The real story about XMRV coming out today?

[xrayspex]

In one way, to me, it doesnt matter if m.e. is more men or women......if docs and researchers think its more women why should that allow them to discriminate more? They can't openly discriminate altho they may have more bias, but man its 2011, is it socially acceptable as a practitioner to say I think you are psychosomatic because you are female? that sounds like a lawsuit waiting to happen to me. Not that I don't understand that happens, but it dawned on me lately that maybe it times i am complicit in this charade of discrimination if don't confront it more openly if suspect its going on. Perhaps it can be as powerful as playing the race card can be (not that I think that always works but I totally support it because racism, sexism, classism is alive and well in post industrial countries) if we confront first the offending practitioner than their boss than their PR staff and start calling more attention to the inappropriate practice of differing care based on gender.

I understand from bio research perspective may want to figure out if more male or female to inform studies. I just expect the same care from practitioners either way, being taken as seriously and tested etc I just found out I have sjogrens, which I knew from self diagnosis, am intrigued by autoimmune component. I did sense tho that the rheumie, while nice and somewhat supportive, didnt seem to think it was big deal.....I suppose compared to lupus may not be as bad, but I woud like to see it studied more and how it ties into m.e. I have been apparently immune stimulated for some time, rarely get colds last 9 years but painful neuro stuff instead.

 

[oceanblue]

That's fine but testing two hypotheses where one is reliant upon the other is, to say least, 'challenging'. Ideally the existence of a gender specific immune response needs to be established separately from testing an infection involvement hypothesis

Er, as far as I'm aware, women generally producing a stronger immune response is more than a hypothesis, eg this from a 2005 review paper

This results in a sexual dimorphism in the immune response in humans: for instance, females produce more vigorous cellular and more vigorous humoral immune reactions

so I wasn't knowingly piling hypothesis on hypothesis.

If gender specific immune response to infection (as against immune response to other environmental agents) is a factor in disease progression then it seems likely it would be evident across a range of infections (unless an immune system hijacking agent in envisaged) and that the defining characteristic would therefore be immune response not specific infections.

The Dubbo evidence is that it does apply across a range of infections (but not necessarily most). They found that with EBV, Ross River Virus and Q fever around 10% developed PVFS - though that means 90% did not. If one particular pathogen was particularly good at triggerig PVFS in vulnerable people that could lead to a high proportion of the patient population having this particular pathogen. That said, I think it's far more likely that CFS has multiple causes, maye they could even all turn out to be pathogens.

 

[oceanblue]

Where did the group selected from originate? My point was that there is already pre-selection in identifying patients before the CCC was even applied. We are dependent on patients and doctors identifying patients for the study in the first place -- before the selection for the study is made. Until we have a way of getting around that obstacle, we don't know that we have a balanced sample.

We're in danger of going well off topic here, but for the record the sample was based on GP practices covering 150,000 patients, more on the study here. Are you suggesting that GPs are failing to pick up CFS in men, thereby artificially creating a sex bias? A large population survey in the US found the same sex bias using very wide selection criteria intially.

 

[Daffodil]

someone mentioned tissue reservoirs. didnt ila singh do autopsy study that found no xmrv in tissues? but i guess if the viral sequences were wrong it wouldnt show

 

[In Vitro Infidelium]

Er, as far as I'm aware, women generally producing a stronger immune response is more than a hypothesis, eg this from a 2005 review paper so I wasn't knowingly piling hypothesis on hypothesis.

I should have been more precise: "Ideally the existence of a gender specific immune response [in which enhanced disease processes are demonstrable]needs to be established separately from testing an infection involvement hypothesis".

That mammals have hormonally mediated gender differentials in immune response is reasonably well established, and the link to this in human autoimmune disease is generally recognised, but neither of these conditions imply exacerbated disease processes as a response to infection. That human females produce (in some aspects) a stronger immune response to a given infection, as compared to human males, doesn't of itself mean that women are more prone to chronic immune activation (they maybe but it's still an hypothesis that needs to be tested). In fact a null hypothesis seems rather obvious - that the less efficient male immune response may provide for increased risk of chronic infection and thus chronic immune stimulation. I'm not arguing against either the existence of a gender differential in M.E/CFS (although I think it needs rigorous testing, given likely widespread diagnostic bias)
nor against an immune activation role as part of the aetilogy of M.E/CFS - just that there is complexity within the likely relevant fields of enquiry, and that complexity demands very careful logically processed examination. The limitations of much previous M.E/CFS research is that it has been structured as giving overarching answers ( XMRV being a case in point) when no such answers can be achieved from single studies or even a series of studies within a single scientific discipline's purview.

