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Xenotropic MLV's can infect many mammals and also (wild) mice


waitin' fer rabbits
South Texas
Hey Urban
You are quite right about the USC and UC (LA) rivalries my apologies and I will make the corrections. I was using the information from the Keck School of Medicine Time line. That can be found here (read more) Some help with the history would be lovely.

Keck School of Medicine | 1880 to Present

The University of Southern California is founded as California’s first research university.

USC's College of Medicine is established with Joseph Pomeroy Widney, M.D., as dean. The school opens on October 7 in a former winery on Aliso Street in Los Angeles. It is the University’s second professional school and the region’s first medical school.

The USC medical school enters into a formal affiliation with the Los Angeles County Hospital and Poor Farm, which had been founded in 1878.

Nine of the original 12 students, including one woman, become the first graduating class of the USC College of Medicine.

Joseph Widney becomes president of USC while remaining dean of the College of Medicine.

The USC College of Medicine opens a modern three-story building on Buena Vista Street, about seven miles from its original Aliso Street location. The faculty had personally borrowed $20,000 for the building’s construction.

H.G. Brainerd, M.D. becomes dean.

USC’s College of Medicine, deep in debt, affiliates with the University of California and becomes the Los Angeles Department of the School of Medicine of the University of California.

USC seeks a new affiliation and the College of Physicians and Surgeons, Medical Department of the University of Southern California is open for Fall term.

Abraham Flexner produces a landmark report for the Carnegie Foundation for the Advancement of Teaching: Medical Education in the United States and Canada. The “Flexner Report” quickly achieves notoriety and has huge impact on medical education and practice in the United States.

USC’s trustees announce the medical school will close until a sufficient endowment can be raised.

The medical school resumes operations following a seven-year closure that began in 1921.

The USC School of Medicine establishes an affiliation with Childrens Hospital Los Angeles.

The 1933 class of medical students, numbering 30 and including five women, celebrate their graduation. It becomes the first class to complete their education at USC’s medical school since the 1928 reopening.

Los Angeles County opens a new modern county hospital on State Street (what is today the Los Angeles County+USC Medical Center).
I'm probably not reading the information correctly. If you can tidy it up that would be great.

Just want to throw this out there-came across an immunization timeline-vaccines have been in existence since the late 1700s, so who knows what they were contaminated with. One of the two Yellow Fever vaccines was extracted from mouse brain tissue (and was not recommended for use after 1961 b/c it was associated with higher incidence of encephalitis). It's likely that there were other vaccines that used mouse cells. This doesn't include animal companion vaccines, which do not undergo the kind of screening that human vaccines do. Vaccines are the one thing that the govt. will do anything to protect, as evidenced by their refusal to acknowledge and withdraw the contaminated (w/ cancer-causing SV40) polio vaccine in the 1960s. Anyway, here is a very interesting history of vaccines to 2008:


p.s.-the Yellow Fever vaccine for humans was announced on April 28, 1932, so the 1935 date may refer to the other vaccine?

