XMRV – Hope and Caution

October 16, 2009

Posted by Cort Johnson

Who Are Those Guys? Gazing at the distant cloud of dust raised by his dogged but mysterious pursuers Butch Cassidy turned to the Sundance Kid and with some awe muttered “Who are those guys?” Despite all  their tricks that posse had stuck on their trail like glue. Has the Whittemore Peterson Institute’s posse caught one of  the slippiest preys in all medicine? Or will a significant subset of ME/CFS patients slither through their hands?

A good part of that answer may depend on  the answer to  “Who are those guys?” Specifically when WPI researchers called the subjects of their study chronic fatigue syndrome (ME/CFS) patients just who were they talking about? And who will end up having this virus? Answering that question will determine if the WPI posse can corral  the whole disease or just a portion of it.

Lets take a close look at just who was in the little study that shook the ME/CFS world.

Putting Your Best Foot Forward - The WPI did not choose your garden-variety chronic fatigue syndrome patients for their first study. They chose the kind of patients that they had the most confidence in with regards this virus. There’s nothing wrong with this;  its standard procedure in the research world. In their first study  researchers usually include patients they think will best make their case. Those patients still fit the definition of the disease but they’ll often have less than subtle differences.  (Given the vague definition of this disease make that very large differences. This is presumably one reason the CDC went to a random sampling scheme.)

An immune researcher would probably try to include pathogen loaded, cytokine upregulated, fluey patients. A endocrine researcher might fit in patients with hormonal problems. Perhaps not surprisingly that first study usually works out pretty well but the second one by an independent researcher who didn’t try and gild the lily, so to speak, often doesn’t.

When scientists want to find a virus, we look for it in the sickest individuals because often this is where there is likely to be the highest levels of a virus, if present.  Dr. Suzanne Vernon

A Special Group of Patients - In this case Whittemore Peterson Institute was refreshingly direct in how they ‘stacked their deck’. They stated  the study participants had ‘severe disability’, low natural killer cell functioning, increased pro-inflammatory cytokine levels (primarily IL-6, IL-8), ‘extremely low’ VO2 max during exercise testing and RNase L dysfunction. During a radio interview we learned that 20% of the patients had lymphoma. Without knowing their functional status it sounds like they are housebound and many very well may have been bedridden.

Outbreaks! (Outbreaks?) – They also came from areas where ‘outbreaks’ had occurred. The WPI took a page from  the distant past when they included outbreaks in the parameters. No one to my knowledge has officially reported an ‘outbreak’ in several decades. Why therefore specifically go back to where ‘outbreaks’ had begun (and therefore not include ‘non-outbreak’ areas)?

Was this to highlight the possibly infectious nature of this pathogen or to draw attention to an important but mostly forgotten era of ME/CFS thinking? Or was it central to their case? Was limiting the participants of the study to known infectious events one way the WPI gilded their lily? (Will ‘non-outbreak’ patients fit the WPI’s  scenario? My guess is that they will but….).

Whatever the answer to  that question its clear that these do not appear to be your ‘normal’ chronic fatigue syndrome patients. A recent Pacific Fatigue Lab study, for instance, found low VO2 max levels in about half their participants. A considerable number of those participants came from Dr. Montoya’s and Dr. Peterson’s pathogen studded patients. Given that these participants had very low VO2  it’s possible that a significant number of even pathogen ridden patients might not have gotten into this study.

This first paper clearly referred to a certain subset of patients. Again this is pretty much expected in the first paper but it does make it difficult to interpolate the results to other patients.

The Big Question - Do I have an XMRV infection? Taking a very conservative view of this question and going strictly off this paper you’d have a good chance of testing positive for it if you had the following characteristics; an infectious onset, extremely low VO2 max levels, low natural killer cell functioning, RNase L. problems and increased inflammatory cytokines. (If you have all of those plus lymphoma you’re almost certainly in – but in a very bad way). Even in these very poorly off patients only two thirds of them tested positive for the virus but that is apparently more a function of a not completely accurate test than a lack of  virus – the WPI is working on a more accurate test right now.

