gag sequences in whole blood genomic DNAs that were negative for mouse IAP and mitochondrial DNA provides strong evidence for infection of humans with MLV-like viruses.”

12. Murine leukemia viruses (MuLV) and Xenotropic MuLV-related viruses exhibit inter-tropic complex recombination patterns

Mattia CF Prosperi , William M Switzer, Walid Heneine and Marco Salemi

“Given the evidence of inter-tropic recombination in MuLV, detection and classification of recombination in XMRV using different MuLV tropism prototypes should be interpreted with caution. Despite using a small dataset, a strong phylogenetic signal in the alignments and highly resolved phylogenies inferred both by full-length and sliding-window approaches, different recombination programs reported conflicting results. These results suggest that identification of parental strains of the potential recombinants is difficult and that recombination in the highly genetically related MuLV have been occurring for some time.”

13. In vitro assembly of xenotropic murine leukemia virus-related virus CA-NC protein

Romana Hadravová, Jitka ¿tokrová, Michal Dole¿al, Iva Pichová, Tomá¿ Ruml and Michaela Rumlová

“We found that purified XMRV full-length CANC, starting with the conserved proline residue at the N-terminus of CA, was not able to assemble into particles. However, a modification of the N-terminus of CANC (modCANC) enabled formation of spherical particles. Moreover, the negative staining of the in vitro assembled particles of XMRV modCANC revealed different organization of protein layers in comparison to CA-NC of M-PMV.”

14. Human infection or lab artifact: will the real XMRV please stand up?

Robert H Silverman

“Xenotropic murine leukemia virus-related virus (XMRV) was first identified in 2005 in a study of human prostate cancer patients with genetic variants of the antiviral enzyme, RNase L. Subsequent investigations in North America, Europe and Asia have either observed or failed to detect XMRV in patients [prostate cancer, chronic fatigue syndrome-myalgic encephalomyelitis (CFS-ME), immunosuppressed with respiratory tract infections] or normal, healthy control individuals. Among the confounding factors are the potential for lab contamination with similar or identical viruses or viral sequences originating in mice. In some studies, relatively contamination-resistant methods (e.g. IHC, FISH, and antibody detection) suggest that either XMRV or a similar type of virus is present in some patients. Evidence for and against genuine infections of humans with this intriguing virus (and/or related viruses) will be discussed.”

15. XMRV infection in human diseases

Otto Erlwein email, Mark J Robinson, Steve Kaye, Myra O McClure, Marjorie M Walker, Anup Patel, Wun-Jae Kim, Mongkol Uiprasertkul, Ganesh Gopalakrishnan, Takahiro Kimura and Kikkeri Naresh

“The novel gammaretrovirus xenotropic murine leukemia virus-related virus (XMRV) was identified in human prostate cancer tissue in 2006, confirmed in 2009 and later linked to a second human condition chronic fatigue syndrome, CFS. These investigations, all carried out in the US, have not been reproduced in Europe or in China.

We found no evidence for XMRV infection in CFS. Moreover, we failed to find evidence of XMRV infection in UK prostate cancer patients and in prostate cancer tissue taken from patients in India, Korea, Thailand and Japan, or in cancers other than that of the prostate.

Our UK CFS patients were consistently XMRV-free. We did, however, generate false-positive results from prostate cancer patient tissue, despite the fact that the no-template controls in our PCR were consistently negative and the PCR for murine mitochondrial DNA was often also negative.

Sources of this contamination will be discussed in our presentation.”

Who Are Our Friends?

Here are a couple of articles sent by friends this morning… link and link. I read them with my morning coffee and both made me feel sick for different reasons. I hated to dignify the first one with a link, because the site is so appallingly illiterate, but this is what the newly diagnosed will find when they go to the net to learn about their illness, since it looks like they aren’t going to get to have a real disease for a little while longer. But not to worry, Kim McCleary says doctors know it when they see it, “like Beethoven’s first symphony”. Oh you have CFS? Too bad. It’s caused by lots of things. Like a “stressful state”. XMRV was all a mistake. Take L-carnitine.