First Generation of Vaccines (pre-1950s)
1798 Smallpox
1885 Rabies
1897 Plague
1917 Cholera
1917 Typhoid vaccine (parenteral)
1923 Diphtheria
1926 Pertussis
1927 Tuberculosis (BCG)
1927 Tetanus
1935 Yellow Fever
1940s DTP
1945 The first influenza vaccines (flu) began being used.
1955 Inactivated polio vaccine licensed (IPV).
1955 Tetanus and diphtheria toxoids adsorbed (adult use, Td)
1959 World Health Assembly passes initial resolution calling for global smallpox eradication.
1961 Monovalent oral polio vaccine licensed.
1963 Trivalent oral polio vaccine licensed (OPV).
1963 The first measles vaccine licensed.
1964 Advisory Committee on Immunization Practices (ACIP), designed to provide CDC with recommendations on vaccine use, holds its first meeting.
1964-1965 20,000 cases of Congenital Rubella Syndrome occurred during the largest rubella epidemic in the United States.
1966 U.S. Measles eradication goal enunciated.
1967 Mumps vaccine licensed.
1969 Rubella vaccine licensed - 57,600 rubella cases reported this year.
1970 Anthrax vaccine manufactured by the Michigan Department of Public Health.
1971 Routine smallpox vaccination ceases in the United States.
1971 Measles, Mumps, Rubella vaccine licensed (MMR).
1976 Swine Flu: largest public vaccination program in the United States to date; halted by association with Guillain-Barr syndrome.
1977 Last indigenous case of smallpox (Somalia).
1978 Fluzone, the current flu vaccine that is made by Aventis pasteur, was licensed.
1979 Last case of polio, caused by wild virus, acquired in the United States.
1980 Smallpox declared eradicated from the world.
1981 Meningococcal polysaccharide vaccine, groups A, C, Y, W135 combined (Menomune)
1982 Hepatitis B vaccine becomes available.
1983 Pneumococcal vaccine, 23 valent
1986 The National Childhood Vaccine Injury Act establishes a no-fault compensation system for those injured by vaccines and requires adverse health events following specific vaccinations be reported and those injured by vaccines be compensated.
1988 Worldwide Polio Eradication Initiative launched; supported by WHO, UNICEF, Rotary International, CDC and others.
1989-1991 Major resurgence of measles in the United States - 55,000 cases compared with a low of 1,497 cases in 1983. Two-dose measles vaccine (MMR) is recommended.
1990 The Vaccine Adverse Reporting System (VAERS), a national program monitoring the safety of vaccines established.
1990 Haemophilus influenzae type B (Hib) polysaccharide conjugate vaccine licensed for infants.
1990 Typhoid vaccine (oral)
1991 Hepatitis B vaccine recommended for all infants.
1991 Acellular pertussis vaccine (DTaP) licensed for use in older children aged 15 months to six years old.
1993 Japanese encephalitis vaccine
1994 Polio elimination certified in the Americas.
1994 Vaccines for Children (VFC) program established to provide access to free vaccines for eligible children at the site of their usual source of care.
1995 First harmonized childhood immunization schedule endorsed by ACIP, the American Academy of Family Physicians and the American Academy of Pediatrics is published.
1995 Varicella vaccine licensed; before the vaccine an estimated 4 million infected annually in the United States.
1995 Hepatitis A vaccine licensed.
1996 Acellular pertussis vaccine (DTaP) licensed for use in young infants.
1998 First rotavirus vaccine licensed.
1999 Rotavirus vaccine withdrawn from the market as a result of adverse events.
1999 Lyme disease vaccine approved by the FDA.
1999 FDA recommends removing mercury from all products, including vaccines. Efforts are begun to remove thimerosal, a mercury based additive, from vaccines.
2000 Worldwide measles initiative launched; 800,000 children still die from measles annually. Measles declared no longer endemic in the United States.
2000 Pneumococcal conjugate vaccine (Prevnar) recommended for all young children.
2001 September 11 results in increased concern of bioterrorism. The United States establishes a plan to re-introduce smallpox vaccine if necessary, a vaccine thought never to be needed again.
2002 Lyme disease vaccine withdrawn from the market by the manufacturer because of lawsuits and lack of demand for the vaccine.
2003 Measles declared no longer endemic in the Americas.
2003 First live attenuated influenza vaccine licensed (FluMist) for use in 5 to 49 year old persons.
2003 First Adult Immunization Schedule introduced.
2004 Inactivated influenza vaccine recommended for all children 6 to 23 months of age.
2004 Pediarix,a vaccine that combines the DTaP, IPV, and Hep B vaccines, into one shot, is approved.
2005 Rubella declared no longer endemic in the United States.
2005 Boostrix and Adacel, Tdap vaccines, are approved for teens.
2005 Menactra, a new meningococcal vaccine is approved for people between the ages of 11 to 55 years of age.
2006 RotaTeq is a new rotavirus vaccine from Merck.
2006 ProQuad is a new vaccine that combines the MMR and Varivax vaccines for measles, mumps, rubella, and chicken pox into a single shot.
2006 Gardasil, the first HPV vaccine is approved.
2007 A booster dose of Varivax, the chickenpox vaccine, is now recommended for all children.
2007 The recommended age for Flumist, the nasal spray flu vaccine, was lowered to two years.
2008 Outbreaks of measles increasing across the U.S. as vaccination rates drop among some communities over vaccine safety fears.
2008 Rotarix, a two dose rotavirus vaccine is approved.
2008 Pentacel, a combination of DTaP, IPV and Hib is approved.
2008 Kinrix, a combination of DTaP and IPV that can be used for children between the ages of 4 and 6 is approved.


