TWiV 123: Contaminated prostates, absolute truth, and bleached worms

42Hosts: Vincent Racaniello, Alan Dove, and Rich Condit

On episode #123 of the podcast This Week in Virology, Vincent, Alan, and Rich talk about XMRV integration sites in prostate tumor DNA, the decline effect and scientific method, and the first virus of Caenorhabditis nematodes.

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51 thoughts on “TWiV 123: Contaminated prostates, absolute truth, and bleached worms”

  1. I have read doctor Deckoff Jones blog.
    and I want to say the following….

    Dear Government, Scientists, doctors & Nurses of the world.
    Please take pity on us.
    Fix what has happened.
    Please help us and please give us the treatment we deserve.
    we are human beings.
    Give us the help we need.

    Just please help us.
    A CFS sufferer.

  2. I posted this on the blog, but it needs mentioning again.

    There is substantial scientific evidence that HGRVs are human pathogens and none whatsoever that they are not.

    Firstly, XMRV integration sites were first discovered in prostrate DNA taken directly from patients. No cell lines of any kind involved. Cell line contamination not possible there.

    Also, the study in question is unable to say where the cell line has been “Analysis of 15 nude mouse strains indicated that none contained XMRV, but some strains potentially used to passage the xenograft contained both PreXMRV-1 and PreXMRV-2.”

    The abstracts posted in CROI present conclusions as fact when they are no such thing. The DU145 cell lines were screened for the presence of XMRV by Dong et al in 2007, and no XMRV was present as provirus or cDNA. Therefore, if integrated sequences were found within the cells, then the direction of transfer was from the human prostate DNA, which contained those sequence, to the cells in question. Similarly, the apparent appearance of XMRV, after the production of xenografts can be explained by the fact that the PCR system used was not sensitive enough to detect XMRV in the original tissue. We certainly have enough examples of that. The testosterone pellets used in the process however would ensure rapid replication of XMRV to the levels which the PCR system used could detect it.

    This is the reference showing how an increase in the level of NF-kappa B increases the replication rate of XMRV, published in the peer reviewed journal of virology.

    How does an increase in the level of NF-kappa B increase the replication rate of a contaminant?

    This is the reference showing the elevated rate of NF-kappa B in DU145 cells.

    If DU145 cells have XMRV integrated into their DNA, can anyone explain why the XMRV does not transcribe and the fact that DU145 cells do not express XMRV, given the high levels of nf-kappa b and oxidative stress known to exist within these cells?

    Finally, Kim et al. has found that XMRV is capable of making three insertions within a 100 kilobase region, and that the integration points for all of the 472 regions mapped were different. If the nucleotide positions were identical to the two sites identified in Garson et al. contamination must have come from the patient sample, not the DU145 cells.

    Now Kearney et al. has apparently been able, and I will use Alan Dove’s word’s here, “to detect XMRV in infected macaque blood (i.e. she can see it when it’s there) but unable to find it in any clinical specimens, including two that Lombardi et al. had reported as positive.” Now the titres in the infected monkeys would be massively higher than in human PMBC’s, with a natural infection pattern. That is artificial inoculation versus natural infection, and can be used to determine tissue tropism.

    The question is, did Kearney use the Lombardi assay to see if she could locate XMRV, which would be adhering to the scientific method?

  3. Cover-up and contamination theories
    While the days, weeks and months pass, the scientific community continues to work on what isn’t, instead of what is. The question of how a lab contaminant produces an immune response in patients hasn’t been addressed by any of the contamination theorists. And how do you manage to contaminate the patients’ samples at a higher rate than the controls when all samples were blinded and run at the same time? In fact, it is the patients that are contaminated with a family of MLV-related retroviruses, not Dr. Mikovits’ lab.