The second article blows my mind, because McCleary didn’t manage to say one thing I can relate to as a patient, other than yes, my daughter and I both have it. The swift decline and no resolution she describes doesn’t even come close to describing the course for many, if not most patients, since recovery to 80 or 90% within a year or two of the first episode is a common history. There are a large number of patients who experienced gradual onset, but wound up in the same place as the ones who remember the moment of onset, and one would expect her to be aware of this. Her description of my disease as “not sexy” is offensive. This woman definitely doesn’t speak for me. She’s the president and CEO of the CAA, the national organization for the disease we have. How did that come to pass? As I’ve said before, I’m a newbie. I only figured it out about CFS as an inseparable entity from treatment resistant Lyme when I read the Science paper. Before that I knew the extant drivel in both the conventional and alternative worlds that espoused the “it isn’t one thing” theory, but I didn’t identify, since the drivel in the Lyme world fit us better.

Now that I’m starting to wonder about the characters and history, which never really interested me before, and trying to consider the most likely motivations of the various players, it’s shaping up to have the makings of a rather twisted tale. History driven by the personal needs of a few people, millions of lives at stake. It may rise to the level of allegory. Our knights in shining armour? There’s the good old CAA. I’ve been sick on their watch for 16 years. Suzanne Vernon was spawned by our captors at the CDC, then went to work with the CAA. Take a look at the Banbury Report, about a meeting that took place a few weeks before the Science paper was published, in which Dr. Vernon states that she thinks one of the things she knows for sure is that it isn’t a retrovirus. Then there’s the HHV-6 Foundation. Dan Peterson is on the board of directors. And let’s see, Konstance Knox is an expert in HHV-6. In fact, Knox/Levy is the first paper she’s ever published that wasn’t about HHV-6. Her lab is heavily invested in an HHV-6 assay. I wonder what HHV-6 Foundation spends it’s research dollars on? And as Mindy Kitei asked here, what’s Dr. Levy’s stake in all this? Ah, what a tangled web… Life is stranger than fiction. Definitely a story fit for an Osler’s Web sequel.

Lots of people seem very committed to it not being a retrovirus. Why would that be? I realize that it can’t possibly be as black and white as it appears. They can’t all be psychopaths. They must at least be lying to themselves, like some of the scientists who said that simple endogenous animal retroviruses couldn’t hurt humans, and don’t even want to learn the truth now, preferring to be dead before the puzzle is solved.

Here’s a letter to Science from patient advocate Chris Douglas, that says it very well. link

Meanwhile, unrepresented patients are starting to organize. This is very important. We need to nurture the sparks of this fire. Don’t let it go out. Thank you, from all of us, to the participants. YouTube and Write up

The WPI is a translational medical institute, a discussion in progress, not expecting all the answers to be in before applying the pieces we do have. The mission of the institute is to cure CFS, but it is a small organization and the virus has turned into such an unexpected fight that defending the prior work is a huge task. Each new salvo triggers a wave of self-examination, trying yet again to find the flaw, but despite the multitude of negative studies, nobody has yet explained the most important thing. Only some of the patients are positive. Not none and not all. Far from requesting a retraction, Science, if truly objective, should be demanding answers with respect to the gaping holes in the arguments of the authors of the negative papers. A number of people have written that they hope the work at the WPI will not be limited to XMRV. The most recent Lombardi et al paper, Xenotropic Murine Leukemia Virus-related Virus-associated Chronic Fatigue Syndrome Reveals a Distinct Inflammatory Signature. Lombardi/Mikovits, helps to define the disease, whatever the cause and adding the clinical practice will further broaden the focus of the research.

What if it was all a mistake for some technical reason (though it’s hard to see how that could be the case). But say it was all a big accident. Then XMRV may still be a signpost. Paprotka et al found a cell line started in the early 90’s that produces it. Although the online supplemental information doesn’t tell us how they derived their number for probability of the event, even assuming they are correct, that it’s a very unlikely event, it happened once, and think how many chances there have been for similar events. This type of random recombination event may not even be necessary for HGRV infection, as already replication competent viruses may be involved, present in mice not susceptible to infection, but xenotropic, capable of infecting the cells of other animals, including human. Am I just speculating? Well, so are they. But if I’m wrong, some time and money is lost, in the attempt to save millions of people. If they’re wrong?