The Dubbo evidence is that it does apply across a range of infections (but not necessarily most). They found that with EBV, Ross River Virus and Q fever around 10% developed PVFS - though that means 90% did not. If one particular pathogen was particularly good at triggerig PVFS in vulnerable people that could lead to a high proportion of the patient population having this particular pathogen. That said, I think it's far more likely that CFS has multiple causes, maye they could even all turn out to be pathogens.

My point was an argument about why the 'M.E/CFS has XMRV involvement' hypothesis was flawed at the outset, it was reliant on multiple untested supporting hypotheses: "XMRV is particularly good at triggerig PVFS in vulnerable people which leads to a high proportion of the patient population having this particular pathogen", "XMRV produces hormoniallymediated immune responses which result in gender differentials in the patient population", the observed gender differential in M.E/CFS is an artifact of diagnosistic bias", etc. There was never any sound reasoning to consider an association between an entity without any evidence of pathogenicity, and for which there was no evidence of human association except in a few older males who provided no basis for wider population representation. Mikovits and WPI are now rewriting th script - "it's not one pathogen, it's lots", these aren't present in 70% but there still lots (how many ?) of M.E/CFS sufferrers with these XMRVs in their bodies" etc, but this is more apologism than scientific thought.

IVI

 

[In Vitro Infidelium]

About different genders' immune systems responding differently to various infections, I have always seen that as mainstream. And an important reason why there are some "women's diseases" and some men's. The variations on how the immune system works, gender wise, is extra evident in auto immune diseases. Do you think differently about that?

I think my reply above answers some those issues. A couple of things I would add: The pattern of gender disproportion is not consistent across autoimmune diseases with ratios typically ranging from 2:1 (MS) to 10:1 (HT), there are also complications in age specific prevalence with differentials increasing with age. Allergy provides a further complicating aspect, for example ashtham is more prevalent amongst boys (3:2 ratio) and parity between males and females doesn't occur until 40+ with prevalence among women exceding that in men, later in life.

Gender difference in M.E/CFS deserves investigation, but at this stage there seems no solid no basis on which to use autimmune studies as definitive support for M.E/CFS research directions - these are two areas of uncertain science, which may have something interesting to contribute to each other but both require separate and internally validated research, although personally wouldn't exlude as logically unviable the proposition that M.E/CFS is at base an autoimmune illness. As to gender difference in infection response - despite the autoimmune evidence and the implication of infective agency as a precursor to subsequent autoimmune illness, there is no consistent evidence that gender mediated difference in immune response leads to difference in observable disease aetiology, that is men and women appear to get sick in roughly equal proportions when affected by the same toxins, bacteria, viruses or parasites.

IVI

 

[Daffodil]

once i asked dr. coffin if the same drugs that work on xmrv would work on the lo/alter viruses and he said "absolutely"

 

[VillageLife]

Just heard this about the blood working group results....

The PMBSs were not preserved in Trizol or any other preserving agent.

 

[redo]

@IVI. I appreciate your thorough posts. :Retro smile:

About gender differences an infectious diseases. Take HIV for example, if you look at the figures for heterosexual contact, there are about twice as many women as men acquiring it. I doubt they couldn't explain why it was like that before they looked for the virus, but as I read you, you think putting forth a hypothesis for gender prevalence should be a prerequisite for even testing the patients for the virus (?).

If the gender prevalence was like 10:1, than I'd for sure agree that it would be an important thing to do forehand. But when the gender prevalence numbers are unsure to say the least, than I can't see why it should be required to put forth such an hypothesis before the testing...

A simple question of 'why is XMRV likely related to M.E/CFS ?' needed answering before bloods were taken and the results published - not muddled through in the aftermath with ad hoc justifications trolled out to answer the very obvious gaps in the hypothesis of a connection between M.E/CFS and XMRV.

IVI

When there's not huge gender differences, and when we know nothing about transmission of (potentially prevalent) gammaretroviruses, and know nothing about how they would behave in a body, I think it's uncalled for to require an hypothesis about why a potential pathogen could affect more of one gender than the other before doing some blood tests.

I might be interpreting you wrong. But what I read between the lines was that an ethics comitee should have stopped the XMRV research before it began - or had them put forth a gender hypothesis.