Room  For Hope - If you go strictly by the study it’s beginning to sound like it might not apply to the ‘average’ ME/CFS patient.  There is considerable room for hope, however, that it will. Dr. Mikovits reported that 95% of a larger set of patients (n=330) tested positive to an antibody tests. The antibody test did not measure active infection but it did indicate that these patients have been exposed to the pathogen.  Dr. Mikovits also stated that she expects most ‘ME/CFS’ patients will test positive for the virus. Dr. Cheney, our only independent guide to the prevalence question right now, contributed 14 patients to  the study and reported that his results were similar to the group as a whole.  That’s encouraging.

It’s also encouraging that  the patients came from me areas across the US. The virus has also been found in some FM patients, autism patients and atypical MS patients which suggests that the number of people with this virus will broaden not diminish.

Thankfully the number of healthy controls testing positive has remained very low throughout; this pathogen – in contrast to all the others associated with ME/CFS – appears to to be quite rare in the general population – an important finding.

Plus the WPI recently stated that not all the people in the study had abnormal RNase L/NK cell results thus it doesn’t appear that you need to have these immune dysfunctions in order for the virus to be present. More and more it’s looking like the broad group of ME/CFS patients may have this virus. Still the only thing that will seal that deal are studies showing that moderately ill patients are infected.

Professional Recomendations – It wasn’t surprising that the first recommendation from the ME Association was for the WPI to begin

Carrying out further and larger studies using different populations of people with ME/CFS, including people at different stages of the illness (to see if the virus is present in the same percentages in both early and late cases) and in all degrees of severity.

Dr. Vernon echoed this when she stated that

“Independent replication studies should also include patients with mild and moderate CFS, at least one chronic disease control group (e.g., multiple sclerosis, lupus) and sex and age-matched healthy controls.”

Who Are Those Guys? So we don’t really know who ‘those guys’ – the ones with the virus – will turn out to be. Sure we have some tantalizing hints that the virus is  found in more types of patients than the Science paper can show but  before most patients  pop the bubbly they should wait to see studies that contain patients that look like them. The good news is that those studies should already be underway.

Beachhead Established – the Jungle Awaits - This is not to criticize the Whittemore Peterson Institute. It’s about being wary in the face of  a complex issue. Given how research happens these problems are inevitable. The WPI’s first job was to establish a beachhead and they’ve established the most biggest beachhead yet in this disease. Their next job is even more difficult – to try and work their way deeper into the jungle that has been ME/CFS. Hopefully they’ll be able to.

**Addendum – some good news has cropped up regarding the possible spread of XMRV in chronic fatigue syndrome patients. It turns out that one of the criteria the WPI used to select their patients in this study – RNase L dysfunction – is not a factor in who carries the infection. People with or without RNase L dysfunction can test positive for XMRN.

How ironic this is since it was the RNase L connection that led Dr. Mikovits to XMRV in the first place. As they say sometimes it’s better be lucky than right. In this case it looks like we were actually lucky.


{ 28 comments… read them below or add one }

John October 16, 2009 at 5:56 pm

To honor the ‘rankly speculative’ aspect of this blog, I wonder if the nature and/or cause of the RNaseL dysfunction is what defines patient cohorts-

For example, the sudden onset cases might be victim of an enterovirus infection that clips the RNaseL, leaving XMRV to proliferate in a certain manner, while gradual onset cases might have their RNaseL disrupted in a different manner, such as by chemical exposure- I remember a study from a few years back where either Lapp or Bell or one of those guys found that RNaseL could be disrupted by viral or chemical exposure. It sounds somewhat plausible given Chia’s new work with enteroviruses and Hyde’s ‘Secondary M.E.’ cases who were victims of chemical exposure, who knows? Then there’s the HERV’s, vaccines, etc. Not to mention the Rituximab B-cell study which hopefully should be coming out in a few months. How about some funding to clear all this up, Uncle Sam?


Kate October 16, 2009 at 9:30 pm

I consider myself a fairly typical CFS patient. I wasn’t part of a cluster, but have been primarily housebound for nearly 22 years, interspersed with periods where I was completely bedbound. My husband was my primary caregiver for 20 years. He showed mild signs of CFS for years (sore throats, swollen glands, chemical sensitivities, etc.) and died of a rare non-hodgkins lymphoma related to EBV three years ago. He was only 49.