    This abstract was presented at CROI a few days ago:
    XMRV Probably Originated through Recombination between 2 Endogenous Murine Retroviruses during in vivo Passage of a Human Prostate Cancer Xenograft. Paprotka
    Many questions arise without the full paper, but it seems that far from showing XMRV to be a lab contaminant, the study shows what may in fact have happened. Human and mouse endogenous retroviruses recombined through subsequent passages in vivo (in mouse) to produce a fully replicative xenotropic exogenous retrovirus, that in fact may prove to be the most infectious human retrovirus yet. In animals, similar viruses are communicated casually. Lombardi et al demonstrated that this new human retrovirus is circulating in the blood of as many as 10 million Americans. A public relations nightmare. So what did the scientists who said this was impossible do? First they denied its existence, then tried to suggest results were the result of mouse parts in their reagents, but none of the arguments have in any way refuted the data of Lombardi et al or Lo et al, who rigorously ruled out contamination. What they have shown is that it is possible to produce XMRV in a lab. Like the murine retroviruses, recombination events produce new pathogenic variants. See my post from September 10 about Sandra Ruscetti’s work: Lessons from the murine retroviruses

    As for the 22Rv1 cell line being the source of XMRV contamination responsible for the whole mistaken affair, none of the labs involved in the Science paper Lombardi et al, have ever used this cell line. They couldn’t have contaminated subjects’ blood with virus produced by a cell line which all three investigators at different institutions can prove beyond a shadow of a doubt never entered their laboratories (personal communication). Sillier still, is the idea that this supposedly singular event was the source of infection, since it has only been around since 1999: A new human prostate carcinoma cell line, 22Rv1. Sramkoski

    My guess is that passing lots of human tissue through mice and then culturing in the laboratory for now more than four decades produced the conditions to enable a very unlikely event- by giving it many chances to occur. A probable place for this to have happened was in the creation of live attenuated virus vaccines where virus is made less virulent with multiple passes through animal cells in tissue culture. The earliest live polio vaccine was made by Hilary Koprowski using Swiss albino mouse brain cells. The first dose was administered to a child in 1950. He also used monkey kidney cells which were implicated in passing SV40 to humans. Albert Sabin’s live polio vaccine was produced from attenutated virus obtained from Koprowski.

    Mouse cells and the cells of other species have also been used over the years in the creation of other vaccines. Some vaccines, including attenuated Measles and Mumps in the MMR, are grown on duck and chick embryo cells. Domestic fowl have endogenous retroviruses, avian leukosis viruses (ALVs or ASLVs), that do very similar things to the gammaretroviruses. Recombination events are involved in pathogenicity and they can infect the cells of other species in tissue culture. XMRV requires the XPR1 receptor to infect cells. The XPR1 receptor is ubiquitous in mammalian cells. Lab mice are resistant by virtue of XPR1 polymorphisms. The alpha retroviruses use a receptor called TVB. TVB is a tumor necrosis factor receptor that is most likely the avian homolog of a TRAIL (TNF-related apoptosis-inducing ligands) receptor. Here is a paper about the receptor: A Fifteen-Amino-Acid TVB Peptide Serves as a Minimal Soluble Receptor for Subgroup B Avian Leukosis and Sarcoma Viruses. Knauss. The abstract contains the following sentence: “This peptide was sufficient not only for binding to ASLV-B but also for activating viral entry into mammalian cells that lacked the cognate viral receptor.”

    Here are two recent papers which should be giving someone pause, but there is no evidence that anything is changing in the status quo at the CDC. Head in the sand or worse?

    * Endogenous retroviruses as potential hazards for vaccines. Miyazawa
    * Isolation of an Infectious Endogenous Retrovirus in a Proportion of Live Attenuated Vaccines for Pets. Miyazawa

