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Plague: An Interview With Judy Mikovits

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By Erica Verrillo

I had the rare pleasure of interviewing Dr. Judy Mikovits at the IACFS/ME conference in San Francisco last March. Dr. Mikovits is best known for her involvement with XMRV research.

Dr. Mikovits is a cellular and molecular biologist with over 30 years of scientific expertise. She has directed programs on HIV, cancer, epigenetics, and neuroimmune disease, with a focus on development of novel drug and diagnostic technologies. Dr. Mikovits holds a PhD in Biochemistry and Molecular Biology from George Washington University. Her dissertation was on HIV latency and mechanisms of immune activation in monocytes. Dr. Mikovits was a Postdoctoral Scholar in Molecular Virology at the Laboratory of Genomic Diversity, National Cancer Institute under Dr. David Derse. Over the past 26 years, she has published 51 scientific papers in peer-reviewed journals.

The riveting story of XMRV, and the subsequent scandal which left her career in ruins, is told in Dr. Mikovits’ forthcoming book, Plague: One Scientist’s Intrepid Search for the Truth about Human Retroviruses and Chronic Fatigue Syndrome, Autism, and Other Diseases. It was a journey that took Dr. Mikovits through the process of scientific research, the thrill of discovery, and ultimately to the high-level corruption which eventually led to her arrest, and the conviction and sentencing to federal prison of her employer, Harvey Whittemore, for federal crimes that, in the words of  Nevada’s highest court, reflected badly on his “honesty, trustworthiness or fitness as a lawyer.”

In spite of the notoriety surrounding XMRV, Dr. Mikovits remains committed to helping people who suffer from ME/CFS and is determined to discover its cause. “To me,” she says, “it’s the patients who matter.”

Dr. Mikovits continues to work on neuroimmune disease and cancer at MAR consulting, an endeavor she shares with Dr. Francis W. Ruscetti.

Plague, “the best scientist-in-jail story since Galileo,” will be released on July 1. You can pre-order it now from Amazon at a guaranteed 30% discount. (Note: This discount will not be available after the release date.) Order here.

For more information, visit Plague the Book.

How did you get involved in ME/CFS research?

That’s a good story. In late November of 2005, I met Kristin Loomis, the head of the HHV6 Foundation. Kristin visited my lab and got excited. Her daughter, who was very sick, had been diagnosed with CFS, but Kristin thought she had HHV6. What I saw in Kristin Loomis’ daughter was an astounding loss of intelligence and cognitive function, which was striking in such a young person.

At the time, my company, EpiGenX Pharmaceuticals, was being sold, and I didn’t have much to do. So, I agreed to work for Kristin as a consultant on HHV6, to put the research together. In 2006, Kristin sent me to the HHV6 meeting in Barcelona where I met Dan Peterson. He gave a very compelling talk. His data showed clonal rearrangement of gamma delta T cells; you don’t get clonalities like that unless you’ve got a frank cancer. He said, “I don’t see where all this cancer is coming from. I don’t know what it means. If anybody can help me, see me after the talk.” I took one look at the slide, and I could not get to him fast enough. He invited me to Reno, where I met the Whittemores.

So, you got hooked because you saw something very strange.

It was the mantle cell lymphoma that was the red flag. Dan Peterson had five patients with mantle cell leukemia in a group of 100, which appeared to be a cluster. The way I’ve been trained, I look at cancers and I look at clusters. So, I thought, “There’s something going on,” because mantle cell lymphoma is incredibly rare.

Did you know anything about ME/CFS before you met Dr. Peterson?

At that time, CFS was really nothing to me, because when I looked at the literature I thought, “Fine, they’ve got an NK problem.” That makes sense, because NK [natural killer] cells only do two things, they recognize viruses and they recognize tumor cells. So, if you can’t clear viruses, you’re going to have NK cell disturbances. After I met Dan, I purposely didn’t read the research, because I wanted to discover what was going on without being influenced by previous research.

The one exception I made was a paper by Paul Levine. His paper was about families that had children who had cancer and CFS. NK function was lowest in the children with cancer. But CFS patients had only slightly more NK function. I carried that paper in my backpack wondering why.

How did you begin working with him?

To me, it’s the patients that matter. I basically saw a sick patient population – and they were so sick. These were young people, the promise of the country. Something had to account for it.

From the day I went into the field, I saw a crippled immune system. That’s what Dan Peterson showed me – a crippled immune system.