Needless to say, I believe the WPI are on to something.


cort October 16, 2009 at 10:02 pm

Please don’t take the last post to mean that I don’t believe they’re onto something. I truly do but after a closer look I’m a little more wary. I want to be careful about not accepting more than has been given so far. So far we know that one group of patients has this virus. That’s pretty darn good.

As the studies progress I sincerely, sincerely hope we find that more and more of the ME/CFS population does. (Why? Because I don’t think I’m in the Incline Village Group and this is the best shot I have at beating this thing). Judging from the signs (Dr. Mikovits statements, Dr. Cheney’s statements, the fact that FM patients may have the virus as well – I think we can certainly be hopeful. But I think I don’t think we should count our chickens before they hatch.


Khaly Castle October 16, 2009 at 10:51 pm

According to you, Cort, WPI “Stacked the Deck” with PWCs who “had’severe disability’, low natural killer cell functioning, increased pro-inflammatory cytokine levels (primarily IL-6, IL-8), ‘extremely low’ VO2 max during exercise testing and RNase L dysfunction. During a radio interview we learned that 20% of the patients had lymphoma.”

While I understand the concept of “stacking the deck” with the sickest of the sick when looking for a virus (because that’s where you’ll most likely find it), what you failed to mention is that these are the very things that defined the disease when Peterson and Cheney were first faced with it. It’s the Incline Cohort that the disease was named for, and anyone who doesn’t have whatever it is that caused THESE people to get ill, doesn’t have CFS. That is not to say they are not sick. That is to say they do not have CFS. CFS is the name that was given to the illness that the Incline Village cohort had. That’s why the Incline cohort studies are vital.

Cort goes on to say:
“They also came from areas where ‘outbreaks’ had occurred. The WPI took a page from the distant past when they included outbreaks in the parameters. No one to my knowledge has officially reported an ‘outbreak’ in several decades. Why therefore specifically go back to where ‘outbreaks’ had begun (and therefore not include ‘non-outbreak’ areas)?”

They went back to the past, to the outbreak areas, to be sure that they were testing people with what THEY know to be CFS. It’s time to let go of any idea that the expansion of the definition of CFS by the CDC (to the point of excluding the original “outbreak” people) makes sense in any dimension of the known universe, or that it will do anything other than muddy the waters when the CDC goes to select their patient base for replication testing.

Any perpetuation of that myth at this point is sheer negligence. Not only is it damaging to finding a cause/cure for those that DO have it, but also for those that don’t. At least if we could drop the charade and come up with a cause for the ORIGINAL CFS, then we could use that as a starting place for those that don’t end up having it….an indicator that their illnesses need to be looked into much further.


cort October 17, 2009 at 6:58 am

You may be right Khaly. The XMRV finding could provide the wedge that distinguishes the ‘original’ CFS patients from those that got added on after the definition was created. That is the group after all that Dr. Peterson – practicing for all these years just up the road from Incline Village – has focused on. I, for one, hope it doesn’t but for a personal reason – this finding provides the best opportunity for a cure that I can see – and I don’t believe that I, with my gradual onset, minimal pathogen involvement fit it. (It was interesting that of all the parameters those patients fit the WPI did not say they had herpesvirus infections (?)).

My sense from reading the original papers is that the Incline Village cohort was pretty diverse though. There were gradual onset patients in there and Dr. Cheney and Dr. Peterson could not distinguish between the two using laboratory findings or by looking at their symptoms. That may be the reason they considered and discarded using the term myalgic encephalomyelitis in their first paper. Maybe something changed later – I don’t know.

A discovery like this obviously has the potential to alter how we look at this disease in several ways!


drew October 17, 2009 at 2:44 am

Cort, I think you make an excellent point. We all need to approach these findings with some degree of caution. While this research offers tantalizing hope to us patients, let’s keep in mind that there are a lot of unanswered questions here.

I, for one, am not “popping the bubbly” yet. (And when it is time to do so, I (and probably lots of other patients) will have to settle for popping the non-alcoholic apple cider!)



