Prions: The Conspiracy to Push Vegetarianism

Smokers' money (via R.J. Reynolds Tobacco) funded Stanley Prusiner's early work on prions, after his funding from Rockefeller University and Howard Hughes Medical Foundation ended. Frederick Seitz merely made site visits to Prusiner's lab, and had nothing to do with tobacco research. The tie appears to have begun in 1975 when John D. Macomber, Vice Chairman of Rockefeller University, joined the RJRI board of directors. Seitz was the former president of Rockefeller.

Setting the Stage

After expending vast sums on the Special Virus Cancer Program without identifying any viruses that cause human cancer (while ignoring the main suspects), the program was shut down - after setting the stage for this new bottomless funding pit.

The Big Push to Suppress Virus Cancer Work

Stanley Prusiner and Prion Research

Stanley Prusiner's 1979 application to RJ Reynolds Tobacco for funding for slow virus research started out by citing progressive multifocal leukoencephalopathy (PML, now known to be caused by polyomavirus) and subacute sclerosing panencephalitis, caused by a measles variant, then shifts its emphasis to "virus-like particles." (Slow Virus Research. Oct. 26, 1979.)

Prusiner application, 1979 / UCSF (pdf, 4 pp)

Frederick Seitz, the former president of Rockefeller University, wrote to RJR Chairman Colin Stokes about former NIH director James A. Shannon's concern that Prusiner was already receiving very large support from the Howard Hughes Medical Foundation. Seitz told Stokes that HHMF's support was being phased out because they were dropping virus research. The letter is dated Feb. 13, 1980, and is on Rockefeller University letterhead. Seitz's presidency ended in 1978, and Shannon, who was his Special Assistant, retired in 1975; the two were conducting site visits together.

Seitz to Stokes, 1980 / UCSF (pdf, 1 p)

Feb. 18, 1980, Prusiner et al.'s new application, "Reynolds Program, Slow Viruses Causing Degenerative Diseases." Nearly all of the relevant citations are to work published after 1976. Expenses include the latest Hewlett-Packard laboratory gear and lots of animals, page 38.

Reynolds Program, 1980 / UCSF (pdf, 49 pp)

Draft of Frank Colby's assessment, Feb. 21, 1980. Colby thought that the subject was not "off the beaten path," and that they should seek funding by the NIH instead.

Colby, Feb 21, 1980 / UCSF (pdf, 6 pp)

Prusiner's contract for $872,500, through the University of California, San Francisco School of Medicine, May 5, 1980, from Henry C. Roemer, senior vice president and general counsel and secretary of R.J. Reynolds, with cc to Seitz. The cover letter for first installment, July 9, 1980.

Prusiner grant, May 5, 1980 / UCSF (pdf, 4 pp)
First installment, July 9, 1980 / UCSF (pdf, 1 p)

Frederick Seitz reported on his site visits to UCSF and UCSD, on Rockefeller University letterhead, to Henry C. "Jack" Roemer, Nov. 18, 1980; with copy to Colin Stokes. He said, "There is little doubt that both of these groups are making excellent use of the Reynolds funds."

Seitz to Roemer, Nov. 18, 1980 / UCSF (pdf, 2 pp)

Seitz letter on Rockefeller stationary to John L. Bacon, Director of Corporate Contributions for RJ Reynolds Industries, June 29, 1981, with copy to Colin Stokes, about the results of his "agreed upon" calls to Prusiner; to Philip Handler (who was leaving Duke University); to James Shannon about veterinary schools in Washington and Idaho; the Sidney Farber Cancer Research Institute; and Charles Heidelberger.

Seitz to Roemer, June 29, 1981 / UCSF (pdf, 2 pp)

RJRI gave Prusiner $500,000 for 1983, with further gifts of the same size planned for 1984 and 1985. The money was given through the University of California, San Francisco School of Medicine. (Horrigan to Prusiner, Feb. 23, 1983.)

Horrigan to Prusiner, Feb. 23, 1983 / UCSF (pdf, 4 pp)

Seitz letter to Roy E. Morse, Vice President of Research and Development of RJ Reynolds Industries, March 21, 1985, on his site visit to Prusiner. He said, "It now seems to be essentially certain that Creutzfeld-Jacob disease, to which humans are susceptible, is a very close relative of scrapie. There still does not seem to be any close relationship with Alzheimer's disease, however."

Seitz to Morse, March 21, 1985 / UCSF (pdf, 3 pp)

RJ Reynolds, "Biomedical Research Contributions (MRC) 1976-89." Joshua Lederberg, the president of Rockefeller University from 1978 to 1990, received $6,100,000 between 1980 and 1988; Prusiner got $3,747,500 during the same period.