So, all that summer I worked with Dan Peterson. We took multiple samples of the most severely ill patients. We took samples every six weeks, so we developed a very good database. It’s important to have a database like the one we were creating, because if you do a snapshot of an immune profile, you capture only one day. You might miss something. The virus(es) may be latent, so you have to take repeated samples over several time points, months apart.

That was how we found XMRV. We didn’t see it in of 67/101 samples, we saw it in 67/101 patients. And we had multiple samples from every patient taken over a two-year period. The reason we needed so many samples was that there could be DNA silencing of the virus by methylation, the very mechanism that was the basis of my startup, EpiGenX.

For me it made perfect sense based on my decades-long work on HIV and HTLV-1. I had published a paper on how methylation of immune modulators in HIV-infected people silenced the virus, and now I was finding something similar with CFS. [DNA methylation suppresses the expression of endogenous retroviral genes. It plays a crucial role in the development of nearly all cancers.]

Do you still believe a retrovirus causes ME/CFS?

We never said cause. It was the adversaries that said cause. What we said was that there was an association. Everyone wanted to make this virus like HIV, but it’s not like HIV. It’s not crippling the immune system so badly that people are dying quickly. And it’s not a large visible cell component that is being crippled, like the CD4 T cell.

If you want to find a retrovirus you’ve got to grow it in a dividing cell, because it needs cellular genes to multiply, and it’s not easy to find. So we used the classic techniques. And the association with XMRV was very strong. We had a transmissible retrovirus from the third family of retroviruses. It was first associated with a cancer, and now we found it was associated with a neurological disease, just like HTLV-1.

If XMRV was a lab artifact, why wasn’t it in all the samples – those from healthy people as well as from those who were sick?

Only the samples we sent to Silverman’s lab got contaminated, but these were all samples from patients. So samples from healthy controls didn’t get contaminated.

In our paper, the hypothesis was that we would find a retrovirus. We did experiments in 2008 that did not quite match Silverman’s XMRV plasmid sequence. Because we couldn’t make the match with Silverman’s XMRV, we modified the parameters. We changed the PCR reaction to capture everything that wasn’t an exact match. This is what we call “wobble” or “variation.” Max Post was the person who captured the variation in our samples.

When we pulled those pieces out and sequenced them, we were getting similar, but not exact matches with Silverman’s XMRV.

Silverman asked for 30 samples, which we provided. But he wouldn’t do his work blinded, so he knew they were from patients. Our work was blinded, but my notebooks were the only way you could figure out which sample was associated with which patient. Silverman provided his own controls.

So, after three tries Silverman still couldn’t get a full-length sequence of the virus we were looking at.  That meant that what we sent him simply was not XMRV Silverman. He said in March 2009, “Let me try again.” We replied, “No, there’s too big a chance of contamination.” But Lombardi cultured the virus and sent Silverman the samples anyhow without telling me. That was a mistake. When Silverman sequenced those samples – which were not blinded – in his laboratory, they got contaminated. Silverman had lots of plasmid in his laboratory, as he had been doing all the sequencing. He notified us in July of 2011 that our samples were contaminated with his VP62 plasmid.

But even if what we found wasn’t Silverman XMRV, it was still associated with two diseases –  the lymphoma in Dan’s patients and CFS. It could have been a family of viruses, or a different strain. For example, there are five strains of HTLV, and only one is pathogenic. What we found could have been just one in a family of retroviruses.

A good example of this problem is Dr. Lipkin’s research. Dr Lipkin says he has found evidence of retroviruses in Montoya’s samples of ME/CFS patients, but he claims this probably doesn’t mean anything because he also found them in the controls. But what if the controls have a non-pathogenic strain? No one has a detailed sequence that would enable anyone to know those answers. And only 5% of the people infected with HTLV-1 ever get disease.

After 40 years we still don’t know the exact mechanisms of how HTLV-1 or HIV cause disease and why the other very closely related strains do not. The point is that healthy people do not express human retroviruses endogenous or otherwise! Of course there are missing links, but to abandon a line of research that could help millions of people is just bad science.

So, if it wasn’t Silverman’s XMRV plasmid, what virus did you find in Dan Peterson’s patients?

We isolated a gammaretrovirus from at least one person. And I believe beyond a shadow of a doubt that it was a new gammaretrovirus that could infect humans. The way we found it was by using a reagent called a 7C10 monoclonal antibody, which was an antibody to murine gammaretroviruses. That antibody recognized all known murine gammaretroviruses.

