Ending Plague

by Francis W. Ruscetti

  One of the things I most appreciate about Shallenberger is his willingness to go on the intellectual journey necessary for new knowledge to be constructed. This is true in all of science but becomes even more vital when we talk about the public’s health.

  Some of you might be saying, “Judy, this guy is saying AIDS isn’t caused by the HIV virus.” My answer is that is exactly what my PhD thesis said, but we did not appreciate all of the data at a molecular level and Shallenberger’s work went against dogma, as did mine.

  That’s the great thing about science. It’s not about the superstition of preconceived ideas. It’s about following the data. None of us knows the ultimate truth, which is why we need to keep all the voices in the conversation, even the dissenting ones.

  I now appreciate and honor the sacrifice of Peter Duesberg, the University of California, Berkeley researcher who clashed so publicly with Robert Gallo and Anthony Fauci about how it had not been shown that HIV caused AIDS. This was a decade before my PhD thesis and the CCR5 delta 32 deletion made it clear. Duesberg simply had the audacity to publicly say that HIV did not meet the classic definition of Koch’s Postulates, in which an infectious agent must have the ability to cause the disease in otherwise healthy individuals, every single time.

  But Gallo and Fauci weren’t interested in having any such nuanced conversations.

  Instead, Gallo and Fauci launched a vicious attack on Duesberg. They couldn’t get him fired from UC Berkeley, but they could so completely choke his research funding that for years he didn’t have the money to hire a single research assistant, run his lab, and could only go to his office, read the latest scientific findings, and maybe teach a few classes.

  As with Dr. Andrew Wakefield and me, Duesberg was subjected to a campaign of vilification which would have given the agents of the Roman Inquisition new ideas in their persecution of Galileo.

  Let me tell you what I believe.

  I think HIV is associated with AIDS, just as XMRV is associated with chronic fatigue syndrome (ME/CFS), autism, cancer, and a host of other diseases.

  But I do not believe the mechanisms of disease causation are well-understood.

  And if we do not understand the mechanisms, we need to continue our efforts so that we may effectively intervene. That should be simple logic.

  What do I think of the attacks launched by Gallo, Fauci, and others on Peter Duesberg?

  Utterly despicable.

  And I think the same of Gallo, Fauci, and others trying to develop AIDS drugs without understanding the mechanisms of disease causation and deliberately ignoring data as the CDC and FDA are doing now with COVID-19. They insured there would be millions of unnecessary deaths, and I consider those to be crimes against humanity.

  For the benefit of those who closely follow the science, and wonder where I might agree and disagree with Peter Duesberg, this is what I believe at this moment in time.

  First, HIV and XMRV do not meet the classic Koch’s Postulates definition of a disease causing infectious agent, which when introduced into a healthy individual will always cause the disease. (Although HIV was considered causative because, in the 1980s, all those with AIDS had evidence of HIV infection. Except the women, of course.)

  Second, Koch’s Postulates need an update to take advantage of more than a century of scientific research, particularly in the areas of genetic and epigenetic vulnerability. Our 2009 Science paper satisfied the best available update, called Hill’s Criteria, but that doesn’t take into consideration the role of defective (incomplete) viral sequences or expression of HERV viruses and recombinants created through vaccine production or other processes.

  Third, those villains who seek to destroy the work and reputations of good scientists asking reasonable questions, as Duesberg did, should be driven out of science and prosecuted for crimes against humanity.

  Fourth, while there is strong evidence that these retroviruses and other viruses are associated with disease, we do not fully understand the mechanisms of disease causation.

  Fifth, we need to understand these mechanisms to guide our treatment protocols, and effectively intervene to improve the lives of people.

  ***

  Frank Shallenberger isn’t a research scientist like me. He’s a clinician on the front lines trying to make people’s lives better. In that, we are united. He was considering the question Duesberg and many others were asking, namely, why were some people catching the virus and coming down with disease, and others weren’t?

  Shallenberger recalled a paper describing how the TH-1 and TH-2 immune systems were functioning in those at risk for contracting HIV and developing AIDS. The TH-1 and TH-2 systems do different things in our body, and Frank believes understanding this difference might be the key to solving many chronic diseases.