Jim October 17, 2009 at 5:01 am

Cort- I’ve been scanning the web since the XMRC announcement looking for a fuller discussion from folks in the ME community, and was glad to find your cautionary and questions. Due to the extraordinary level of these findings I find them less easy to dismiss as just another “we’ve found it” disappointing finding, but there is a lot to be checked out before we really know what this means. I’d like to hear some more discussion from you, Cort, given how hooked into the policy issues in the community, on the CDC’s “reaction” to the XMRC research, and why it took a private foundation to pursue this work. There’s some important history on the NIH and CDC’s history in regards to virology and ME that bears review here.


cort October 17, 2009 at 7:30 am

I’m kind of amazed at the CDC’s response. I would have thought that no matter what they felt privately they would have simply said it was possibly an extraordinary finding that they were going to check it out. But to publicly question whether Science should have included it in their journal and to state that they didn’t think they were going to be able to replicate the results just seems to me, a laymen, out of bounds.

Based on a closer look at the paper I think it’s pretty clear, though, that they can’t replicate the results. In fact the WPI has made it impossible for the CDC to replicate the results – at least using their old samples which is, I believe, what they’re doing. The CDC doesn’t know which of their participants met the Canadian Consensus Definition. They’ve never done a single RNase L. test or NK cell test or aerobic exercise test. They have no idea which of their participants met those standards. So they’re going to be testing a very different group of patients.

I assume that Reeves was included in the NIH conference in August I think it was. If he was he’s probably already been testing samples. It may very well be that when he says he doesn’t think he’s gonna be able to replicate the results that he already knows that.

With regards to history of viral testing at the CDC. I think I mentioned in the Game Changer post the CDC did two studies retroviruses early in the 1990′s. The first did not replicate Dr. DeFreitas findings, the second looked at a variety of retroviruses and other viruses and did not find any. It’d interesting to go back and see which patients they used. The first study turned out to be rather controversial. It bears mentioning though that Dr. Gow in the UK – still a CFS researcher – also failed to replicate Dr. DeFreitas results and a Japanese team the next year to find evidence of retroviruses in CFS patients. I can’t imagine that these findings would have any bearing on the WPI findings because technology has changed so much in the past 15 years. I just point this out to note that several different teams did look for retroviruses after Dr. DeFreitas findings came out – it wasn’t just the CDC. After that the search for retroviruses effectively ended in chronic fatigue syndrome. (The NCF reportedly looked for evidence of Dr. DeFreitas virus after 2000 and failed).

As I noted in ‘Puppet Master’ this was the discovery that was waiting to happen. The RNase L problems in chronic fatigue syndrome have been well known for around a decade now. Dr. DeMeirleir and Dr. Englebienne wrote an entire book on them! Once the XMRV virus was found in prostate cancer patients with reduced RNase L. activity the game was on. Quite frankly I’m surprised that Dr. De Meirleir didn’t jump on it right then. Maybe he tried – who knows but it didn’t take a flash of genius to think maybe we should check ME/CFS patients for that virus. Oddly enough the idea that RNase L dysfunction is tied to XMRV expression in prostate cancer patients has taken a hit recently. Maybe if Dr. Mikovits had waited a year or two she would’ve decided there was no connection and never tried.

Oddly enough the CDC is focused on the same interferon pathway that RNase L is a part of but they aren’t interested in the viral aspect of the pathway – hence no they have no interest in RNase L and therefore missed the connection – a strange thing for a bunch of virologists. (Dr. Reeves and Dr. Jones are virologists).

We’re going to see the same process but magnified here. The CDC, the Dubbo Team and probably several other teams that have samples or are currently recruiting patients for a study and can get some money together will be trying to replicate this. Of course the WPI will be going full bore as well. Its hard to judge but it could be that we’ll have more answers than within six months.


Anonymous October 17, 2009 at 6:23 am

I understand the point of comparison between various claims of ‘THIS is it’ but it’s worth noting that De Meirleir’s H2S theory has met with a great deal of criticism and has nowhere near the rigorous testing the WPI is basing their claim on.


cort October 17, 2009 at 7:31 am

Good point anonymous and I amended the blog to reflect that the two research efforts are really apples and oranges in their degree of magnitude. Thanks!