    Beta retroviruses, e.g. mouse mammary tumor virus (MMTV), may also be present in tissue culture of murine cells. The first PubMed paper seems to have been published in 1948 when the “milk factor” was first identified on electron microscopy in tumor prone mice:
    A particulate body associated with epithelial cells cultured from mammary carcinomas of mice of a milkfactor strain. Porter
    MMTV is a vertically transmitted endogenous retrovirus that causes cancer when it inserts near an oncogene. Vertical transmission of murine breast cancer by adoptive nursing was demonstrated in 1936 by Dr. John Joseph Bittner. It was formerly classified as a simple retrovirus, but transcribes a regulatory protein similar to HIV, so is the first complex murine retrovirus identified. MMTV codes for a superantigen that stimulates T lymphocytes which in turn stimulate B cell proliferation. At puberty the virus enters the mammary glands with migrating lymphocytes and infects proliferating epithelial cells. MMTV can be transferred exogenously or endogenously through the germ cell line; the later infection produces virus present in every cell of the body. Mice that acquire the infection this way have a higher incidence of tumors. In lymphocytes, it may cause a T cell leukemia. MMTV has an enhancer region in its U3 long terminal repeat that activates the virus in mammary cells. It is activated by estrogen and other glucocorticoids, including progesterone. It is especially responsive to the synthetic steroid Dexamethasone which is used to induce lactation in the dairy industry. And a few new MMTV papers.

    * Mouse Mammary Tumor Virus Molecular Biology and Oncogenesis. Ross
    * Mouse mammary tumor like virus sequences in breast milk from healthy lactating women. Johal
    * Mouse Mammary Tumor Virus in Anti-Mitochondrial Antibody Producing Mouse Models. Zhang
    * Prolactin-induced mouse mammary carcinomas model estrogen resistant luminal breast cancer. Arendt

    Gamma retroviruses are used as the backbone for gene vector therapy. It is known that retrovirus-mediated gene therapy of SCID-X1 can lead to leukemia and lymphoma because proto-oncogenes can be activated as a consequence of vector integration. Gammaretroviral vectors preferentially integrate near transcriptional start sites and CpG islands.

    * Insertional oncogenesis in 4 patients after retrovirus-mediated gene therapy of SCID-X1. Hacein-Bey-Abina
    * A novel model of SCID-X1 reconstitution reveals predisposition to retrovirus-induced lymphoma but no evidence of gammaC gene oncogenicity. Scobie
    * Murine Leukemias with Retroviral Insertions at Lmo2 Are Predictive of the Leukemias Induced in SCID-X1 Patients Following Retroviral Gene Therapy. Davé

    Another place for it to have happened or to be happening, as demonstrated by the Paprotka CROI presentation, is in the creation of human to mouse xenografts. It turns out that by transplanting human tumors into mice and passing the tissue through subsequent generations, it becomes possible to establish tumor cell lines that couldn’t be established before. Also xenografts are used to study tumors, e.g. specific tumor immunogenicity and response to treatments. Why the presumption that the recombination that occurred in the Paprotka experiment was a unique event? They were fiddling with mouse viruses in the lab in the 1930s. The first outbreak of Epidemic Neuromyasthenia was in LA in 1934 and involved hospital staff. And suddenly the CDC is worried about lab workers and testing archived specimens. It would be funny if it weren’t so incredibly sad.

    Take a look at this fascinating paper that covers a lot of material including the problems with xenotransplantation:
    The discovery of endogenous retroviruses. Weiss

    Are we to believe this recombination event occurred only once and that a pathogenic MLV-related human retrovirus is only produced by one particular cell line? Told to us by some of the very scientists that said it was impossible? Anyone smell a cover-up? Much easier to destroy a seminal work than admit that there may in fact be a family of XMRVs. Careful reading of the Science paper shows that the monoclonal antibody used to detect XMRV envelope in Lombardi et al detects all known xenotropic, polytropic and ecotropic MLVs. Antibodies made by patients recognized specific envelope and gag proteins. PCRs were optimized for sensitivity, not specificity. And quite possibly there are many other recombinant animal retroviruses infecting humans as well, created in laboratories and injected into almost everybody in the industrialized world, because of arrogance.

    Putting it all together, it seems quite plausible that batches of vaccines containing retroviruses that are infectious to humans have been going out for over half a century. Much of what I’ve written here has been known but ignored for a long time. The assumption was made that endogenous animal retroviruses couldn’t harm people. It’s becoming clear that this was a very incorrect assumption.

