ProHealth: Plague: An interview with Judy Mikovits

Firestormm

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Plague: An Interview With Judy Mikovits

1 June 2014



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.”

...

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 dilemma 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....

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.

Read more: http://www.prohealth.com/library/showarticle.cfm?libid=18960
 
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natasa778

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more good bits

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. We may have avoided something that could have infected everyone, because Silverman was sending XMRV all over the world.)

How many people did we save by learning that XMRV could be aerosolized and spread to immune-compromised individuals or lab workers?

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.
 

Firestormm

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So what would motivate her to use this description do you believe?
I guess you would have to read her book and possibly find out. Of course talking of ME or CFS (whatever your preference of name) as a 'plague' is rather sensational.

Nice word isn't it? Implies an infectious virus or bacteria. Mikovits was ever talking about XMRV and retroviruses and how it was spread through the air.

Kent Mc. is not someone I would take seriously either. Indeed them teaming up to write such a book made me even less likely to buy it or into their notions. Check out his 'work' on Austism and his promotion of quackery on his sites: actually I wouldn't. It's a risk to your health.

Doing my best here to be polite.

Non-HIV AIDS as a banner has been doing the rounds for a while. Promoted by some user called something 'Boston' if I recall. And it stemmed out of XMRV fiasco. Might also have been influenced by Klimas and what she said in her often misused quote.

When Nancy said 'I would rather have HIV than ME' the full quote was in relation to her work - with HIV and ME patients - and how relatively better understood, funded and treated HIV patients were. It was a good quote. But has been cut short in places - at least it was - to give a heightened sense of... I don't know what the word is.

Comparing ME to AIDS is inherently wrong in my view and for what it's worth. But people do. AIDS comes up and sometimes in the context of the organisation - the working together to find a cause to find funding to gain better research and reduce the stigma - these lessons would be better used in our 'community' but tend to get lost to the notion that ME is AIDS by a different name.

It's like a lot of things that are not currently understood and are marginalised. Some people choose to sensationalise to grab attention. Reaching for theories based on nothing or on very little. Andrew Wakefiled and MMR and Austism being another example...

I could go on. But will probably find this comment deleted when next I return.

Apparently we can't criticise anyone in this 'community' if we don't agree with them. Got to tow the party-line. Whatever the heck that is these days.
 

Firestormm

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@Lillybelle

Here's a Q&A with Klimas I just found. I haven't time (need to get to doctors for exam) to dig out her oft-cited remarks about HIV and CFS but it's similar in context to this. It comes from Oct. 2009 so just following publication of the XMRV-CFS paper:

http://consults.blogs.nytimes.com/2...-fatigue-syndrome/?_php=true&_type=blogs&_r=0

Links Between H.I.V. and XRMV?

Q.
I found the comparison to H.I.V. (all because it happens to be another retrovirus) to be alarmist, unnecessary and at worst, the kind of sensualist factoid reporting that’s more typical of a tabloid! From what I gather … the link between the two is weak and general at best.

What angers me is that the comparison to H.I.V. is completely out of context; there are many retroviruses that are not known to cause any pathologies at all – comparing it to the one that is most well known and feared is simplistic and quite simply wrong. We should not forget that retroviruses have been common through out human history, and while some do not cause disease at all, most are nowhere near as extreme as H.I.V.

To compare the virus to H.I.V. is to create undue alarm and suffering to people who are already dealing with a difficult disease. Not only is the comparison useless outside its context, it does nothing to provide useful information to the reader.

I ask that you think of the moral consequences of your sloppy comparison — the horror and anguish of those that might have thought that it might be as debilitating as H.I.V., as well as the dread of the thought of potentially passing it on to another person.
David

A.
Dr. Klimas responds:

You make a good point. This is one study, the results needs to be validated, then the next study will look at treatment options. And you are right, some retroviruses are seemingly benign, whereas others are pathogens.

But I hope you are not saying that C.F.S. patients are not as ill as H.I.V. patients. My H.I.V. patients for the most part are hale and hearty thanks to three decades of intense and excellent research and billions of dollars invested. Many of my C.F.S. patients, on the other hand, are terribly ill and unable to work or participate in the care of their families.