Breaking good news, for a change, from the International Conference on Human Retroviruses, in session now in Belgium, evidence that some labs can find XMRV in human tissue:

A Prototype RT-PCR Assay For The Detection of XMRV In Multiple Human Sample Types. Tang/Abravaya found positives in formalin fixed paraffin embedded prostate cancer specimens and urine pellets, using 22Rv1 for their spiked control, rather than a VP62 clone. Here’s a twist- Graham Simmons appears on both this paper and Knox et al. He didn’t tell the team he was on that couldn’t find it about the team he was on that could? How strange. But the important thing is this group was able to distinguish negatives from positive controls, even though the positive control was not a human isolate, and they found it in human tissue (not blood).

And these papers sound promising, but no abstracts:

XMRV replicates preferentially in mucosal sites in vivo: Relevance to XMRV transmission? Villinger/Silverman  

Detection of MLV-like gag sequences in blood samples from a New York state CFS cohort. Hansen/Bell

We also heard this from the Invest In ME conference held in London last month:

The final presentation was by Wilfried Bieger (Munich, Germany). He mentioned their earlier studies to detect XMRV, which had been negative.  His team had then collaborated with Judy Mikovits and set up a highly sensitive, specific and uncontaminated protocol for virus detection, sequencing of viral DNA and antibody testing with western blot. Viral DNA and RNA were not detected in fresh blood, but after cultivation of PBMCs for 6 weeks under stimulation and using partly co-culture with virus permissive LnCap cells, culture cells turned positive in some patients. Presence of XMRV was confirmed by sequencing XMRV specific DNA. There have been approximately 40% positives so far.

It’s more than smoke. It will burst into fire, despite the best efforts of some to smother it. We need to fan the flames. Don’t let them forget us again. There are future generations at stake that can’t be allowed to go through what we have.


When I started this blog, I was a sick patient, excited about a process of discovery that was unfolding for me. I had a lot of anger and dismay at the information vacuum surrounding the situation. My motivation was to inform and do whatever I could to move the process along. Since then, I’ve recovered a large degree of function and have returned to private practice in Hawaii. I also work for the WPI, as an independent contractor, in very specific capacities, still intending to help open the clinic in Reno. At this point, of the many perspectives I share in this epic, I identify most with being the mother of a patient, and of a healthy 16 year old son, who has some of the same little things my husband, daughter and I do. I have suspected that he has what we have for eight years. He had the most positive tick borne disease tests of anyone in our family. Dr. Charles Ray Jones, who I believe to be a very fine doctor, decided wisely not to treat him for Lyme. He has done very well, can push the envelope. But under the circumstances, I worry, as we all do for our unaffected children. So my motivation for writing remains essentially unchanged. I only want the truth, so that Ali can have a life and my son not lose his. It’s not because of any affiliation, or being invested in anything other than getting to the bottom of it, so that we can all have some meaningful treatment, finally. I want the medicine to move forward, and it shouldn’t have to wait until the scientists dot all the i’s and cross the last t.

When I learned of the request from Science for retraction of Lombardi et al and the EEC, I cried off and on for a day. The thought that brought on tears was “the work is going to stop.” Nobody will put their grad students on it, because it will ruin their careers. No one will spend the money because Knox et al are trying to put the nail in the coffin. This can’t be allowed to happen. I’m not the best person to pick the paper apart technically, though it has some obvious flaws that the scientists will address, I’m sure. But the logical flaw is more basic than any of the details. Unless someone has a test that can identify a sick person, a negative study, using different methods from the original study, doesn’t contribute anything new. Absence of proof is not proof of absence.