RJR Biomedical Research Contributions, 1976-89 / UCSF (pdf, 15 pp)

Seitz sent a letter to J. Paul Sticht, retired chairman of R.J. Reynolds Industries commending the company for research grants it provided to Prusiner during the 1980s. (RJR Grants Assist Nobel Prize Winning Research. Caravan 1997 Nov;31(10):9.)

RJR Grants Assist Nobel Prize Winning Research / UCSF (pdf, 16 pp)

From "Nobel Gas," by Gary Taubes. Slate 1997 Oct. 11: "Prusiner's proposition has been controversial from the get-go. The researcher who did Prusiner's lab work at the University of California at San Francisco quit over the publication of Prusiner's very first prion paper in 1982, arguing that Prusiner was overinterpreting the available data to push the prion hypothesis.

"Over the next 15 years, Prusiner won over virtually everyone to his prion hypothesis -- the lay press, the scientific press -- but not the researchers in his field... By 1985, when Prusiner's own papers were still suggesting that the prion hypothesis was at best a long shot, he won a $4-million congressional award 'to determine the structure of prions and how they cause disease.' In 1991, Prusiner reported at a major conference that he had proved that the infectious agents of these diseases were proteins free of nucleic acids. In particular, he had created mice with a genetic mutation that caused what was a normal protein -- the prion protein, in Prusiner's lingo -- to beome abnormal and produce disease. He then took brain matter from these mice and injected it into new mice, which promptly got sick, showing that no viral particles were necessary to transmit the disease. But there was still no paper proving the results to the scientific community.

"Two years later, when he presented the same mice work at another conference, the news pages of Science and Nature wrote it up as if it cinched the prion hypothesis. Although Prusiner's work had not been replicated by anyone and he had still not published these supposedly seminal findings that prions cause disease in a peer-reviewed journal, he won the prestigious Albert Lasker Award in October 1994. (The Lasker Award is considered a short-list for the Nobel.)...

"Prusiner's boilerplate response to prion critics has been that if mad-cow disease or any of the other 'prion diseases' is caused by a virus, then surely that virus would have been discovered by now. The fact is, it's damned hard to find a virus in a mishmash of animal brains, which is where you have to look. One reason a virus hasn't been found -- if indeed a virus causes these diseases -- is that no one is doing the laborious and expensive work to find it. It can take researchers decades to find culpable viruses -- hepatitis C is a famous example. But at least those researchers got funded to look, which is not the case in the prion field. Prusiner has received in the neighborhood of $40 million in funding from the National Institutes of Health since 1985. Qualified critics who request money from the NIH to look for viruses are told by NIH bureaucrats that if the virus turns out not to exist, then their study will have been 'of insufficient significance and scientific merit' and thus not worth doing.'

"One member of the Nobel Committee says his colleagues were aware of unanswered questions in the prion hypothesis but awarded Prusiner the prize in recognition of the wealth of information he has unearthed on mad-cow-like diseases. But if it turns out that viruses do cause the diseases, then Prusiner will have won the prize for the discovery of something spectacularly wrong."

Taubes / Slate 1997

"Scientists have not found any nucleic acid associated with a prion, however, despite intensive efforts in many laboratories." (Answer to: What is a prion? By Shaun Heaphy of Leicester University Dept. of Microbiology and Immunology. Scientific American, Oct. 21, 1999.) = !! = USING WHAT FOR FUNDING? From whom? Prusiner was the Number One NIH Fat Cat in basic research in 2000, receiving $12.5 million, and he has been generously funded from the very beginning - unlike those who disagree, whose funding (if any exists) doesn't even show up on the radar screen. And these facts make a mockery of how Prusiner is being marketed to the public as a "heretic."

Heaphy, 1999 / Scientific American

And an interesting point is revealed on Heaphy's website, which lists the symptoms of CJD as "loss of motor control, dementia, paralysis wasting and eventual death, typically following pneumonia." (Sean Heaphy website.) PNEUMONIA! Of course, the Syndicate expects us to have been conditioned to stampede past this clue like a herd of cattle and uncritically embrace their prion hypothesis. It has happened before. In 1955, Charles S. Cameron, Medical and Scientific Director of the American Cancer Society wrote in his book, The Truth About Cancer: "It so happens this condition [viral pneumonia] seems to occur with surprising frequency in patients with cancer of the lung - and early in the course of the disease at that." It is now 50 years later, and we are still awaiting investigation of this link. Furthermore, when passive smoking studies didn't ignore it, they carefully excluded recent cases, as if they were conscientiously trying to avoid implicating infection.