I split my clinical time between the two illnesses, and I can tell you if I had to choose between the two illnesses (in 2009) I would rather have H.I.V. But C.F.S., which impacts a million people in the United States alone, has had a small fraction of the research dollars directed towards it.

Despite these limitations, there has been considerable effort to understand the cause and develop effective treatments. The Whittemore Peterson Institute should be congratulated for its outstanding work, performed in a brand new center paid for with private donations, state money and N.I.H. collaboration. Creative research and creative financing!
Things have changed obviously since then. But I think you can get the point she is making. Her point is still repeated now - but of course XMRV was proven a contaminant. Still I think Nancy would happily state her patients with CFS are less well cared for than those she sees with HIV and very sick. Shame the same can't be said for patients with HIV in other parts of the world of course who don't get treatment and do develop AIDS and die - horribly.

But those who still believe some sort of retrovirus - undiscovered/unreported/unresearched - might be responsible (or even is responsible) or even those who think it could be a virus: might also think 'NON-HIV AIDS' is a useful name for CFS or ME.

I do not.
 

Lillybelle

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@Lillybelle

Here's a Q&A with Klimas I just found. I haven't time (need to get to doctors for exam) to dig out her oft-cited remarks about HIV and CFS but it's similar in context to this. It comes from Oct. 2009 so just following publication of the XMRV-CFS paper:



Things have changed obviously since then. But I think you can get the point she is making. Her point is still repeated now - but of course XMRV was proven a contaminant. Still I think Nancy would happily state her patients with CFS are less well cared for than those she sees with HIV and very sick. Shame the same can't be said for patients with HIV in other parts of the world of course who don't get treatment and do develop AIDS and die - horribly.

But those who still believe some sort of retrovirus - undiscovered/unreported/unresearched - might be responsible (or even is responsible) or even those who think it could be a virus: might also think 'NON-HIV AIDS' is a useful name for CFS or ME.

I do not.
@Firestormm I appreciate the information and the thoughtful evaluation you have given this response. I have been researching the Mikovitz story trying to understand the whole retrovirus hypothesis and put it into context with Cheney's virus outbreak proposal in Nevada in the 80's.

When I first saw Dr Mikovitz background in cancer/HIV, and her dedication to M.E./CFS research I was impressed and even though the viral proposal (I hadread) had come to a dead end I was surprised upon reading the interview above that, it seemed that she believed a virus was involved still (2014). However she does say in interview above she didnt believe causality, rather correlation which are 2 different things statistically.

What I thought was interesting was how the mouse research (allegedly?) created arange of new retroviruses via the research process. I'm not sure if this is true? Are there other studies demonstrating this?
Anyway, I feel (1 person sample) that the immune system is compromised by this disease M.E./CFS. Well I most certainly didnt have constant mucous, middle ear infection and fluid in the perycardium (chest pain) forno reason before I got sick. So whilst fatigue isa problem, I most certainly have a comprimised immune system.

So whilst I agree it is sensational and alarmist to use a label like non HIV aids. I do believe ME/CFS is an acquired Immune system deficiency. In regards to Boston, (Karen Lambert)she has been on her plight for many years. Here is testimony to the Chronic Fatigue Syndrome Advisory Committee (CFSAC) Meeting Day 2 June 14, 2012(?) in the US about her Negative HIV AIDS. Here is her testimony:

And website:http://www.cfsstraighttalk.blogspot.com.au/

I dont buy into this by the way. But its interesting.
 

Sean

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Kent Mc. is not someone I would take seriously either. Indeed them teaming up to write such a book made me even less likely to buy it or into their notions. Check out his 'work' on Austism and his promotion of quackery on his sites: actually I wouldn't. It's a risk to your health.
Also check out Kent's comments here on PR a while back about Lipkin (read through to the end of the thread). Disgraceful smear merchant.

I am appalled that Mikovits has chosen to team up with Heckenlively.

As I said, I will be donating the price of their book to the microbe discovery project.
 