    So is there motivation for the cover-up and baseless attacks against Dr. Mikovits? They cannot attack the data because it is impeccable. Coffin and Stoye wrote the commentary in Science. Have they retracted it? Coffin said at the CFSAC in October 2009 that “This is as good as it gets…”. If this were HIV/AIDS, the year would be 1983. We have much still to learn about human MLV-related viruses. Is it even remotely possible that the findings reported in Lombardi et al were the result of contamination of their reagents? No more likely than that the retrovirus described by DeFrietas et al in 1991 was contamination. Had the CDC done something then, we could have prevented the autism epidemic and a second generation of infected people. Instead they buried DeFrietas’ work by withdrawing all funding. Deja vu?

  4. I have ME/CFS and tested positive for XMRV through WPI’s lab. I want to make it clear though that I do not believe in cover-up and conspiracy theories that people continuously discuss in the comments. Also ME/CFS patients as a whole just want the truth it is just the small vocal minority that insists that science and government is some how trying to cover this up.

    I really wanted to thank you Dr. Racaniello for your continued discussion on this topic. It really helps break down the science to a point that I can understand. I would love to see a TWiV with Dr. Mikovits and see what her counter arguments to many of the recent XMRV papers.

  5. “Now the titres in the infected monkeys would be massively higher than in human PMBC’s, with a natural infection pattern.”

    [citation needed], as they would say on Wikipedia.

  6. Agreed dr Dove.
    We need answers I think this group of patients have been mistreated for far to long – its time for some serious answers!

  7. If we are dealing with human retroviruses from a lab, We have to treat this as a public health emergency!

  8. Jamie Deckoff-Jones MD

    I wrote the piece posted above. I am a doctor, not a virologist, and this post covers a lot of ground that is tougher than rocket science. I have many questions and much to learn, but I’ve rewritten the sentence in the second paragraph that starts with “Human and mouse…”. Dr. Racaniello, is this correct?
    Endogenous retroviruses recombined in or infected human tumor cells through subsequent
    passages in vivo (in mouse) to produce a fully replicative xenotropic exogenous retrovirus..

    Jamie Deckoff-Jones MD

  9. On day 275, two animals (RIl- 10 and RYh-10) were administered 0.308 ml of a cocktail of recombinant XMRV proteins including gag p15 (2.3 μmole), gag p12 (1.1 μmole, gag p30 (3.1 μmole, gag p10 (2.9 μmole) – Onlamoon et al (2011)

  10. Doctor Deckoff-Jones.
    I supported what your saying in my post, I did mean what you described.
    (Human retroviruses) which were made in the lab from mice.

  11. Which part of your lengthy comment are you asking Vince to fact-check? Correcting the whole screed would take a very, very long time.

  12. Nobody has established what a “natural infection pattern” is for XMRV in humans, so you can’t possibly know whether the monkeys’ titers are higher, lower, or the same.

  13. Only that one sentence. It was the most difficult sentence for me in the whole piece. I didn’t post my blog here; someone else did. I actually changed that sentence on the blog shortly after I posted it. I’m looking forward to seeing the full paper.

    Jamie Deckoff-Jones

  14. Searching PubMed for “Schalberg”[Author] returns 0 hits. Searching instead for “xmrv pbmc” gives a cultured cell study, a negative study on CFS, and the Lo et al. paper. Given how new this whole field is, it’s not surprising that we don’t have any definitive answers on what a “natural infection pattern” looks like. Getting that answer would require a fairly robust clinical screen of a reasonable number of people, but a prerequisite for that is having more than one lab that can reproducibly detect XMRV in clinical specimens. We’re not there yet.

  15. Lo et al. virus sequence per 4000 PMBCs 1000 viral copies per 8ml of blood several orders of magnitude less than the concentration of viral sequences used to inoculate the monkeys. There are many labs now finding XMRV in both prostate cancer and ME/CFS.

  16. Schlaberg et al.

    “determined XMRV proviral loads in these tissues. Using XMRV
    plasmid DNA as a standard, we estimated that qPCR-positive
    prostate cancers contained 1–10 copies of XMRV DNA per 660
    diploid cells”

    XMRV is present in malignant prostatic epithelium and is associated with prostate cancer, especially
    high-grade tumors.