waitin' fer rabbits
South Texas
Thank you for the really nice vaccination history list but I'm not following your reasoning. If the XMRV-XPR19(x) is not in any mouse then how would it get transferred to mass vaccine production? If the ability to create the XMRV virus itself in any animal didn't pop up until the 1800's at the earliest how would that figure into the timeline. My understanding of early vaccines is that an infected but recovered patient was scratched with a needle and then a person to vaccinated was scratched with the same needle. So there were no use of animals in early vaccines and later vaccines were developed using mice but then the XMRV -XPR1(x) virus does not inhabit laboratory mice so I'm not making the connection. Could you elaborate please?


disjecta membra
Los Angeles, CA
George, I guess the relevant question would be: What were the likely exposures of doctors and nurses at the Los Angeles County Hospital in 1934 that could account for them getting something-that-looks-like-ME when the patients did not get it? It looks like we may be stretching a point to see if those staff members would have been in contact with lab mice; couldn't it just as easily have been something like the Truckee school where people in staff areas were jammed closely together and exposed to....what? By-products of wild (house) mice or lab mice? Mouse poop dust, mice nibbling on things in the staff kitchen, friendly office cat? Ok, that last maybe isn't so likely in a hospital, even in 1934.

Are we speculating that the jump may have been from Lake Casitas wild mice into humans? For some reason I have an image of some staff members having a weekend getaway in Ojai or something and coming back to work with some unwelcome viral passengers...not any crazier than any other wild speculation.

Of course, the year 1934 is most significant in LA for the catastrophic floods that occurred at New Year's, which wreaked a lot of destruction and disrupted many wild as well as populated areas. The kind of event that could conceivably have rearranged some wild animal habitats, forcing various species into new areas, etc. The 20s and 30s were also a time of lots of development and population growth in LA, when many people began living in newly built suburbs close to what we now call the urban/wildland interface. The kind of rearrangement of (human) habitat that often leads to unintended consequences. We notice it most when giant areas of Southern California burst into flames in the summer and fall, but it could have other consequences as well.

All of the above is pure wild speculation, of course. But it's fun. I'd have to dig a little bit more into the specific history of the County Hospital to know what things were like around there in that year. Brand new building in 1934. And were medical practices such at the time that lab mice would be kept anywhere near patient care areas? I know that lab animals were used for some diagnostic tests in times past (e.g., the infamous "rabbit test") but my knowledge of the history of medical practice runs a little thin after that.


waitin' fer rabbits
South Texas
Hey UT
Your speculations sound as good as any I've heard. (grins) And the possibility of the LC mice actually being the vector is reasonable. Could be the LC mice had some fun with lab mice and that's how the potential ended up in the lab mice. I get the feeling most people have a kind of "immediate onset" view of ME/CFS but I'm not so sure that's the case. (Yet another thing that remains unclear) This could have entered the human population from wild mice, rats, rabbits or cat's, dogs far earlier than 1934. The outbreak may have been triggered rather than spread.

I base that on a lot of anecdotal information, regarding gradual onset or stories of histories of ME/CFS going back generations like in my case as well as the supposition that autism may be triggered by vaccines. Most of talk about getting (fill in the blank) and then never getting well. We know that all of the different viruses EBV, glandular fever, Q fever, or the various triggers like auto accidents, traumatic medical procedures can't all be the "cause" of ME/CFS so they must be the trigger mechanisms for the XMRV virus. So then what if the 1934 outbreak was a trigger for the virus? And what would doctors and nurses be exposed to over a period of months or years that patients wouldn't? I've been trying to figure that out now for 13 months. (big grins)

Any way ya slice it, it keeps coming back to California in the early part of the century. That's about the only thing I can figure for sure.


waitin' fer rabbits
South Texas
Thought I'd post this from the December issue of The Journal of Virology. If anyone has access to the entire paper that would be lovely

Common Inbred Strains of the Laboratory Mouse That Are Susceptible to Infection by Mouse Xenotropic Gammaretroviruses and the Human-Derived Retrovirus XMRV {triangledown}
Surendranath Baliji, Qingping Liu, and Christine A. Kozak*