Personally, I think the way ethics committees have gone from being pretty absent to being 'everywhere' is a ditch to ditch response. It used to be no barriers to doing medical research (examples not needed I guess), to the way it is now where there is a roadblock no matter where you turn. Even for noninvasive procedures.

 

[Undisclosed]

Just heard this about the blood working group results....

The PMBSs were not preserved in Trizol or any other preserving agent.

This is a rumour. The person that started this rumour has failed to provide proof of this. It seems the person promoting this rumour is posting it on different websites using different usernames (that's just a rumour too). Does anybody have any proof. It is doubtful that any seasoned researcher would not use a preserving agent.

 

[VillageLife]

Yes I heard it on another forum. I also wondered if it was correct?

 

[ixchelkali]

Those are extraordinarily vague statements from the BWG. Why not provide a precise breakdown or chart of what labs tested what controls with what methods?

If the WPI were only given a couple control samples which they signed off on (and therefore had little overall say in the negativity of the control group), the BWG could still make the following statements (which you bolded) and be semantically correct. I've included in brackets the hidden implications that drastically alter the meaning of these claims:





The issue again, is details. But instead of details in this regard, the BWG offered us only vague, equivocal statements that could cover a wide range of scenarios. Your assertion that "At any rate, the WPI agreed that the controls were negative before they were blinded" is a reinterpretation of these vague statements that lends them even more power. This part of the BWG paper reads like a political press release, and that alone should raise questions about why the precise details of this process were omitted.

Read the supplemental materials. The details are there. The WPI was not "only given a couple control samples which they signed off on"; they tested each of the negative controls themselves and agreed they were negative.

http://www.sciencemag.org/content/suppl/2011/09/21/science.1213841.DC1/Simmons-SOM.pdf

I dont see that this is vague at all. It specifies that the three negative laboratory controls were tested by all 9 laboratories participating in the study. The 12 samples from blood donors were sent to five of the participating laboratories, including the WPI (as well as Los, the CDC, Mary Kearneys HIV lab at the NCI, and Frank Ruscettis NCI lab). So the WPI tested all of the negative controls and concluded that all 15 were negative, before they were blinded.

Remember, the WPI is part of the Blood Working Group. Judy Mikovits is one of the authors of the study. When you say that the BWG is being vague, or suggest that the WPI would sign off on the negative controls without having tested them, you are saying that the WPI did sloppy work in this study. That does not appear to me to be the case, and you don't help the WPI or ME/CFS patients by saying that.

 

[In Vitro Infidelium]

About gender differences an infectious diseases. Take HIV for example, if you look at the figures for heterosexual contact, there are about twice as many women as men acquiring it. I doubt they couldn't explain why it was like that before they looked for the virus, but as I read you, you think putting forth a hypothesis for gender prevalence should be a prerequisite for even testing the patients for the virus (?).

If the gender prevalence was like 10:1, than I'd for sure agree that it would be an important thing to do forehand. But when the gender prevalence numbers are unsure to say the least, than I can't see why it should be required to put forth such an hypothesis before the testing...

HIV is a rather unhelpful comparison for M.E/CFS. In the early days of HIV research science had to confront a major acute public health issue where patients faced deeply unpleasant illness and death. There was a de facto acceptance that the illness was a disease of gay men and intravenous drug users, this actually led to unhelpful lines of research but in the face of the mammoth investment that was made, such dead ends were compensated for by alternate directions. With proper description of HIV it is now possible to understand why certain populations are affected by higher infection rates, which are largely functions of behaviour and exposure. However if one takes HIV out of the context of the developed worlds self concerned panic, and considered how AIDS could have been researched across cultures, rather than the research being solely focussed on seeking a cure for the west, the behaviour and exposure issues would have been far more explicit which would in turn likely have provided valuable epidemiological evidence at an earlier stage.

M.E/CFS is not HIV, there is no evidence of an epidemic and thousands of young people are not dying every day in ten of countries across the world. The science of M.E/CFS can be pursued in the most effective way, (necessarily) using a fraction of the resources applied to HIV, without the pressure that HIV researchers faced in the 1980s and 1990s. Hypotheses can of course be produced at the drop of hat the question in science is whether they are testable or not you can only test an hypothesis against what is known; merely coming up with evidence say the presence of virus - in patients with a particular condition, doesnt of itself tell you anything unless what is known about the virus has some relationship to the character of the disease. In the case of M.E/CFS that character includes (on all the available evidence) a very noticeable gender disproportion and that is a huge deal !