The problem was that every time we put our sequence in the database it came up with XMRV, because that’s all there was. There was nothing else to compare it to. When De Freitas did her work in 1990 she had the same problem. She found HTLV-1 and HTLV-2-like virus because, back then, that’s all there was in the database.

So, every time we put a sequence in the database, it came up with XMRV because there was nothing else to check it against. But you have to remember that XMRV isn’t a single virus, it’s a family of viruses. And there may be many other retroviruses that are similar to it that may be pathogenic to humans. We just don’t have a way of identifying them through a database right now.

If you found a new retrovirus, why was the paper you published in Science retracted?

The paper should not have been fully retracted. It should have been partially retracted. The only reason the paper was fully retracted was because I was jailed and had no access to our data.

One of the things that was so wrong about what happened is that they threw out all my research. They destroyed it all. And this is the saddest part; we came up with a study that showed who would do well on Ampligen. 30% of the people with ME/CFS had antibodies to spleen focus-forming virus (SFFV), and these were the patients who responded to Ampligen.

What we had found was a biomarker – the antibody to SFFV-env recognized by 7C10. This finding was later validated in the Lipkin multicenter study. The assay in our original paper was replicated in every study we did, but now all of that original data is lost. If I hadn’t been so thoroughly discredited, and my research destroyed, Ampligen could have been approved.

But I look at it this way, if that Science paper on XMRV had never come out, would we have the research that is being done today?

Why did you call your book Plague?

One of the reasons we called it Plague was not so much because of the disease itself, but because of the increasing numbers we are seeing of people developing related health problems, such as autism, neuroimmune disease, and cancer. If we do nothing, in another decade one in two families will have one of these neuroimmune diseases.

From another standpoint, the title refers to the plague in science. There is a plague in medical research. We don’t want to believe that medical research is corrupt. We don’t want to think that if they saw a child who was sick, researchers wouldn’t do something. But yet, the government is corrupting science – just as they did with ME/CFS and XMRV – by controlling the funding and the message, which ultimately determines what the journals publish.

What have we learned?

That is the question I ask myself.

XMRV was made in recombination with mouse cells. Before we could grow cells in labs we would pass cells through mice in order to attenuate them. But we found that by passing cancer cells through mice we could grow tumors; the cells had recombined with a retrovirus. Everyone before 1980 did this. It was standard laboratory procedure. We learned that anything we passed through animal tissues could make replication competent recombinant retroviruses in only ten days. All of our NIH research is based on mouse research. And those cell lines I worked with daily for more than 30 years have the potential to produce novel retroviruses.

So, here’s the question: How many of these recombinant retroviruses are now in our environment and playing a role in all of these neuroimmune diseases?

If XMRV had mutated only two amino acids in its genetic envelope we could have had a true plague. Nobody could have predicted that XMRV could remain stable on a bench for months, or that it could be aerosolized and transmitted in dust, in saliva. But because our immune systems spotted it, we developed an antibody. (Many of the lab workers such as Max and myself seroconverted, meaning we developed the antibody from our lab exposure.)

How many people did we save by learning that XMRV could be aerosolized and spread to immune-compromised individuals or lab workers? We may have avoided something that could have infected everyone, because Silverman was sending XMRV all over the world.

But, exposing Silverman’s XMRV as a lab artifact should not have ended the research. The work Frank Ruscetti and I did to find the epitope that the antibody recognizes in humans should have been completed. Currently 6% of the population carries an antibody that recognizes a gammaretrovirus envelope protein. Six percent is 20 million Americans!

Last year, Gary Owens published a research paper that showed the envelope protein of MLVs alone could cause vascular leak and aggressive tumors. He had previously published data identifying XMRV-2, now called B4RV, on November 10, 2009. That was only one month after our paper was published. We worked with Gary and found those sequences and proteins in some of our original patient samples. The virus Gary Owens found causes the very things I saw in Dan Peterson’s patients and which are found in so many of the complex chronic diseases that affect our  population today. So why was this work suppressed for three years, and why is it being downplayed now? How many new retroviruses have we created through all the mouse research, the vaccine research, gene therapy research? More importantly, how many new diseases have we created?