Laboratory of Molecular Microbiology, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892

Received 2 September 2010/ Accepted 1 October 2010

Laboratory mouse strains carry endogenous copies of the xenotropic mouse leukemia viruses (X-MLVs), named for their inability to infect cells of the laboratory mouse. This resistance to exogenous infection is due to a nonpermissive variant of the XPR1 gammaretrovirus receptor, a resistance that also limits in vivo expression of germ line X-MLV proviruses capable of producing infectious virus. Because laboratory mice vary widely in their proviral contents and in their virus expression patterns, we screened inbred strains for sequence and functional variants of the XPR1 receptor. We also typed inbred strains and wild mouse species for an endogenous provirus, Bxv1, that is capable of producing infectious X-MLV and that also contributes to the generation of pathogenic recombinant MLVs. We identified the active Bxv1 provirus in many common inbred strains and in some Japanese Mus molossinus mice but in none of the other wild mouse species that carry X-MLVs. Our screening for Xpr1 variants identified the permissive Xpr1sxv allele in 7 strains of laboratory mice, including a Bxv1-positive strain, F/St, which is characterized by lifelong X-MLV viremia. Cells from three strains carrying Xpr1sxv, namely, SWR, SJL, and SIM.R, were shown to be infectable by X-MLV and XMRV; these strains carry different alleles at Fv1 and vary in their sensitivities to specific X/P-MLV isolates and XMRV. Several strains with Xpr1sxv lack the active Bxv1 provirus or other endogenous X-MLVs and may provide a useful model system to evaluate the in vivo spread of these gammaretroviruses and their disease potential in their natural host.

* Corresponding author. Mailing address: NIH, NIAID, LMM, Bldg. 4, Room 329, 4 Center Drive, MSC 0460, Bethesda, MD 20892-0460. Phone: (301) 496-0972. Fax: (301) 480-6477. E-mail: ckozak@niaid.nih.gov


Senior Member
Logan, Queensland, Australia
Hi everyone,

I like reading these theories, but they are just speculative. Any one could be right, any one could be wrong.

I am currently (with the science as it is) of the view that XMRV causes ME by a two hit mechanism. First you get X infected. Then after it has a foothold and lots of time to spread (weeks, months, years, decades) all the X infected are exposed to something at the same time. This could be almost anything, from pesticides and carbon monoxide, to a severe flu or mold exposure. Then we get an outbreak of ME. X is slow, and can cause sporadic cases (there could be some in the 20s that were undocumented). When a cluster trigger occurs, we have an apparent epidemic. The problem is that, in this model, the virus is far more widespread and clusters are really clusters of something else, something that results in ME. Now that something might be merely showing X to our immune systems, and we are just the tip of the iceberg.

(Iconic image: I can see a huge blue iceberg in the early morning light over the ocean. Carved/sculpted into the tip is a gigantic X that goes down to the waterline.)

Let me illustrate my caution by looking at what might be an unpopular theory: vaccination as a cause. It is quite right to doubt that X (easier to type than XMRV, and we are not likely to get it wrong; also it could make a good slogan: the X Virus) is in vaccines. It is far more likely that we have both XMLVs and PMLVs in vaccines. The "age of vaccination" may have meant that thousands or millions of people were vaccinated with both types of these MLV contaminants. Any one of these people could have had the X/PMLV crossover event, and the creation of X. Indeed, X could have been created many many times in different locations, and this could be ongoing.

This could mean that any specific X virus has a defined geographic spread. Worldwide, it is likely that this would be a huge number of blotches (think of coffee stains on a map) all over the world. Superimpose both the X distribution and the MLV distributions and the only places not covered are probably deep ocean, isolated islands and remote locations including the deep arctic circles. If you want to get away from X, go live on Mars - but don't take X with you.

Mold is unlikely to cause ME, or be infected by X. It is very likely to be a trigger and may interact with X. Indeed, we can envisage scenarios in which X depresses the immune system so we can't fight many molds that normally would not be a problem. Then the molds co-infect the host, depressing the host so that it can't fight X. This then becomes a permanent state, or perhaps the cycle can be broken only to have the person become infected again from mold in the environment. Substitute Lyme or herpes family viruses and you get a similar picture.