    Robert Schlaberga,1, Daniel J. Choeb, Kristy R. Browna, Harshwardhan M. Thakerb, and Ila R. Singha,b,2

    aDepartment of Pathology and Cell Biology, Columbia University Medical Center, 622 West 168th Street, New York, NY 10032; and bDepartment of Pathology, University of Utah, Emma Eccles Jones Medical Research Building, 15 North Medical Drive East, Salt Lake City, UT 84112

    Communicated by Stephen P. Goff, Columbia University College of Physicians and Surgeons, New York, NY, July 20, 2009 (received for review April 29, 2009)

  17. And many more labs failing to find it. The prostate cancer studies are all over the map – XMRV is there in non-tumor cells, or there in tumor cells, or not there at all. Lo et al. didn’t find XMRV anywhere, only murine-like viruses that look disturbingly similar to some that were shown to be contaminants in another lab. It’s a proper mess.

    As I said, there aren’t enough data to say what a “natural infection pattern” looks like in humans, if indeed it occurs. Until the studies reported at CROI are published, you really have no idea how sensitive or insensitive their assays were anyway, so please stop blowing smoke.

    The jury is still out. However, it looks like the bailiff is saying “all rise,” and the court is coming back into session.

  18. Negative studies prove nothing, neither do beliefs that fail to meet the minimum standards of a hypothesis. Lo et al. confirmed Lombardi et al. It is the same virus. They look nothing like mouse viruses as you well know. Lombardi et al. never used 22Rv1. Where could this imaginary contamination have come from? It doesn’t exist, as there is zero evidence for it.

    I’m afraid we know plenty from the abstracts and presentations at CROI. None of it is holding up to scrutiny as I have easily demonstrated. So too have I presented the evidence on the natural infection pattern of the virus.

  19. Here is further evidence.

    EID Journal Home > Volume 16, Number 6–June 2010

    Volume 16, Number 6–June 2010


    Xenotropic Murine Leukemia Virus–related Gammaretrovirus in Respiratory Tract

    Nicole Fischer, Claudia Schulz, Kristin Stieler, Oliver Hohn, Christoph Lange, Christian Drosten, and Martin Aepfelbacher
    Author affiliations: University Medical Center Hamburg-Eppendorf, Hamburg, Germany (N. Fischer, C. Schulz, K. Stieler, M. Aepfelbacher); Robert Koch-Institute, Berlin, Germany (O. Hohn); Leibniz-Center for Medicine and Biosciences, Borstel, Germany (C. Lange); and University of Bonn Medical Centre, Bonn, Germany (C. Drosten)

    The concententration of XMRV virions is between 100 and 1000 copies per ml from the quantitative PCR used in the above study.

    In prostate studies serological methods are consistently more sensitive in detecting xmrv than PCR and using VP62 to calibrate PCR has been proved to be unable to detect XMRV in clinically positive samples. That totally explains the results in the studies that failed to finda human gammaretrovirus.

  20. The really worrying thing is that, if XMRV really is just a contaminent and leads on to nothing for CFS, patients are going to be stuck with the worthless quackery they’ve already had to endure for 20 years.

    Rather than lumping together all patients suffering with severe ‘fatigue’ and trying to manage them, work needs to be done to identify the different causal mechanisms for their disabilities.

  21. To debunk crackpot conspiracy theories, I’ll charge a nuisance fee of $5,000/hour. Prospective clients must make a non-refundable payment for the first 8 hours up front, and pass a basic test of logic, critical thinking, and reading comprehension.

    I do not suffer fools cheaply.

  22. It appears that John Coffin disagrees with Alan Dove.

    Science Now, “Now Coffin is convinced that “it is all contamination.”

  23. It appears that John Coffin disagrees with you Alan. Please see the Science now article.

    Now I realise this is not your area, so you may think he means contamination with a mouse virus, but in this case he is referring to recombination, where two harmless “fossilised” viral segments in mouse DNA recombine to form virulent pathogenic viruses.

    Alan you do know what XMRV is don’t you?

  24. I’m sure you would like to know why the negative studies are negative, so here it is.

    All the negative studies used the VP62 clone.