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heapsreal

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I would like to see the early 1990s retrovirus looked into. Dam i can't remember her name, the scientist from back then in oslers Web. And some type of comparison, was it the same 'thing' they were looking at or 2 different retroviruses and is technology different now and could show things differently to the 1990s retro? ?

deFreitus virus???
 

Iquitos

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Since AIDS means Acquired Immune Dysfunction, and I believe that's what ME is, I'm fine with calling it non-HIV AIDS. The latest research on AIDS finds the retrovirus imbeds itself in the patient's DNA and then the immune system can't deal with it. There's plenty of ME research that indicates the distinct possibility that some pathogen, perhaps several pathogens, do the same in ME.

And yes, it was Elaine DeFreitas. Info on her patent, which mentions a retrovirus she calls CAV:

http://forums.phoenixrising.me/inde...ng-revelations-from-wistars-world-patent.115/
 
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Here is my problem. I think you need certain parameters to be considered for AIDS. I am not there, yet I have ME.
Again maybe a subgroup.
I DO NOT HAVE LOW CD4, I HAVE LOW CD56.
Is like saying Sojern is AIDS (low CD3), Lyme (CD57)...... Argggggg.:bang-head::bang-head::bang-head::bang-head::bang-head::bang-head::bang-head::bang-head::bang-head:

Idiopathic CD4+ T-lymphocytopenia, or ICL, is an immunodeficiency syndrome in which human immunodeficiency virus, or HIV, cannot be detected. Because HIV is the causative agent of acquired immune deficiency syndrome (AIDS), ICL can be referred to as Non-HIV AIDS. As in AIDS patients, Non-HIV AIDS patients exhibit reduced numbers of CD4+ T-lymphocytes, and many Non-HIV AIDS patients have developed the opportunistic infections or otherwise rare cancers associated with AIDS.
 

heapsreal

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In Japan they call cfs natural killer cell disease as they find many with low nk function. Thats pretty much getting to the common aquired immune defiency without having to relate it to another disease,?? Researchers have also found many cfsers have poor cd8 t cell function.

NK/ T cell dysfunction i think describes us quite well going by whats found in research so far??
 
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Frequent Detection of Infectious Xenotropic Murine Leukemia Virus (XMLV) in Human Cultures Established from Mouse Xenografts

Purpose

To investigate the frequency of xenotropic murine leukemia virus (MLV) presence in human cell lines established from mouse xenografts and to search for the evidence of horizontal viral spread to other cell lines.

Results

Six of 23 (26%) mouse DNA free xenograft cultures were strongly positive for MLV and their sequences had greater than 99% homology to known MLV strains. Four of five available supernatant fluids from these viral positive cultures were strongly positive for RT activity. Three of these supernatant fluids were studied to confirm the infectivity of the released virions for other human culture cells. Of the 78 non-xenograft derived cell lines maintained in the xenograft culture-containing facilities, 13 (17%) were positive for MLV, including XMRV, a virus strain first identified in human tissues. By contrast, all 50 cultures maintained in a xenograft culture-free facility were negative for viral sequences. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3218386/


Generation of Multiple Replication-Competent Retroviruses through Recombination between PreXMRV-1 and PreXMRV-2 2013 Aug 21

1. Krista Delviks-Frankenberrya, Tobias Paprotkaa*, Oya Cingözc*, Sheryl Wildtd, Wei-Shau Hub,

2. John M. Coffinc and Vinay K. Pathak

Retroviral recombination allows the reassortment of mutations and genetic polymorphisms, leading to the generation of RCRs from otherwise defective parental viruses.In addition, these studies indicate that retroviral recombination is crucial for generating recombinants by combining functional cis and trans elements from the parental proviruses and that selection for these functional elements results in the formation of novel RCRs.

Conclusion: To determine their potential to generate RCRs (replication-competent retroviruses), 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. http://jvi.asm.org/content/87/21/11525.long


Xenotropic MLV envelope proteins induce tumor cells to secrete factors that promote the formation of immature blood vessels.