Heaphy / Leicester University

Stanley B. Prusiner is a Trustee of the University of Pennsylvania. One of the Trustees Emeritus is Paul F. Miller Jr., retired senior partner in Miller, Anderson & Sherrerd, and the former treasurer of the World Wildlife Fund.

Trustees / University of Pennsylvania
WWF / Undue Influence

New inhibitors of scrapie-associated prion protein formation in a library of 2,000 drugs and natural products. DA Kocisco, GS Baron, R Rubenstein, J Chen, S Kuizon, B Caughy. J Virology 2003 Oct;77(19):10288-10294. "Several classes of compounds were represented in the 17 most potent inhibitors, including naturally occurring polyphenols (e.g., tannic acid and tea extracts), phenothiazines, antihistamines, statins, and antimalarial compounds... The fact that many are approved human drugs or edible natural products should facilitate their use in animal testing and clinical trials."

Kocisco et al, 2003 abstract / J Virology

Prion hype at the Milwaukee Journal Sentinel! Those lackeys tell us that "Maverick [sic] scientist Stanley Prusiner" [who has gotten millions and millions of dollars from Rockefeller, RJ Reynolds, and NIH for years] "prevailed over enough doubts about his theory to win the Nobel Prize," as it's about pure scientific excellence instead of pure political pull. Prof. G Richard Olds of the Medical College of Wisconsin breathlessly tells us that "They're practically indestructible" [although according to reseach dating back at least to 2000 scrapie prion is easily inhibited by a variety of common natural and man-made compounds]. They concede that the prion itself is not sufficient and call the mystery factor "Protein X." It is estimated to cause one death per million people per year, which in the "minds" of the media (to use this term loosely) vastly overshadows the tens of thousands of deaths per year known to be due to influenza (ho hum, that's old news, so it doesn't count). The featured victim (young, of course) had a rapid heartbeat and a fever of 103 degrees F; "most likely an infection, possibly pneumonia," but who cares, when there will be millions more dollars to spend searching for "Protein X." (A New Kind of Killer. By John Fauber and Mark Johnson. The Milwaukee Journal Sentinel, Oct. 27, 2002.)

Fauber & Johnson, 2002 / Milwaukee Journal Sentinel

Retrovirus infection strongly enhances scrapie infectivity release in cell culture. P Leblanc, S Alais, I Porto-Carreiro, S Lehmann, J Grassi, G Raposo, JL Darlix. EMBO J 2006 Jun 21;25(12):2674-2685. "Here we report that moloney murine leukemia virus (MoMuLV) infection strongly enhances the release of scrapie infectivity in the supernatant of coinfected cells. Under these conditions, we found that PrPC, PrPSc and scrapie infectivity are recruited by both MuLV virions and exosomes. We propose that retroviruses can be important cofactors involved in the spread of the pathological prion agent."

Leblanc - EMBO J 2006 abstract / PubMed

Cells infected with scrapie and Creutzfeldt-Jakob disease agents produce intracellular 25-nm virus-like particles. L Manuelidis, ZX Yu, N Banquero, B Mullins. Proc Natl Acad Sci U S A 2007 Feb 6;104(6):1965-1970. "We had repeatedly found approximately 25-nm-diameter virus-like particles in highly infectious brain fractions with little prion protein (PrP), and therefore we searched for similar virus-like particles in situ in infected cell lines with high titers. Neuroblastoma cells infected with the 22L strain of scrapie as well as hypothalamic GT cells infected with the FU Creutzfeldt-Jakob disease agent, but not parallel mock controls, displayed dense 25-nm virus-like particles in orthogonal arrays. These particles had no relation to abnormal PrP amyloid in situ, nor were they labeled by PrP antibodies that faithfully recognized rough endoplasmic reticulum membranes and amyloid fibrils, the predicted sites of normal and pathological intracellular PrP. Additionally, phorbol ester stimulated the production of abnormal PrP gel bands by >5-fold in infected N2a + 22L cells, yet this did not increase either the number of virus-like arrays or the infectious titer of these cells. Thus, the 25-nm infection-associated particles could not be prions. Synaptic differentiation and neurodegeneration, as well as retroviruses that populate the rough endoplasmic reticulum of neuroblastoma cells, were not required for particle production. The 25-nm particle arrays in cultured cells strongly resembled those first described in 1968 in synaptic regions of scrapie-infected brain and subsequently identified in many natural and experimental TSEs. The high infectivity of comparable, isolated virus-like particles that show no intrinsic PrP by antibody labeling, combined with their loss of infectivity when nucleic acid-protein complexes are disrupted, make it likely that these 25-nm particles are the causal TSE virions that induce late-stage PrP brain pathology."