  The suggestion of this TH1 to TH2 shift as being responsible for the devastating consequences of AIDS was first proposed by two researchers in 1993 in the journal, Immunology Today:

  This viewpoint proposes that an imbalance in the TH1-type and TH2-type responses contributes to the immune dysregulation associated with HIV infection and/or progression to AIDS is dependent on a TH1 to TH2 dominance. This hypothesis is based on the authors’ findings that: (1) progression to AIDS is characterized by loss of IL-2 [interleukin-2] and IFN gamma [interferon gamma] production concomitant with increases in IL-4 and IL-10; and (2) many seronegative, HIV-exposed individuals generate strong TH1-type responses to HIV antigens.37

  What had been recognized was that there were subsets of functional T-cells, defined by the cytokine to which they responded and produced. The shift is a functional shift. If the cytokine expression of the T-cells changes, then the downstream immune response changes. One of my post-doctoral projects was defining, at the molecular level, the change in the response.

  What we knew was that the promoter, the on/off switch of IL-2 and interferon gamma, was different by a single CpG nucleotide. We hypothesized the difference between a cell that expressed IL-2 versus one expressing interferon gamma was the methylation and silencing of that single CpG nucleotide.

  Dr. Howard Young, an interferon expert and longtime colleague, suggested a clever way to test the hypothesis. There were enzymes that recognized and differentially cut methylated and non-methylated sites. One enzyme was called SnaB1. With Dr. Young’s guidance, I designed a PCR test to determine if methylation of that single CpG nucleotide could distinguish at the molecular level a TH-1 versus TH-2 response.

  If the CpG site was methylated the PCR product was present and it would produce interferon gamma.

  If it was unmethylated, we’d get IL-2, showing there was a functional shift of T-cells from TH-1 to TH-2 status.

  It worked.

  We understood that even though only one in ten thousand T-cells might be infected, there was a functional shift of the T-cells toward a TH-2 response, generating IL-4, IL-5, and IL-10, shifting the immune system toward antibody production and away from the antiviral response. This was a simple test to determine whether an HIV-infected individual was likely to develop AIDS.

  Frank Shallenberger recalled a paper he’d read looking at gay men who had AIDS and those who did not: (I wondered if he saw the paper from my PhD thesis, as I did that work in healthy, HIV-infected men.)

  In this paper, they took a bunch of homosexual men and divided them in half. Half of them had AIDS, and the other half was not diagnosed with AIDS. Then they looked to see how their TH1 and TH2 systems were working. And the gist of the paper was that every single one of the men with AIDS had a TH1 to TH2 shift. Every single one. Then they looked at the control group and only 35 percent of them had a TH1 to TH2 shift. So, I’m looking at that and thinking, “Wow! Are you telling me that of these young and healthy males, 35 percent of them have already had a TH1 to TH2 shift? That can’t be good. Are those 35 percent the next group about to develop AIDS?38

  The AIDS heretic, Peter Duesberg, had suggested that the heavy use of recreational drugs and promiscuous gay sex, par
ticularly anal sex, resulted in multiple immune system traumas to the body leading to the immune system collapse of the patients.

  Duesberg didn’t seem to be far off the mark.

  As Frank Shallenberger recalled the change in his thinking:

  I started to realize, that what’s going on with these diseases, whether it’s AIDS or chronic hepatitis, or chronic Epstein-Barr. It’s not the infectious agent itself that’s the problem. The problem is that the particular person is not responding to the agent with an immune system in a proper manner. And ozone therapy is one way we can make you respond in a proper manner. When you’ve got all these people walking around, many with these TH-1 to TH-2 shifts, they’re vulnerable. Along comes a virus to which these people, and they may never recover.

  They don’t have the ability to control the virus. That’s my theory. So, I’m going along and I’m treating people for viruses, and every single one of them gets better. I don’t care what the virus is. Sometimes it’s Hanta virus, or West Nile virus, or influenza. Most of the time I don’t know what it is. I just know it’s a clinical viral infection. Every single one of them gets better almost instantaneously when I apply ozone.39

  This gets into the classic debate over whether it’s the pathogen or the health of the organism which determines whether one develops a disease.