This could mean that simply looking at X evolution is a mistake. We need to look at how it co-evolves with all the co-pathogens that we routinely find. I would bet they are evolving together, and each puts pressure on the other's evolutionary path.

Please also keep in mind that some molds may have been co-evolving in many hosts with MLVs for even millions of years.

Don't get me wrong: I am very intrigued by the evidence pointing to a convergence in California in the early 1930s. It is certainly worth digging into to see if we can uncover more. Using my earlier model, if we can identify early clusters of ME such as in LA, then we have a clue as to where people were becoming infected, and therefore where X might have originated. It just might not be only in LA.



disjecta membra
Los Angeles, CA
I'm going to try to go to original sources on this 1934 outbreak in LA, because from what I've been able to see by a casual glance at newspaper archives is that there is a lot of talk of a polio outbreak in LA that summer, as well as in other cities. (Everyone lived in fear of polio outbreaks in the first half of the twentieth century, and they commonly occurred in the summer and fall.) There was so much actual polio going on that this "atypical polio" may be hard to suss out.


Senior Member
I've been reading through this one and there are some intriguing observations in there:

Observations on the Epidemic of Polio-Encephalitis in Los Angeles, 1934:

The whole "yuppie flu" business and the claim that CFS affects the middle class more than the poor, is of course part of the history of ME/CFS, and is generally disputed as a prejudice, a myth, and explained by psychologists with ideas such as "they read it in the papers and convinced themselves they had it". But these observations of a disproportionate distribution of ME/CFS amongst the middle classes are surely subject to none of these factors and can't be explained away by any of the theories from either side. What on earth could be going on here? Genetic susceptibility is an obvious idea that comes to mind, but again, this seems to me to be a hypothesis driven more by our assumptions than anything else. I suspect that the answer lies in some environmental factor, and in the means of transmission. The observation about upper stories and high sides of hillsides looks like a massive and overlooked clue. All these observations, both in this paper and historically, seem to be pointing at some environmental factor that is present in what we might think of as clean, sanitary, desirable environments, where the air is, theoretically, somewhat cleaner - or perhaps the heat, or some other aspect of environment - were the middle classes more likely to have something like central heating for example?

Please bear in mind that all the above speculation is a vague and approximate sketch: it's more of a "discussion document" intended to spark ideas in those more specialised in the relevant disciplines than myself. I look forward to the thoughts of George and others on the above...may be it's time to call in the mold warriors...:D
Many times when people talk about whether CFS is a new disease, they point to the diagnosis of "neurasthenia."

This was a diagnosis popular from about 1870 to 1920. It mostly was given to affluent women, and had the same symptoms as mild-ish CFS (e.g. Fukuda). People are bedridden, lacking in energy, cognitive dysfunction, non-specific pain, appear to have nothing physically wrong on exams, dismissed as psychological.

Usually the question of why it was not diagnosed in less well-off people is attributed to the idea that these folks didn't get proper diagnoses and/or couldn't afford to lollagag about in bed.

However, one clue is the fact that Stachybotrys was first found in an indoor environment in Germany in about 1850. it only can grow on cellulose....in that case wallpaper (and now, mostly, on drywall and on wall insulation).

Only wealthy people at the turn of the 20th century could afford wallpaper.

Below is a section of a story called "The Yellow Wallpaper," written by a woman with neurasthenia. Sounds to me like that wallpaper was really moldy anyway.

I don't know if ME/CFS has an affluent component to it these days. In Osler's Web, one of the doctors (Grufferman?) suggested that maybe it was a "Yuppie" disease because people were exposed in lovely glass tower office buildings and on airplanes, which recirculated air with pathogens in it.

Office buildings like that and airplanes tend to be especially bad with molds and other "Sick Building Syndrome" problems.

Whether any of this has anything to do with the LA Hospital epidemic, I don't know.

I'm not sure what to say about the rest of the questions, yet.