The only thing new in the Knox study was Dr. Peterson’s participation, the authors trying to suggest some sort of uniformity of patient selection with the original study, as if patients are hard to come by. Since they weren’t the patients from the original study, the fact that they came from his practice contributes nothing. That only means that they came from a doctor with a conflict of interest. All the paper shows, along with some inane speculation, is that Knox’s lab couldn’t reproduce VIP Dx’s results. I am guessing that Abbott developed the serology test which didn’t work that was used in the study, but the discussion of their negative serology data is too superficial to consider seriously. Serology, in the end will be the clinical key. Patients don’t make antibodies to contaminated specimens and PCR is clearly too finicky. Serology has been left out of most of the discussion to date. We know so far that tests derived from monkeys infected with a VP62 clone don’t work on humans. We don’t think the currently available test from VIP Dx is sensitive enough. We believe that positives are true positives, but there are false negatives, including people with positive cultures. The right test should be a goldmine for someone. It’s not that it’s a problem for us if someone makes money on our disease, it’s that sometimes the quest to own the patent supercedes the good of the patients. If greed is the motivator, so be it, as long as it leads to progress. In this case, people went to a lot of trouble to slow progress.

I accept that there will be some people who don’t like me for speaking out. Now that I’m not powerless anymore, I’m supposed to be more circumspect. Use my inside voice. It’s worth it for me to take the flak, for the many patients who say that sharing my thoughts helps them to think about their illness and options. So let’s see what I’ve said that’s so inflammatory. Konstance Knox once had a relationship with the WPI, that didn’t end well. Easily verifiable. Dr. Peterson also had a relationship with the WPI that didn’t end well. I am not discounting all of the work that he did for ME/CFS in the past, but that was then, this is now. If he was concerned that there was a problem with the testing, why didn’t he use the resources at his disposal to work on it with the scientists at his own institute? Instead he gave specimens to a scientist with a conflict of interest. All of this must have been a confusing nightmare for the patients involved. What did he accomplish? Res ipsa loquitor.

As I’ve said, I don’t know Dr. Peterson personally, but I am working with the same people he did and I know what motivates them. The Whittemores have put it all on the line. They are dedicated to getting to the bottom of the illness, whatever the answer, for the most personal of reasons. Dr. Mikovits is an honest person who cares deeply for the patients. I am proud to call her my friend and it breaks my heart that she has to live through this. She in no way deserves to have her integrity questioned. She has no financial stake. She is staying to weather the storm for us, the patients. It started out for her as science, but getting to know the patients has really affected her on a personal level. Nobody wants to get to the bottom of it more than she does. She should be getting assistance, not a bunch of people trying to discredit her.

I don’t believe that my writing should alienate anyone who truly wants to help. I hope that at the very least, it makes the protagonists consider their own motivation. I haven’t criticized anyone whose heart is with us. I am being cast by some as an angry conspiracy theorist. In my opinion, human frailty is almost always a better explanation than nefarious schemes. Greed, ego, shame, desire for revenge are generally enough to explain what moved a particular situation. In this case, there was a joint effort involving disgruntled former contributors, people working for a company that makes it’s money on lab tests, and a doctor in an academic setting (about whose motivation I know nothing). It doesn’t really qualify as a conspiracy, but it smells. And Science’s cooperation with it smells. Harmful to patients everywhere if it stops research. As for anger, I’m mostly not angry anymore. When I’m not agitated about the lack of scientific progress, I’m a pretty happy person. However, the events of the weekend, really shook me up, made me very mad, and sad. And scared, that the work could stop.

The idea that 22Rv1 was created in a lab after CFS already existed, therefore proving that XMRV is a lab contaminant and nothing more, is another logical fallacy. It’s pretty clear at this point, that XMRV isn’t the whole story. Similar events to the one described in Paprotka et al, with other proviruses could have happened before that, including naturally, even before modern tissue culture or xenografting techniques. Neuromyasthenia is hardly a new phenomenon, first described a few hundred years ago. What is new, is how common it has become. I can’t imagine why there isn’t more concern that the cell line produces a fully replicative exogenous retrovirus capable of infecting human cells. But we can all relax now because Konstance Knox says that human serum restricts it in vitro, in some unspecified way and any antibodies that might be found are only some kind of “autoantibodies”. Well, that’s a relief for the human race.