HVS October 17, 2009 at 9:27 am

If XMRV is truly only at the root of the illness of very classic Incline Village cohort patients, at least those without XMRV will have narrowed the search for their problems a bit. They can look at environmental toxins, Lyme, etc. etc.
…Not much a of a silver lining, but all information helps.


Khaly Castle October 17, 2009 at 11:28 am

Cort, I understand your statement about hoping it does not delineate a difference between original cohort CFS and your illness, for personal reasons. I think this is precisely why advocacy has been so split and bitter, so difficult to unite. People are afraid that they will be Un-Diagnosed if something like this comes along and starts weeding out people.

We can’t look at it that way, though. If we were to test negative for XMRV, should it be the calling card for CFS, then at least we know what we DON’T have. This doesn’t mean we are not sick. This would be a great first step in the process of elimination, a tool that says we need to look elsewhere, as HVS said.

The fear of being Un-Diagnosed is really baseless. The vast majority of us don’t have a real CFS diagnosis anyway. We have the one that doctors slap on you when they think it’s AIYH.


cort October 17, 2009 at 11:59 am

Hi Khaly,

It’s more a personal issue for me – I want to get well and be able to exercise, etc. and I think this is the best opportunity for treatment that we’ve ever seen. Actually I agree with you about the process of elimination – I think that even if XMRV ends up being present in only a subset of patients that it will help everybody .

One reason is that those XMRV or rather XAND patients would be split off from the rest of the patients in research studies. That means we’ll have a more homogenous group to research and this should lead to better results. Basically simply splitting any group off should lead to better research results in all the other groups. I think its all good.


Jim October 17, 2009 at 3:29 pm


u said “the idea that RNase L dysfunction is tied to XMRV expression in prostate cancer patients has taken a hit recently.” could u tell me where u learned this?




Keith October 17, 2009 at 4:31 pm

Cort don’ you think it’s possible outbreaks still occur but since the CDC doesn’t believe in them or educate doctors in them they either are ignored or not recognized. I was part of a cluster and I can tell you it was never reported or recognized at the time by any of the doctors I saw. I’m sure the same thing has happened many times elsewhere. Part of the CDC education and CAA education should have always been that clusters do occur in this illness. But since no doctors have been educated to thet effect of course non will have beeen reported. And if they were reported the CDC would ignoree thee report. Heck the biggest cluster we know of we are only aware of because of Cheney, Peterson and Hillary Johnson for the most part. If not for them it would have never been accknowledged by anyone.


cort October 17, 2009 at 5:44 pm

Sure. I met someone from Atlanta, I think it was who saw person after person after person around her felled by a mysterious illness that no one could identify. Dr. Chia has talked of seeing different ‘waves’ enteroviruses show up his patients. Apparently different kinds of enteroviruses sweep through communities regularly. If you don’t look for these outbreaks or have a way to report them – how would we – the public – ever know that they happened?

I’m a little unclear why they stopped being reported though. The CDC, of course, didn’t have anything to do with monitoring the early outbreaks. Perhaps as the medical system got more and more organized – the CDC became the clearinghouse for infectious events – and the buck stopped there – I don’t know.


Alyson October 17, 2009 at 5:52 pm

Hi Cort – Thanks for this post. It gave me a lot to think about.

On a side note, thanks for your blog and all that you do. I appreciate it!


John October 17, 2009 at 7:00 pm

On the CDC website, it mentions that they investigated outbreaks of CFS but never reported on them, and that outbreaks were reported but never got investigated. That’s why it’s so important that outside researchers get access to CDC datasets.

Jim, the prostate cancer thing was from a study done in Germany. They didn’t find any XMRV at all. The author of the original study, Silverman, noted that they use substantially different techniques, I believe. You can google xmrv’, possibly combined with ‘germany’ and it should show up. PS- If you’re interested in the CDC and it’s reply to CFS, or lack thereof, I can’t recommend the book ‘Osler’s Web’ enough. It’s truly a work of art. Hillary Johnson’s website is oslersweb.com and it gives a flavor of what the book is about, but the book is just extraordinary.

When a study fails to find any association whatsoever, that raises a red flag to me. Kind of how Evengard reported not finding any enterovirus whatsoever in either patients or controls in her study on enterovirus/CFS, it seems like by statistical chance alone she should have found at least a couple cases.