    The Urismans primers were set for VP-35 gag. The only thing Lombardi et al kept for their RT-PCR assay were the cycling condtions, but they used different outer primers, and then they dropped the annealing temperature so that the gibbs free energy for template primer formation would be more negative. Thereby lowering the stringency of the primers.

  25. I’m sure you would like to know why the negative studies are negative, so here it is.

    All the negative studies used the VP62 clone.

    The Urismans primers were set for VP-35 gag. The only thing Lombardi et al kept for their RT-PCR assay were the cycling condtions, but they used different outer primers, and then they dropped the annealing temperature so that the gibbs free energy for template primer formation would be more negative. Thereby lowering the stringency of the primers.

  26. Actually I lied, there were plenty of other changes the other group chose to make in order to not find the virus.

  27. Actually I lied, there were plenty of other changes the other group chose to make in order to not find the virus.

  28. I would write it as follows: “Two endogenous murine retroviruses
    related to XMRV recombined in human prostate tumor cells that were
    passaged in mice. The recombinant retrovirus produced is nearly
    identical to XMRV that has been isolated from patients.”

  29. Yes I would say that as well.

    and I would say please anyone who can put right what is wrong please do so.

  30. 22Rv1 has not been fully sequenced, and multiple labs are finding a greater diversity than originally published. It is also not certain if the assays used in Pathak et al is capable of detecting XMRV in low levels.

  31. I can’t edit that post below, so here are my additions.

    Lets not forget that XMRV was first isolated by urisman and others from the polyadenylated RNA of prostate cancer sufferers. If the recobinant proviral DNA entered the human population in this way, then Urismans findings mean that it is now replicating.

    The problem once again is that Pathak et al. did not establish the fact that his PCR assay could detect XMRV in vivo conditions which means that he simply does not know whether XMRV was present in the prostate tissue prior to xenografting.

    The “appearence” of XMRV can easily be explained by the increase in transcription induce by the testosterone used in xenografting raising the titre to a level where his assay had the clinical sensitivity needed to detect XMRV in the cell line.

    Nearly identical is a very loose term and not a scientific description, what is the sequence homology in percentage terms in the integrase and VRA and VRB region.

    Moloney murine leukaemia virus could be described as nearly identical to XMRV, can you explain what you mean by nearly identical?

    Pathak cannot even establish that the mouse strains containing what he terms as pre XMRV were even used in the formation of the cell line.

    Can you give an example when two ervs have been known to combine to form a replicative virus?

  32. Prostate tissue of XMRV positive patients were tested by IHC by urisman and found to be positive.  Contaminants dont make proteins, replicating viruses do.

    “IHC on human tissues was performed on a Benchmark Ventana Autostainer (Ventana Medical Systems, Tucson, Arizona, United States). Unstained, formalin-fixed, paraffin-embedded prostate sections were placed on electrostatically charged slides and deparaffinized followed by a mild cell conditioning achieved through the use of Cell Conditioner #2 (Ventana Medical Systems). The concentrated R187 monoclonal antibody against SFFV p30 Gag was dispensed manually onto the sections at 10 μg per ml and allowed to incubate for 32 min at 37 °C. Endogenous biotin was blocked in sections using the Endogenous Biotin Blocking Kit (Ventana Medical Systems). Sections were washed, and biotinylated ImmunoPure Goat Anti-Rat IgG (Pierce Biotechnology, Rockford, Illinois, United States) was applied at a concentration of 4.8 μg per ml for 8 min. To detect Gag protein localization, the Ventana Enhanced Alkaline Phosphatase Red Detection Kit (Ventana Medical Systems) was used. Sections were briefly washed in distilled water and counterstained with Hematoxylin II (Ventana Medical Systems) for approximately 6 min. Sections were washed, dehydrated in graded alcohols, incubated in xylene for 5 min, and coverslips were added with Cytoseal (Microm International, Walldorf, Germany). Negative controls were performed as above except without the addition of the R187 monoclonal antibody.”