In HIV its always been possible to show that infection is a function of exposure, neither homosexually men in the US, nor heterosexually active women in the developed world are in anyway physiologically notable in terms of HIV they just happen to be groups who have high exposure because of freely chosen or economically or culturally imposed behaviours. In contrast there is no evidence that female M.E/CFS patients have been in some way more highly exposed by lifestyle to some specific pathogen than the male population that they live alongside. Of course such evendence may be there to be found, but to date it has not been made explicit.

When there's not huge gender differences, and when we know nothing about transmission of (potentially prevalent) gammaretroviruses, and know nothing about how they would behave in a body, I think it's uncalled for to require an hypothesis about why a potential pathogen could affect more of one gender than the other before doing some blood tests.

I might be interpreting you wrong. But what I read between the lines was that an ethics comitee should have stopped the XMRV research before it began - or had them put forth a gender hypothesis.

In medical research any difference in gender ratios is significant differences of the order 1:2+ are hugely important because they dont happen for no reason, they tell us something profound about the nature of the condition. Other than exposure, there is no evidence for gender specific differentials in infectious effect (notwithstanding that there are some differences in male and female immune functioning) a thousand women and thousand men exposed to the same bug will on average get equally sick. M.E/CFS isnt like that, as far as anyone can currently tell, for every 1,000 women with M.E/CFS there are no more than 500 men that doesnt reflect any known infection although it does of course reflect the position in autoimmune disease. The question then is not whether investigating XMRV or HGRVs in M.E/CFS is unethical, but that there simply isnt any compelling scientific reason to follow that line of research, unless there is a testable hypothesis of why there should be a gender differential in an infective disease. This is scientifically essential because the gender differential is a key descriptor of the condition under investigation it should be one of the reasons why a particular pathogen were being looked for. The alternative is to randomly select pathogens that look likely and keep plugging away at say $500,000 per research cycle per lab year. After how many $millions and how many lab years do you decide that the search is fruitless ? M.E/CFS isnt AIDS, there isnt going to be half a billion dollars for research; tracking down single pathogens without some clear logical basis for doing so is misdirected science and other than on the basis of some lucky break, doomed to failure. Lombardi, Mikovits and WPI have singularly failed to explain why XMRV could have had any relationship to M.E/CFS, it would be foolish beyond belief to continue down this particular cul de sac without having some clear scientific justification that is related directly to the known characteristics of M.E.CFS; anything else is just micturation contra aeolian.

 

[Christopher]

M.E/CFS is not HIV, there is no evidence of an epidemic and thousands of young people are not dying every day in ten of countries across the world.

No - millions of people of all ages are dying incredibly slow, torturous, deaths due to gross negligence of the scientific community. How revolting.

 

[ukxmrv]

I think IVI that you have different value judgements here from patients when you compare HIV and CFS & ME.

Although patients were dying of HIV more quickly than patients with CFS and ME are dying, we are still dying. None of us will get our lost lives back if and when a cure is found.

We don't know how many patients in the UK or the USA have ME and we don't know how many die each year. No one keeps the figures on the patients who are living and dying in misery.

You seem to be arguing that because the HIV deaths were quicker they are somehow more important and that resources were more urgent. That's not the case. Each ME patient needs these urgent resources spent now.

I would argue differently to you. When I die at 70, 80 whatever I will still be dead and my death will be important as any person who died of HIV. It's already been (nearly) 30 years that I have lived with this disease and I've lost patient friends through suicide, early cancer and early heart problems. I'm facing and living a deeply unpleasant life until I die.

That's what you do not seem to understand about ME and CFS. This makes me wonder if you know about these diseases. It is deeply insulting to argue that ME patients should wait 10, 20, 30, 40, 50 years without understanding of the disease and a cure.

If I had died during the initial acute viral onset (I was admitted to hospital) at least I would have been spared the last 30 intolerable years. Many HIV patients took their own lives as their health deteriorated as they found the suffering intolerable. ME patients are finding their own suffering intolerable.

This is not a comment on your understanding of science. This is a comment on your understanding of ME and CFS.