  I think it’s both.

  Try to limit exposures to pathogens, but also try to make sure you have a healthy immune system to battle any microbes to which you might be exposed.

  As Shallenberger further explains, “You do not want a TH-1 to TH-2 shift ever.”40 You want to maintain balance. Homeostasis. That may be one reason why antiparasitic drugs are beneficial in COVID-19, Ebola, and HIV/AIDS. I always remember Dr. Dietrich Klinghardt telling me at a conference in Fuld, Germany on April 1, 2017, that he’d never seen a retrovirus associated disease where there was not a co-morbidity of a parasitic infection. Frank Ruscetti and I always say “pathogens rarely travel alone,” citing the 2009 paper, “War and Peace Among the Microbes” by the Margolis lab.

  Shallenberger is not a molecular biologist, but as a clinician he’s trained to see patterns in his patients with chronic illness. Shallenberger states:

  There is always a trigger. I’m just a clinician. I’m a doctor and I don’t know much about viruses. But I do know what makes people sick and well. And I can tell you it’s darned unusual to see a patient come in with a chronic illness that can’t tell me, you know, this all started with a particular series of events twenty years ago.

  The event was some kind of trauma to the body. It might have been a blood transfusion. It might have been a bad viral infection. They might have hit their head and had some concussion. Or they could have been big time into stress. All of these things can cause a TH-1 to TH-2 shift.41

  Shallenberger also noted that some of his patients claimed a vaccine was a trigger for their chronic condition and he began to think more deeply about the question.

  I’ve never really liked vaccines. Something about them I just didn’t like. At that point I asked myself, ‘What’s the definition of a successful vaccine?’ It’s one that induces the formation of antibodies. [That’s not the same as lifelong immunity.] Where do these antibodies come from? They come from the TH-2 system. And while the TH-2 system is busy making all these antibodies, it is also secreting cytokines that shift you from a TH-1 state to a TH-2 state. That is exactly what happens every time you get a vaccine. It shifts you from TH-1 to TH-2.

  And I thought, ‘We’re taking kids and adults and we’re shooting them up with more and more vaccines.’ And you have to wonder, ‘How many of these kids are growing up with a normally functioning TH-1/TH-2 balance. How many are going to develop all manner of diseases and chronic conditions as a result of the shift?’ There are going to be some pretty strong kids for whom it won’t matter. But there’s got to be a subset of the population for which it’s going to be disastrous.42

  Before reading Plague of Corruption, Dr. Shallenberger had a negative view of vaccines because of the TH-1 to TH-2 shift, but after reading the book, he told my coauthor, “Now you guys tell me, oh by the way, these vaccines are loaded with all these animal viruses! I thought, ‘Oh my God! What are we doing?’”43

  Like me, Shallenberger is hopeful that with proper therapies, people can get better, and can often be cured. He claims that when people come to him, they’re usually the cases nobody else has been able to help. While it may take up to eight months, he estimates 85–90 percent of his patients experience substantial improvement, if not resolution of their symptoms. When the patient really commits to the program, Shallenberger believes the number increases.

  We’re all on a journey. But when I think of people like Dr. Frank Shallenberger, I know it’s a journey I’m making with good thinkers who want to make the world a better place.

  EPILOGUE

  Doing the Right Thing in a World Gone Mad

  Success is a collection of problems solved.

  —I. M. Pei

  I guess Robert Gallo can’t help being a thief.

  First, he stole credit for the discovery HTLV-1 and IL-2 from Frank Ruscetti. Then he tried to steal credit for the discovery of HIV from Luc Montagnier. Finally, in 2016, he tried to alter the history of human retrovirology. Maybe it shouldn’t come as a surprise. Gallo reminds me of one of those aging bank robbers who just can’t pass up a chance for one more heist.