Anyways, what I came here to ask was about the 67% figure. Why only 67%? Did the other 33% not have XMRV, was the test just not sensitive enough to detect it in all patients, were the remaining 33% somehow containing the virus, possibly poorly? I think the NIH or NCI found 7 of 11 patients positive for XMRV- same questions as above. Any ideas?


Heidi Bauer October 17, 2009 at 7:05 pm

This was posted today on the WPI’s new Facebook fan page. I found it helpful in understanding who they used and what the guidelines/definitions were.


“XMRV is strongly linked to patients with ME/CFS. This initial finding was confirmed in three different laboratories, the National Cancer Institute, the Cleveland Clinic and the Whittemore Peterson Institute.
Patient samples were donated from different locations around the US. This was not one cohort. All patients met the Fakuda and Canadian definitions for CFS and the study included age and sex matched controls with zip codes but Science did not feel that information was important to this publication. Not all patient samples that were positive had the biological markers of low NK cell function and RNase L defect.
The importance of this finding is two fold. One that XMRV is an infectious retrovirus found in significant numbers in the blood of people who are ill with CFS and only in a very few without symptoms of ME/CFS. Number two is that it was found in 4% of healthy controls which means that 10 million Americans may be infected with this retrovirus.
What you ultimately call this disease is not important. We must now try to understand how this virus is acquired and how that relates to disease and immune deficiencies. Human infectious retroviruses are not ubiquitous or benign. This virus should not be confused with benign endogenous retroviral particles that we all have in our genome. This is only the third human infectious retrovirus found to be replicating in the blood of humans to date, the other two are HIV and HTLV-1 & 2. It is a gamma retrovirus not a lenti retrovirus which means it is a simple vs. a complex retrovirus. “


cort October 17, 2009 at 8:16 pm

Thank you Heidi – that helps greatly. In particular, for me – this statement: Not all patient samples that were positive had the biological markers of low NK cell function and RNase L defect. I think that opens the door wide open for many other patients. Thanks.


cort October 17, 2009 at 7:24 pm

Yes the test did not find the virus in a third of the patients BUT the WPI and is developing a more accurate test which they believe will find the virus in a higher percentage of individuals. (I forgot to mention that in the paper. The antibody test kind of confirms this – it indicates that 95% of the patients they’ve tested have at least been exposed to the virus.

It’s very important that the number of healthy controls testing positive for antibodies to the virus is still remain very low. That, of course, means it is not in the general population – and gives a strong boost to the theory that this is a major factor in ME/CFS.

Check out this statement from a lab that’s apparently associated with these studies.

“Some patients have also asked about the test available for RNASE panels at VIP lab, which tests for the original immune defect that pointed to XMRV. We found this test does not have clinical value, nor does it seem to show whether a patient is likely to have XMRV. A recent study of 38 CFS patients at GMA, tested with the RNASE panel, found it was not helpful in directing treatment at this time. Dr. Mikovits’ study on CFS patients also found the RNASE panel did not indicate who would have XMRV.”

This is good news for ME/CFS patients at large. It means you do not need to have the RNase L defect to carry the virus. This suggests that those special parameters I worried about (RNase L, IL-6, IL-8, etc.) may not apply and makes it more likely that the ‘run of the mill’ CFS patient has the virus.


John October 17, 2009 at 7:51 pm

Yes, I know of a patient who reports they are currently on antivirals and who had what they said were very high levels of RNaseL which were brought down to very low levels following antiviral treatment. Problem is, they didn’t appear(from what I have read) to fall under the ‘responder’ profile, ie no initial worsening of symptoms, no cognitive improvement, etc. They’re also not doing much better on antivirals, from what I gather. So to me this agrees with the lab above and shows how inconclusive the RNaseL testing is at this time, because for this person it doesn’t appear to have much linkage to how well or not well they’re doing clinically. Maybe it shows something, but who knows what.


Heidi Bauer October 18, 2009 at 5:24 am

I’m happy it was helpful for you Cort. I was focusing on the same part. As a patient who has not had a full work up for all those immunological abnormalities, I’ve wondered if I would test positive for XMRV.