  33. X-MLV’s were originally believed to not be capable of infecting cells of their mouse host. Yet, this has clearly been shown to not be true. The authors of Pathak et al. should have realised this. The transfer has been from the infected cell line to the mice in the experimental environment. Their conclusions are not supported by the evidence.

  34. Xenotropic MLVs by definition do not infect the mouse host. That is
    why implantation of a human tumor was required to allow infection by
    the endogenous XMRVs and generation of a recombinant virus.

  35. “The mouse xenotropic MLVs (X-MLVs) were originally defined by their inability to infect cells of their natural mouse hosts. It is now clear, however, that X-MLVs actually have the broadest host range of the MLVs. Nearly all nonrodent mammals are susceptible to X-MLVs, and all species of wild mice and several common strains of laboratory mice are X-MLV susceptible. (Kozac ,2010)”

    Pathak’s own researchers have let him down in this matter, because his conclusion that lab mice could not have been infected by PCR negative XMRV and thus must have been transfered to the cell line from the mice, that might have been used in xenograft formation, is in the light of the above evidence totally unsupportable.

    Xenotropic MLV class virus were once thought to not be able to infect mice, but xenotropic MLVs are now known to have the widest host range of all MLV class viruses.

    Viruses which are classified as xenotropic can infect wild and lab mice. There are any number of them, would you like any examples?

    Viruses with the same structure as XMRV are known to infect mice.

  36. Note that not all lab strains of mice are infectable with xenos. But
    it doesn’t matter what you think about the ability of xenos to infect
    mice. The fact is that the human prostate tumor did not contain XMRV,
    while the tumor acquired it after passage in mice as did the 22Rv1
    cell line. But you should wait to read the paper when it’s released,
    as it might address all your concerns.

  37. From Urisman et al, 2006.

    “Phylogenetic trees constructed using available mammalian type C retroviral genomes and representative full-length proviral sequences from the mouse genome (Figures 3 and S2) showed that the newly identified virus is more similar to xenotropic and polytropic than to ecotropic genomes. Based on these findings we propose the provisional name Xenotropic MuLV-related virus (XMRV) for this agent.”

    This virus is very similar to MLV viruses once considered not to be able to infect mice, but now it is known that these X-MLVs have the widest host range of all up to and including laboratory mice.

  38. No, it is not fact. The observation can be readily explain that the PCR assay was not good enough. Remember also that it has not been proven that this mouse strain had any part to play in the creation of the 22Rv1 cell line. I am quiet happy to explain why, if you would like?

    Here is an example of xenos in mice:

    Common Inbred Strains of the Laboratory Mouse That Are Susceptible to Infection by Mouse Xenotropic Gammaretroviruses and the Human-Derived Retrovirus XMRV

    Surendranath Baliji, Qingping Liu, and Christine A. Kozak*

  39. The only fact was that they were unable to detect XMRV in the cells before xenograft formation. It is not fact that XMRV was not present.

    Many PCR assays have simply been unable to detect XMRV in people known to be infected.

    The authors should have used a more sensitive assay, or at least a PCR assay with a proven ability to detect XMRV in tissues if present.

    It is not a matter of what I think. The ability of MLV viruses described as xenotropic to infect mice is now scientific fact.

    It is of note that involvement of the mouse strain described by Pathak in the creation of the 22Rv1 cell line has not been established

    The conclusions presented by Pathack are a hypothesis and not fact. As his observations are quite unable to explain how XMRV was first isolated from polyadenylated RNA, extracted from the tissues of prostate cancer patients. The hypothesis cannot even be regarded as a scientific hypothesis.

  40. This matter concerns a lot of very sick people that are suffering greatly and by any measure haven’t gotten the research they deserve over a very long period of time. As a host of this podcast you should really take the high road and cut out the mocking. At best you make a fool of yourself, at worst you provoke and perpetuate the very cynicism and mistrust from the commenters that seem to bother you.

    Its fine if you are persuaded by the arguments of the above studies at this point and have come to the conclusion that they refute the original lombardi paper. But some of us would like to see more direct evidence before coming to that conclusion.

    Have some compassion.

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