Murgai M1, Thomas J, Cherepanova O, Delviks-Frankenberry K, Deeble P, Pathak VK, Rekosh D, Owens G. 2013 Mar 27;

CONCLUSIONS:
Together these results indicate that xenotropic MLV envelope proteins are sufficient to induce the production of factors by tumor cells that suppress vascular SMC differentiation, providing evidence for a novel mechanism by which xenotropic MLVs might alter tumor pathogenesis by disrupting tumor vascular maturation. Although it is highly unlikely that either XMRV or B4Rv themselves infect humans and are pathogenic, the results suggest that xenograft approaches commonly used in the study of human cancer promote the evolution of novel retroviruses with pathogenic properties. http://www.ncbi.nlm.nih.gov/pubmed/23537062


Infection of xenotransplanted human cell lines by murine retroviruses: a lesson brought back to light by XMRV 17 June 2013 Front. Oncol., | doi: 10.3389/fonc.2013.00156

Heidi A. Hempel1, Kathleen H. Burns1,2, Angelo M. De Marzo1,3 and Karen S. Sfanos1,3*
  • 1Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD, USA
  • 2Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA
  • 3The Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, MD, USA
Infection of xenotransplanted human cells by xenotropic retroviruses is a known phenomenon in the scientific literature, with examples cited since the early 1970s. However, arguably, until recently, the importance of this phenomenon had not been largely recognized.

The emergence and of Xenotropic Murine leukemia virus-Related Virus (XMRV) as a cell culture contaminant as opposed to a potential pathogen in several human diseases, notably prostate cancer and Chronic Fatigue Syndrome, highlighted a potential problem of murine endogenous gammaretroviruses infecting commonly used human cell lines.

Subsequent to the discovery of XMRV, many additional cell lines that underwent xenotransplantation in mice have been shown to harbor murine gammaretroviruses.

Such retroviral infection poses the threat of not only confounding experiments performed in these cell lines via virus-induced changes in cellular behavior but also the potential infection of other cell lines cultured in the same laboratory.

Thus, the possibility of xenotropic retroviral infection of cell lines may warrant additional precautions, such as periodic testing for retroviral sequences in cell lines cultured in the laboratory.


How Can Xenotropic Murine Leukemia Virus-Related Virus (XMRV) Contamination be Prevented
February of 2014. This study looked at how to prevent the infection of lab workers. The publication describes XMRV as a lab creation which is capable of infecting human cells and integrating its genome into that of the host. Therefore, XMRV virions and XMRV-infected cells are considered as biosafety level 2 organisms. http://aem.asm.org/content/early/2014/02/10/AEM.04064-13.abstract
 

Lillybelle

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Thanks @Ernie in laymans terms then. Yes, experimenting on mice can cause new viruses which can then infect lab workers and contaminate the mice involved in the experiment. Great:) sounds like a top job for the poor lab technicians. Or does it make them9lab technicians) immune to the new virus. And is the virus then passed on by breathing, touching coughing etc?
 
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Infectious Disease Risk to Public Health Posed by Xenografting

This chapter was drawn largely from the workshop Session II: Infectious Issues. Thus, the majority of the chapter summarizes workshop presentations. Where useful for background, some sections have been supplemented with additional information. The chapter, however, is not intended as an in-depth analysis and summary of the field of animal-to-human infectious diseases. 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.
 
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Conclusions and Recommendations
The following conclusions and recommendations are based on workshop presentations and discussions, as well as review of relevant materials and extensive discussions among the committee. This chapter presents those conclusions and recommendations along with the key points that underlie them, but it does not duplicate in detail material presented in previous chapters of this report.

The progress of basic science in the field of xenotransplantation has been rapid, and clinical trials of specific applications of xenotransplantation are under way. 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. The committee concludes that, although the degree of risk cannot be quantified, it is unequivocally greater than zero.
 

Lillybelle

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Infectious Disease Risk to Public Health Posed by Xenografting

This chapter was drawn largely from the workshop Session II: Infectious Issues. Thus, the majority of the chapter summarizes workshop presentations. Where useful for background, some sections have been supplemented with additional information. The chapter, however, is not intended as an in-depth analysis and summary of the field of animal-to-human infectious diseases. 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.
So, is this what definitely happened with Mikovits xmrv virus research and how the samples were contaminated?
If so do those lab workers and Mikovits herself nowcarry one of these new retroviruses? Or is that unknown?