 

[Bob]

In medical research any difference in gender ratios is significant differences of the order 1:2+ are hugely important because they dont happen for no reason, they tell us something profound about the nature of the condition. Other than exposure, there is no evidence for gender specific differentials in infectious effect (notwithstanding that there are some differences in male and female immune functioning) a thousand women and thousand men exposed to the same bug will on average get equally sick. M.E/CFS isnt like that, as far as anyone can currently tell, for every 1,000 women with M.E/CFS there are no more than 500 men that doesnt reflect any known infection although it does of course reflect the position in autoimmune disease. The question then is not whether investigating XMRV or HGRVs in M.E/CFS is unethical, but that there simply isnt any compelling scientific reason to follow that line of research, unless there is a testable hypothesis of why there should be a gender differential in an infective disease. This is scientifically essential because the gender differential is a key descriptor of the condition under investigation it should be one of the reasons why a particular pathogen were being looked for. The alternative is to randomly select pathogens that look likely and keep plugging away at say $500,000 per research cycle per lab year. After how many $millions and how many lab years do you decide that the search is fruitless ? M.E/CFS isnt AIDS, there isnt going to be half a billion dollars for research; tracking down single pathogens without some clear logical basis for doing so is misdirected science and other than on the basis of some lucky break, doomed to failure. Lombardi, Mikovits and WPI have singularly failed to explain why XMRV could have had any relationship to M.E/CFS, it would be foolish beyond belief to continue down this particular cul de sac without having some clear scientific justification that is related directly to the known characteristics of M.E.CFS; anything else is just micturation contra aeolian.

IVI, your argument re the gender issues has weaknesses.

You are overlooking a number of different reasons why women could become ill, but men not become ill, when exposed to the same pathogen.

1. If a virus is sexually transmitted, there could be a reason why women are more vulnerable to infection than men.

2. People who are infected with HIV do not necessarily show any signs of illness, or have any symptoms. So it is possible that an equal amount of men and women are infected with a retrovirus (e.g. an HGRV) but that women are more likely to become ill. One such reason could be that the virus is stimulated or reacts in some way to female hormones. Or another reason could be that there is some tissue unique to females that the virus thrives in. Remember the macaque study, and how XMRV seems to prefer tissue to blood. I think there has been some research, or at least a hypothesis, about why XMRV might be stimulated by hormones, but I'm afraid that I can't remember the details.

I don't think that HGRV research should be stopped just because IVI doesn't know the reason why there are gender differences.


Personally, I wouldn't call XMRV research a waste of resources, whether or not the virus is associated with ME.
Not only does the research advance our understanding of retroviruses, but we have also discovered that XMRV is a man-made virus that pollutes many labs. (Assuming, for the sake of discussion, that any XMRV research is now valid.)
This alone is reason to investigate further.
A previously unknown virus, which lives in human tissue, contaminating labs, puts people at danger of infection.
Lab workers could be infected, and vaccines are at risk of contamination.

I also wouldn't call XMRV a 'random' virus.
What ever the current state of play, XMRV has been detected by various researchers in the general population, and related viruses have been detected in ME patients by at least two researchers.

It doesn't seem like a very good idea to me to shut down research just because the answers aren't clear to us, and IVI isn't convinced that an infective agent could behave differently in men and women.

And if you think that a retrovirus could not explain the symptoms of ME/CFS then you probably think that ME/CFS patients just feel tired all the time.
The multiple symptoms that ME/CFS patients experience could well be explained by a virus.
And actually, even a sole symptom of tiredness or fatigue could be explained by a viral infection. Why do you think that chronic fatigue could not have a viral cause?
All viruses behave differently, and it doesn't seem like good science to pre-determine how you expect a virus to behave.
For example, a flu virus behaves very differently to Herpes viruses etc etc etc.

Another reason why I believe that XMRV has been useful for CFS/ME research is that it has brought new funding, new attention, and new researchers into the field.
As just one example, Ian Lipkin now seems very interested in working on CFS, whether XMRV is involved or not. He will bring new funding into ME/CFS research.
He seems to think that a pathogen is involved in CFS/ME, and has said that he will continue to work in the field of CFS/ME and hunt down the pathogen.
Who could have expected that someone like Ian Lipkin, or Harvey Alter for that matter, would have been interested in CFS/ME a couple of years ago? They probably hadn't ever done any work in the field before.

 

[asleep]

The details are there.

No, they are not. Please point me to a chart that shows exactly which lab tested which control with which method. Or, lieu of that, please show me where it states in no uncertain terms that the WPI itself tested every single control with whatever methods they desired.

These are the things that constitute details. Not three vague sentences with many possible interpretations. And given how crucial the determination of genuine negatives is, the lack of detail here should be seen as shocking, not convincing.