When they destroyed all of our work, and discredited everything I or Frank Ruscetti had ever published, and arranged for the publication of my mug shot in Science, the NIH very deliberately sent the message to researchers everywhere about what would happen to any honest scientist who dared ask those important questions.

If HHS gave you the power to re-name CFS, what would you call it?

Non-HIV AIDS. It is an acquired immune deficiency, beyond a shadow of a doubt.

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8 thoughts on “Plague: An Interview With Judy Mikovits”

  1. Katharina says:

    Thank you for this great Interview! Thank you, Dr. Judy Mikovits! We owe you so much! And science also!

  2. Katwilm says:

    This is why I feel that diseases like this may well have come from vaccines. There are animal molecules in our vaccines which are injected into our bodies. More and more all the time. Like Dr. Mikovits asks “how many new diseases have we created?” Thank you for your honesty.

  3. me/cfs says:

    I know this will not be a popular viewpoint, but I see the situation differently.

    Dr Mikovits is fanning the flames of fear in the patient community rather than promoting scientific truth and the hope that it brings. I say this because of the language she is using to convey her message. Words like plague and Non-HIV AIDS are powerful, yet they do not match the truth of our illness. While AIDS is a disease caused by a single, identifiable virus, ME/CFS is not. Many pathogens have been identified in ME/CFS patients. This points to a totally different source for the illness. In fact, it is an indication that the many infectious agents which exist to a degree in all humans are taking advantage of an opportunistic situation brought on by a dysfunction of the immune system. But there is no indication that any one pathogen is the singular cause behind the dysfunction. It is an important distinction from AIDS.

    By publishing her earlier findings on XMRV without verification by other labs and researchers, Dr Mikovits set back our cause. It has given credence to the wider medical community consensus that holds to the mistaken notion that our disease is simply not a medical problem. I say this because I have heard it from physicians I have seen. Good physicians who seem intent on finding the truth behind the cause of ME/CFS.

    1. WillWiegman says:

      Thiocyanate is the only antioxidant that can prevent White Blood Cells from self-destructing when they try to clean up toxins, kill bacteria or process vaccines. We can’t live without it but it is all gone from our foods in the US now, processed, overcooked or GM’s out for sweetness.

  4. anomar says:

    I don’t know what happened to Dr. Mikovitz, but I have ordered her book to get her perspective.

    Pioneers often look and sound over the edge because they are reacting to the very real oppression they are seeing around them.

    After 40 years of suffering, I am not interested in being polite and not rocking the boat. As someone who once aspired to be a scientist, I couldn’t be more disillusioned with the profession as a whole.

  5. Robyn_E says:

    John Coffin was able to produce replication competent retroviruses in only 10 days from Pre-XMRV1,2, and human kidney cells. Generation of Multiple Replication-Competent Retroviruses through Recombination between PreXMRV-1 and PreXMRV-2 – This research from Dr. John Coffin and Dr. Vinay Pathak showed that replication competent murine leukemia retroviruses can be produced in a relatively short period of time. From their abstract, “To determine their potential to generate RCRs,we transfected PreXMRV-1 and PreXMRV-2 into 293T cells and used the virus produced to infect fresh cells; the presence of reverse transcriptase activity at 10 days indicated the presence of RCRs.”

    Or how about the fact they are finding Infectious MLV retroviruses in xenograft cell lines and cell lines that are just housed in the same building: Frequent Detection of Infectious Xenotropic Murine Leukemia Virus (XMLV) in Human Cultures Established from Mouse Xenografts – This research suggests that the murine leukemia retroviruses have the potential to become airborne. In their conclusion the team warned, “Laboratories working with xenograft-derived human cultures should be aware of the risk of contamination with potentially bio-hazardous human-tropic mouse viruses and their spread to other cultures.”

    Another: Xenotropic MLV Envelope Proteins Induce Tumor Cells to Secrete Factors that Promote the Formation of Immature Blood Vessel – the results suggest that xenograft approaches commonly used in the study of human cancer promote the evolution of novel retroviruses with pathogenic properties.

    Oh and this one is very important. It is the 1995 National Academies analysis for xenotransplantation (still in use today), which includes xenografting human and animal cells – Infectious Disease Risk to Public Health Posed by Xenografting, The possibility that infections can be transmitted from animals to humans is of concern not only because of the threat to the health of the recipient, but also because such infections may be transmissible to others, creating a public health hazard. Further, such infections may be due to previously unrecognized organisms, making detection difficult if not impossible. If the time from infection to clinical symptoms is long, the risk of widespread transmission is greater, because during this time the new organism may silently spread from person to person, as happened with human immunodeficiency virus (HIV).