The over the top concern about the use of antiretrovirals seems the height of paternalism, especially when you consider that HIV drugs are used to prevent transmission to healthy high risk people and unborn babies. Here’s an exciting article, suggesting another possible long-term benefit of antiretrovirals for us: Mouse viruses and human disease. Stewart/Cameron

I’ve been asked now and again why I don’t wait until I know the outcome of the therapies we try before reporting. Whether a particular therapy does or doesn’t help us is almost irrelevant, as many things help a few people and not lots of others. The important thing is to share the ideas in order to further the discussion. We are beginning to have enough information to think ahead. Physicians are supposed to connect the dots to help their patients. In this case the dots turn into a pretty frightening picture. It is unfortunate that writing about the implications of human gamma retroviral infection makes one sound like Chicken Little. But the sky really is falling.

A Sad Day For Patients

The apparently concerted effort to deny patients an answer or treatment for our disease continues. Science Magazine published two negative papers today, along with an Editoral Expression of Concern, or EEC. Dr. Mikovits was informed on Friday, before Memorial Day weekend, though the second of the two papers was accepted for publication on May 15. The co-authors of Lombardi et al have unanimously refused to retract.

Here is Dr. Mikovits’ response to the EEC, link, Annette Whittemore’s response, link, and the response of the WPI’s Clinical Advisory Board, link, sent to Science over the weekend.

The timing of the EEC seems “premature”, to put it mildly, with Dr. Lipkin’s and Dr. Maldarelli’s findings still pending. There is nothing new in either paper that should have precipitated this.

I receive many questions about why Dr. Peterson is no longer working with the WPI, which I have generally tried not to answer, because I wasn’t there. But, as of today, I think it safe to say that not only is he not working with us, the people he is collaborating with seem intent on destroying the institute that bears his name. I am in the middle of it, and it is unfathomable to me. I have never met Dr. Peterson, but here is my best guess, as the one following in the wake of this attempt to destroy the institute. It has to be all about intellectual property, and revenge. Nothing else makes sense. Why would he provide already tested specimens to Konstance Knox, who has a vendetta against the WPI? Knox worked as a consultant for VIP Dx and left under “difficult circumstances” related to her business practices. Science should have been aware of this history and made a serious inquiry of it. They were alerted to it, but proceeded to publish this morning anyway.

Taking the sordid details out of it, the Knox paper is yet another entirely negative paper where they proved they couldn’t find it in anyone. Again, there was no real attempt to replicate Lombardi et al, only the innuendo that it was somehow disproved by this paper, by virtue of it being Peterson who provided the specimens. How could Science, a premier journal, publish such shoddy work, sloppier than the Singh paper, though with the same logical fallacy? It can’t be both a contaminant and not there at the same time. Which is it? The totality of the evidence says neither. Why is no one asking the real question? How is it that VIP Dx finds approximately 4 out of 10 patients positive, not zero and not 100%? How do you explain contaminating only some of the specimens in the same run?

And why do all of these scientists feel compelled to practice medicine without licenses? When Konstance Knox gets sick from the infectious contaminants in her lab, shall the doctors remind her that she said to the press that patients shouldn’t have the right to try antiretroviral drugs for the viruses that she is too incompetent to find (or wasn’t really trying to find in the first place)?

Why would scientists who know better reach obviously incorrect conclusions about their own work? Why would anyone want to make XMRV go away, when there’s so much smoke? The money involved is enormous. Did anyone notice that a few of the co-authors on the Knox paper work for Abbott Diagnostics? Do you think Abbott would like to own The Test?

It may be that the sequence diversity from patient to patient is too large to detect by PCR for a particular strain of HGRV (human gamma retrovirus). Replication competence probably involves recombination events. It may be that it isn’t even a few viruses, but many. PCR only finds what it’s looking for. It is going to require rapid deep sequencing. The science is up to that technology, but it is still too expensive to use on the likes of us. They’ve sequenced the entire mitochondrial genome of a Neanderthal. When will they take a look at ours?

So if they make it go away, they can rediscover it later, with enough sequence variation to call it something else. And while the vultures fight over the carrion, new babies are born with it, teenagers are collapsing with an incurable illness and old people are dying prematurely, after decades of relentless suffering without help. Today is 600 days since Lombardi et al was published. It is shameful. Please express your outrage to Science.