Best, Lisa

From "The Yellow Wallpaper" by Charlotte Perkins Gilman (1899)

I'm feeling ever so much better! I don't sleep much at night, for it is so interesting to watch developments; but I sleep a good deal in the daytime.
In the daytime it is tiresome and perplexing.
There are always new shoots on the fungus, and new shades of yellow all over it. I cannot keep count of them, though I have tried conscientiously.
It is the strangest yellow, that wall-paper! It makes me think of all the yellow things I ever saw--not beautiful ones like buttercups, but old foul, bad yellow things.
But there is something else about that paper-- the smell! I noticed it the moment we came into the room, but with so much air and sun it was not bad. Now we have had a week of fog and rain, and whether the windows are open or not, the smell is here.
It creeps all over the house.
I find it hovering in the dining-room, skulking in the parlor, hiding in the hall, lying in wait for me on the stairs.
It gets into my hair.
Even when I go to ride, if I turn my head suddenly and surprise it--there is that smell!
Such a peculiar odor, too! I have spent hours in trying to analyze it, to find what it smelled like.
It is not bad--at first, and very gentle, but quite the subtlest, most enduring odor I ever met.
In this damp weather it is awful, I wake up in the night and find it hanging over me.
It used to disturb me at first. I thought seriously of burning the house--to reach the smell.
But now I am used to it. The only thing I can think of that it is like is the color of the paper! A yellow smell.
There is a very funny mark on this wall, low down, near the mopboard. A streak that runs round the room. It goes behind every piece of furniture, except the bed, a long, straight, even smooch, as if it had been rubbed over and over.
I wonder how it was done and who did it, and what they did it for. Round and round and round--round and round and round--it makes me dizzy!


Senior Member
Sofa, UK
We know that all of the different viruses EBV, glandular fever, Q fever, or the various triggers like auto accidents, traumatic medical procedures can't all be the "cause" of ME/CFS so they must be the trigger mechanisms for the XMRV virus. So then what if the 1934 outbreak was a trigger for the virus? And what would doctors and nurses be exposed to over a period of months or years that patients wouldn't? I've been trying to figure that out now for 13 months.
It's so frustrating isn't it?!

We always just seem to be missing one piece of the puzzle somehow! There are these great big blatant clues sitting there and yet we can't quite work out what they mean!

As well as only the nurses and doctors getting sick, also there are those references to the wider outbreak disproportionately affecting middle class families - that idea turns out to go right back to 1934 and it keeps coming up: myth or not? - and affecting people living on the top floors of buildings and in houses on the high side of streets on the sides of hills. What on earth could that mean? What is different about top floors? Having lived on the top floor of everywhere I've ever lived, one thing I do know is it gets a lot hotter in summer and colder in winter. I also always seem to be at the extreme end of the central heating system, which can be a real nuisance. Beyond that, I can't think of anything. But that observation they made wasn't just a coincidence I think - it means something.

By the way, that report also mentioned that there were several cases where several members of the same family all got sick at the same time.

I have generally been thinking more in terms of a 2-strike or 3-strike theory rather than a continuous exposure over months or years. I've wondered whether the two strkes could be infection by 2 or 3 different X/P MRV variants, or pre-existing XMRV infection plus some environmental trigger.

1955 Royal Free Hospital has at least one key piece of the puzzle in common with LA. Again, it was doctors and nurses who got sick, and not the patients. That seems to shout that this point has to be significant, and that it can't be a viral trigger, or at least, if it is a viral trigger, then the doctors and nurses had some pre-existing factor that the patients didn't.

The other thing about Royal Free that looks like a vague but very suggestive connection is that on the chronology, 1955 was the year of another new polio vaccine. I've seen no evidence that the staff at Royal Free got a polio vaccination in the years before - maybe an early or experimental one - but if I learned that they did, it wouldn't surprise me. It's the fact that in both LA and Royal Free there was a new polio vaccine around at the time that seems most suggestive.

I too thought the New Year flood was likely to be significant. I read some about the history of that and it was a major catastrophe affecting the region; UT is right that would have changed the region's ecology dramatically, and I accept that conventional zoonosis should be the most likely explanation; there's no real need to look for anything else I guess.

Still can't quite let go of my point about the paper I mentioned earlier though. George you keep saying XMRV had to pass through another host, but my point about that lab work I was talking about before was that it seemed to fit well with what you were requiring there. The samples were from people who had died from encephalitis from all over the US, those various infectious agents had therefore passed through them, and samples of their infected brain tissue were then passed back through mice, and a virus was then recovered from the mice. Sorry to keep banging on about that one but it just seems to fit well with what George is saying is required for human X/P XMRV to evolve.