    Emergence of a new public health risk appears to be a two-step process (Morse, 1995). First, a new infectious agent is introduced into a given human population from other human populations, animals, or environmental exposures. Frequently these new agents are zoonoses, defined as animal microbes that can infect humans as well as the animal species from which they come. The second step is establishment and dissemination of organisms that prove to be infective and transmissible from person to person. The first step, introduction of a potentially transmissible agent into a human, could be accomplished by transplanting an organ that was infected with the agent. It is the second step of establishment and dissemination, however, that raises public health concerns, particularly if the agent is viral since current therapies for viral illnesses are limited.

    Basis For Public Health Concern
    Historic experience with many zoonotic diseases suggests that the potential for human infection with xenogeneic pathogens has implications for the community that extend beyond the individual transplant recipient.

    “examples demonstrate that some zoonotic infections have the potential to extend beyond the individual and into the community. Thus, the risk of xenotransplant-associated infection is not restricted to the xenotransplant recipient alone. The potential for xenogeneic infections to be transmitted through human populations is real and poses a public health concern. Further, the risk for health care workers in close contact with the xenograft recipient is probably higher than for the community at large.”

    The potential for the introduction of a new retrovirus into human hosts via implanted xenogeneic tissue is of public health concern due to the long period of clinical latency associated with all known human retroviral infections. This long latency period provides the opportunity for silent person-to-person transmission to occur before pathogenicity is evident.
    There are concerns that xenogeneic viruses may recombine or reassort with viruses latent in human tissues and result in variants that possess either a broader host range or an increased pathogenic potential. What options are available for risk management of xenotransplant-associated infectious public health risk? One option is to eliminate all risk by avoiding all use of xenogeneic tissue in humans.

    Conclusions and Recommendations

    Xenotransplantation may also be valuable for the treatment of human diseases. However, it is well recognized that infectious agents can be transmitted from animals to humans and that organisms benign in one species can be fatal when introduced into other species. Further, it is known that the pathogenicity of infectious organisms can change under a variety of conditions and that the effects of infection by some organisms, such as the human immunodeficiency virus, are delayed for years or even decades. Because xenotransplants involve the direct insertion of potentially infected cells, tissues, or organs into humans, there is every reason to believe that the potential for transmission of infectious agents (some of which may not even now be recognized) from animals to human transplant recipients is real. If established in the recipient, the potential for transmission to caregivers, family, and the population at large must be considered a real threat.
    However, all members of the committee agreed that some mechanism is needed to ensure attention to and reduction of the risk of infectious disease transmission.

  6. Robyn_E says:

    Guidance for Industry: Source Animal, Product, Preclinical, and Clinical Issues Concerning the Use of Xenotransplantation Products in Humans

    The use of the different xenotransplantation products has the potential for transmission of infectious disease from nonhuman animals to humans.

    Potential public health risks posed by the use of xenotransplantation products include:

    transmission of infectious agents that are pathogenic for humans but may not be pathogenic or even detectable in the source animal host; transmission of organisms that may not normally be pathogenic in humans but can become so in the immunosuppressed or immunocompromised individual; and,
    recombination or reassortment of infectious agents, particularly viruses, with nonpathogenic or endogenous human infectious agents, to form new pathogenic entities.
    Furthermore, it is difficult to predict the infectious agents that may cause disease in a recipient of a xenotransplantation product solely on the basis of analysis of naturally occurring zoonoses because there are major differences between normal contact of humans with animals and contact of a recipient with a xenotransplantation product. For example, the physical barrier or distance is eliminated in the recipient due to transplantation and vascularization of xenotransplantation products, or even due to implantation of nonvascularized cells or tissues, or ex vivo manipulations that cause intimate proximity or contact of xenotransplantation product materials with recipient cells, tissues, or fluids. The potential for viral adaptation in immunocompromised or iatrogenically immunosuppressed hosts and the potential for undetected spread of previously latent viral infections are of particular concern.

  7. WillWiegman says:

    Dr. Judy, read about Thiocyanate and the Lactoperoxidase-Thiocyanate-Hydrogen Peroxide System of the mucus membranes of the lungs, mouth, sinuses, and throat.

    Also read this, very informative:

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