Amy October 19, 2009 at 2:25 am

Hi Cort,

Thanks very much for your excellent blog and website. I’m finding your commentary and thoughts about the XMRV research really interesting and helpful in making sense of it all. You might be interested to know that, if you haven’t already seen it, the Wall Street Journal’s article on the news included the following quote from Dr Judy Mikovits:

“Just like you cannot have AIDS without HIV, I believe you won’t be able to find a case of chronic fatigue syndrome without XMRV,”

Wow!- a pretty confident statement from someone who seems so measured!

I have had severe ME/CFS for 18 years, since I was 15, and like everyone else I’m just desperate to know whether the findings will relate to my case. I’m in the UK, so dread to think how long it might be before testing is available here. (In fact if you ever get any information about whether samples can be sent from other countries once testing is available in the US I’d be extremely grateful to hear it).


martin October 20, 2009 at 4:48 pm

How does this xmrv virus account for epidemic forms of ME/CFS? They say it is not contracted through the air (airborne). So how does the incline village, royal free, icelandic outbreak, new york school kids epidemics happen then if it isn’t airborne????????


Erik Johnson October 20, 2009 at 9:30 pm

How can a virus not be airborne?
It seems to me that if someone with an active viral infection were to cough or sneeze, does the possibility even exist that a certain number of viri would not be emitted in the act?
Could it be possible that we simply defined it as not being transmisssible by airborne means, because we had no prior understanding of a mechanism by which a very few copies of DNA could breach the lower customary limits of immune surveillance and reproduce?
But that perhaps, considering that the virus occasionally acted in a manner that appears to transcend this artificial boundary we impressed upon it … that we should look very hard for that mechanism?


kim October 22, 2009 at 7:19 pm

I’m disturbed by the direction of some of these posts, such as Erik (10.20.09, 9:30pm): “How can a virus not be airborne? It seems to me that if someone with an active viral infection were to cough or sneeze, does the possibility even exist that a certain number of viri would not be emitted in the act?”

Be careful here. First of all, this is not an ordinary virus, not influenza, not EBV, not Lyme, not enterovirus, not not not. It’s a retrovirus, a very different animal, with a different profile from common viruses.

Second, we’ve been down this path before. Surely some of you are old enough to remember the hysteria around AIDS in the early days of the epidemic. People made the same wild speculations about casual contact or airborne ‘viri’ then too – which swiftly led to all sorts of witch hunts against AIDS patients, including children who had gotten AIDS from blood transfusions. Even the memory of those dark days is horrible to recall. DO NOT GO THERE again with this retrovirus!!! The retrovirus HIV is not an airborne virus, so it is indeed possible, and likely, that this new retrovirus is not airborne either.

It is as utterly irresponsible to indulge in wild speculations of casual transmission of XMRV as it was with HIV back then. We should be concerned about potential pathways of transmission known for HIV, a heavy enough burden for us to contemplate, and be very wary of further raving beyond what we know as fact so far.


Dorothy October 22, 2009 at 9:53 pm

I agree with Kim. There’s no reason to assume this virus might be spread by airborne transmission. It’s not a respiratory virus like influenza or the common cold. Plenty of nasty viral diseases are NOT transmitted by coughing or sneezing – a few that come to mind are Dengue fever (spread via mosquitos), Yellow Fever (mosquitos) , Ebola virus (direct contact with body fluids), Hantavirus (exposure to rodent urine or droppings), Norwalk Virus (“cruise-ship” virus, spread by contaminated food prepared with unwashed hands), and West Nile Virus (mosquitos).

Speaking of mosquitos – it’s supremely ironic that Dr. Reeves’ dad, William C. Reeves Sr, was greatly admired for his work in identifying and preventing mosquito-borne viruses and credited for saving many lives – while his son has actually increased the suffering of patients! There’s a very interesting bio on the elder (now deceased) Reeves at


Too bad the acorn fell so far from the tree!

At any rate, I hope the mystery of how this retrovirus spreads is cleared up quickly. I thought I read somewhere that WPI was checking out close contacts of patients? Obviously people have gotten sick in clusters, but I have to wonder if XMRV might quietly infect people then get triggered by an airborne virus that spreads quickly through a population. Of course, that doesn’t explain how people get infected with XMRV in the first place.


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