  I’m sure it must have been humiliating to have that report issued from the Office of Research Integrity in 1992 which drove him from the center of the scientific universe to the relative obscurity of the University of Maryland, where he has languished in exile like Napoleon on Elba for the last quarter century. Medical students of today may well have no idea that Gallo was the most quoted scientist of the 1980s and 1990s, the Anthony Fauci of his time.

  But nobody today can doubt that a few scientists have become the effective rulers of our world, rather than the servants they were supposed to be.

  I believe we are in a time of unprecedented danger for humanity.

  Let me explain how Gallo, in his sunset years, tried to rewrite the history of XMRV research, robbing humanity of so much more than credit.

  ***

  In November 2013, approximately four years after the publication of our groundbreaking article on XMRV and chronic fatigue syndrome (ME/CFS) in the journal, Science, and two years after I’d been erased from the scientific literature and textbooks, I delivered a talk called, “The Exotic Biology of Xenotropic Murine Leukemia Viruses (XMRVs).”1

  I reviewed the literature as to how the retrovirus had first been identified in 2006 in approximately 10 percent of prostate cancer tissue samples by a team led by Joseph DeRisi from the University of California, San Francisco, and Robert Silverman from the Cleveland Clinic.2

  I presented the data from our 2009 paper, which showed our original samples were negative for the VP-62 plasmid (molecular clone) positive for natural XMRV, but when those samples came back from the Silverman lab, they contained the plasmid.

  What does that mean?

  The VP-62 plasmid contamination was probably from Silverman’s lab, which makes the most sense because Silverman and his research partner, J. Das Gupta, created VP-62 plasmid in their own lab, before I was ever in Nevada. Or did the retrovirus escape on its little viral legs from the Cleveland Clinic to my lab in Nevada?

  I displayed the phylogenetic tree of XMRV, showing its close association to other mouse retroviruses, as well as how Adi Gazdar demonstrated in 2011 that the virus could spread through the air, a genuine nightmare scenario.3

  I showed the work of the Gary Owens lab at the University of Virginia, identifying what I believe should be called XMRV-2, but has since been named B4RV. Additionally, it was found that the envelope proteins alone could cause the microvasculature changes and pathologies, not only in prostate cancer, but also in ME/CFS.4

  In one of my slides Frank and I summarize these three points from the Owens a
nd Coffin labs’ paper:

  1. B4 tumor cells harbor a retrovirus sharing 93% homology to XMRV-1 – we have designated it XMRV-2.

  2. XMRV-2 is capable of infecting and stably integrating into the genome of a human prostate tumor cell line LNCaP which contains a loss of function deletion mutation within the RNAsel familial prostate cancer susceptibility gene-1.

  3. XMRV-2 infected LNCaP cells show multiple functional changes associated with increased tumorgenicity and/or metastasis including increased growth, altered migration and adhesion, and secretion of factors that decrease vascular SMC differentiation.5

  This is exactly what one would expect with a newly discovered virus. There would be variants. Gary Owens had found a variant. Why did it get named B4RV? Because when he called it XMRV-2 at an XMRV meeting at the Cleveland Clinic presided over by John Coffin on November 10, 2009, it would have supported our Science paper one month after it was published.

  XMRV would no longer be an orphan retrovirus, but would have a family attached to it.

  And what of our claim that I believe is the reason we were attacked so viciously? That common lab experiments, mixing tissue from different animals could quickly produce variant replication competent retroviruses? That work was done by none other than the John Coffin lab. The article was entitled, “Generation of Multiple Replication-Competent Retroviruses through Recombination between Pre-XMRV-1 and PreXMRV-2.”6

  Coffin and his team found that you could generate new replication-competent retroviruses in ten days by the mixing of tissue from different types of animals and growing them in immortalized cell lines in fifty gallon fermenters!

  XMRV was likely to be the tip of the iceberg of an entire asylum of manmade viruses.

  If honest, ethical public health officials read and understood that paper, their first action afterward should have been shutting down all labs in which animal and human tissues are combined.

  Scientific laboratories were likely becoming the greatest breeding ground in Earth’s history for the creation of new and potentially dangerous pathogens.