Manuelidis - Proc Natl Acad Sci U S A 2007 abstract / PubMed

Mechanistic Insights into Prion Curing by Novel Anti-Prion Compounds. S Webb, T Lekishvili, C Loeschner, S Sellarajah, F Prelli, T Wisniewski, IM Gilbert, DR Brown. J Virology 2007 Oct;81(19):10729-10741. "Congo red has little therapeutic potential for the treatment of these diseases due to toxicity and poor permeation of the blood-brain barrier. We have prepared two Congo red derivatives, designed without these liabilities, with potent activity in cellular models of prion disease. One of these compounds cured cells of the transmissible agent... Congo red derivatives that are effective at the cure of prion disease increased the degradation of abnormal PrP by the proteasome. Therefore, the principal mechanism of action of the Congo red analogues was to prevent inhibition of proteasomal activity by PrPSc."

Webb / J Virol 2007 abstract

Five Questions on Prion Diseases. A Aguzzi, C Zhu. PLoS Pathog 2012;8(5): e1002651. "Here we review the current knowledge on five issues relevant to prion diseases: (1) how do prions enter the body, (2) how do prions reach the central nervous system, (3) how do prions damage the CNS, (4) do mammals have an antiprion defense system, and (5) how can the prion problem be resolved for good." As for (4) Prnp -/- mice mice develop more or less normally yet cannot replicate prions... Upon inoculation, residual infectivity all but disappears within 4 days, indicating that prions—commonly regarded as the sturdiest pathogens on earth—can be cleared in vivo with astonishing efficiency and speed." For (5), they propose PrPC farm animals.

Aguzzi & Zhu / PLoS Pathog 2012 full article

A Proautophagic Antiviral Role for the Cellular Prion Protein Identified by Infection with a Herpes Simplex Virus 1 ICP34.5 Mutant. M Korom, KM Wylie, H Wang, KL Davis, MS Sangabathula, GS Delassus, LA Morrison. J Virol 2013 May;87(10):5882-5894. "We found that deletion of PrP in mice complements the attenuation of Δ68H, restoring its capacity to replicate in the central nervous system (CNS) to wild-type virus levels after intracranial or corneal infection. Cultured primary astrocytes but not neurons derived from PrP(-/-) mice also complemented the attenuation of Δ68H, enabling Δ68H to replicate at levels equivalent to wild-type virus. Ultrastructural analysis showed that normal astrocytes exhibited an increase in the number of autophagosomes after infection with Δ68H compared with wild-type virus, but PrP(-/-) astrocytes failed to induce autophagy in response to Δ68H infection."

Korom - J Virol. 2013 abstract / PubMed

Prions-Not Your Immunologist's Pathogen. MD Zabel, AC Avery. PLoS Pathog 2015 Feb 19;11(2):e1004624. Commentary/Review. The innate immune system responds, but not the adaptive immune system.

Zabel & Avery / PLoS Pathog 2015 full article

Frederick Seitz and the Anti-Smoking Subhumans

The anti-smokers' juvenile make-believe about Frederick Seitz should be a laughingstock - but consider everything else the scum have gotten away with.

Seitz has become the target of PeeCee lie & smear brigades for failing to follow their party line about global warming. "One scientist who joined both propaganda efforts was Dr. Frederick Seitz, a former president of the National Academy of Sciences. My colleagues at Vanity Fair magazine and I recently revealed that Seitz received $45 million from the RJ Reynolds tobacco company in the 1970s and 1980s for research that found no connection between smoking and cancer." (Global Warming — Bush's Climate of Fear. Script by Mark Hertsgaard. LinkTV, Sep 1, 2006.) This is nothing but a baldfaced lie. No such research exists. Is this fraud trying to pretend that because the prion research didn't even look at the issue of smoking and cancer, it's therefore guilty for not finding any? Hertsgaard and his corrupt colleagues at Vanity Fair magazine invented this garbage from whole cloth! They're nothing but lying sociopaths.

Global Warming — Bush's Climate of Fear / markhertsgaard.com

Articles in PubMed by Seitz (some of which may be his, others by someone else). Seitz died in 2008. Note that the New York Times parroted Hertzgaard's lies as if they are legitimate journalism, rather than pure fabrication, and made no attempt to determine whether any such research existed. (Frederick Seitz, Physicist Who Led Skeptics of Global Warming, Dies at 96. By Dennis Hevesi. New York Times, Mar. 6, 2008.)

Search: Seitz F / PubMed
Frederick Seitz, Physicist Who Led Skeptics of Global Warming / New York Times

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cast 02-21-15