But anyway, like George keeps reminding me, it's good to keep coming back to what we know. California, early 20th century, birth of ME/XMRV. That all seems solidly confirmed now by this paper, and that's truly a historic breakthrough.


Phoenix Rising Founder
Arizona in winter & W. North America otherwise
I did not come away with the conclusion is ruled out. I came away with the conclusion that it was lessened but was still possible. This is from an article - it suggests that X ERV's could be in lab mice and they could possibly produce XMRV

- the Endogenous Xenotropic Retroviruses (XMV’s) - Of course we’re concerned with the mouse X MRV’s - the endogenous retroviruses most closely related to XMRV because researchers worried about contamination will most likely turn to these ERV’s . Work has recently been done to determine where and how active these ERV’s are.

Most X ERV’s, fortunately, are not able to produce infectious retroviruses but some are. Kozak found two types of lab mice which contain X ERV’s that are able to produce high levels of XMLV’s (but not necessarily XMRV.) She also found that subjecting some laboratory mice cells to various stressors (chemical induction, bacterial lipopolysaccharides (LPS)) could induce them to produce the XMLV viruses).

She’s been able over the past months to identify four active ‘proviruses’ embedded in mouse genomes that are able to produce X ERV’s ; one of which (Bxv1) is found in about 1/3rd of the common strains of inbred mice (lab mice?). She’s identified two strains of lab mice that can produce high levels of X ERVS, nine that can produce intermediate levels and four that rarely produce them (Table 2).


Phoenix Rising Founder
Arizona in winter & W. North America otherwise
This is what I came up with regard to the actual viruses.

The Laboratory Mice - Since laboratory mice are probably the key figures in any contamination scenario the big question is whether or not their cells have receptors that susceptible to XMRV. It turns out that most of them don’t. In fact ,lab mice appear to be the only mouse group that carry a receptor that able to completely block X MLV (and therefore XMRV infection).

This is not completely surprising given that most laboratory mice are derived from house mice which differ in their susceptibility to XMLV’s. However she also notes that house mice trapped at ‘various sites throughout Western Europe and the Americas’ do carry the receptor (Xpr1 svx) that allows X-MLV entry - so it is available in that population. But did that X-MLV receptor make its way into some lab mice?

It turns out that it did. While not nearly as variable genetically as wild mice laboratory mice did come from a variety of mouse populations some of which did carry the ‘wrong’ receptor. While the majority of lab mice do carry the ‘anti-XMRV receptor’ some strains of lab mice carry a ‘permissive’ receptor that readily allows X MLV’s to infect them. In fact Kozack recently penned an paper titled ‘Common inbred strains of Laboratory Mouse are Susceptible to…..Human Derived Retrovirus XMRV”. http://www.ncbi.nlm.nih.gov/pubmed/20943975. which states that she found three inbred laboratory mice that could be infected by XMRV.

Overall the possibility of a contamination from a lab mouse appears to lower for XMRV than for other MLV’s it is still present. This finding appears to be at odds with recent unpublished reports that no other mouse or other species have yet been found to harbor XMRV. Perhaps the possibility of infection does not necessarily denote the presence of infection.


waitin' fer rabbits
South Texas
Hey Cort you're right that the door was left open a crack. (grins) I read that as normal scientist speak. It's so rare this early in the game to hear them be diffinative. This seemed pretty definitive for a first and follow up paper. In answer to the earlier question about the 80 years. I apologize for not being clear. I set the 80 year mark. The first lab mice were breed in 1907 and where shipped to the west coast before 1928. That's all the for sure info and that was from investigating CC Little the father of the lab mouse. Hope that helps.


Senior Member
I did not come away with the conclusion is ruled out. I came away with the conclusion that it was lessened but was still possible. This is from an article - it suggests that X ERV's could be in lab mice and they could possibly produce XMRV
You talk about laboratory mice. But the laboratories in the WPI study never worked with laboratory (or any) mice.
Now, if I find a mouse in my house I would not assume he is a laboratory mouse, would I? So, do you think that a laboratory mouse would come to the WPI's lab because he knows it's a laboratory and only feels comfortable where there are centrifuges and PCR machines?