The WPI was not "only given a couple control samples which they signed off on"; they tested each of the negative controls themselves and agreed they were negative.

Well, the point is we don't know, because we were not given this information in unambiguously explicit terms. In my previous post, I demonstrated how the words in this passage could semantically apply to a situation in which the WPI signed off on only a subset of control samples, through the use of hidden implications. (As an exercise, assume for the sake of argument that the WPI was only sent samples from a couple controls and that cumulatively all the labs together signed off on all the controls using an accumulation of many methods. Now re-read this passage from the SOM. It still reads as valid, though it describes a very different picture.)

Your assertion that "they tested each of the negative controls themselves and agreed they were negative" is simply one possible interpretation of their description. Given the other possibilities (one of which I have shown), your interpretation relies on assumptions and trust without the backing of evidence. You have, of your own accord, breathed the most generous meaning into their words.

I humbly suggest that you might be mistaking the implications of language with concrete details.

Remember, the WPI is part of the Blood Working Group. Judy Mikovits is one of the authors of the study. When you say that the BWG is being vague, or suggest that the WPI would sign off on the negative controls without having tested them, you are saying that the WPI did sloppy work in this study. That does not appear to me to be the case, and you don't help the WPI or ME/CFS patients by saying that.

This doesn't necessarily imply that they did sloppy work. Given the centralized nature of this study, who knows what discrepancies existed between what the WPI thought was happening and what was actually happening. One can only speculate.

I realize this may seem like reaching for straws (and I certainly reserve the right to be shown wrong), but if the past two years have taught anything it is the power of words to obscure the truth in plain sight. This is why I insist upon raw details, not second-order interpretations (especially if the results are being billed as "conclusive").

 

[floydguy]

Great comments Bob and Asleep. I am not one of those who is completely attached to the HGRV theory but I think it's the best current disease model. Aside from childhood trauma, Wessely's false illness beliefs, EBV/HHV-6 what are the more compelling models that we have to work with? Everything else seems to be looking at the effect rather than the root cause.

 

[floydguy]

I'm inclined to agree with you, Floyd, although I think some of the research into genetic immune abnormalities combined with infections are also promising.

I'd agree with you there as I am in several of the genomic NIH/CDC studies . My core symptom is a severely dysfunctional immune system. The question seems to be is there a pathogen that is no longer present, is a pathogen still present and/or is there some defect in the immune system? I have no problem considering non-HGRV scenarios. I just hate to do it to go back to childhood trauma research.

 

[In Vitro Infidelium]

I think IVI that you have different value judgements here from patients when you compare HIV and CFS & ME.

Differently from patiients , ALL patients ? I claim to be an affected by M.E/CFS does having a differing opinion exclude me (and indeed others who arent vocal) from an M.E/CFS diagnosis ? In any any event argumentum ad populi is hardly a basis for approaching a discussion on science.

Although patients were dying of HIV more quickly than patients with CFS and ME are dying, we are still dying. None of us will get our lost lives back if and when a cure is found.We don't know how many patients in the UK or the USA have ME and we don't know how many die each year. No one keeps the figures on the patients who are living and dying in misery.You seem to be arguing that because the HIV deaths were quicker they are somehow more important and that resources were more urgent. That's not the case. Each ME patient needs these urgent resources spent now.

Some statistical evidence of fatality would be useful. Saying we dont know haow many are dying because we dont know how many are ill, is simply saying theres no statistically valid evidence of fatality from M.E/CFS. HIV IS (not was, IS) a virulent disease that kills millions of course its more significant if someone dies in 6 months than if they die in sixty years because, in the first case youve got a small window of oportunity it is more urgent ! And HIV is easily transmittable it is a major public health issue which will command public resources. It doesnt matter how serious we consider M.E/CFS to be the rest of the world just isnt going to take anyone who claims M.E/CFS is somehow equivalent to AIDS, seriously. That means the resources available for research are always going to be less, and less by orders of magnitude than were available for HIV research, and that means there can be no useful comparison between how HIV was researched in the 1990s and how M.E/CFS can be researched in 2011 2021.

I would argue differently to you. When I die at 70, 80 whatever I will still be dead and my death will be important as any person who died of HIV. It's already been (nearly) 30 years that I have lived with this disease and I've lost patient friends through suicide, early cancer and early heart problems. I'm facing and living a deeply unpleasant life until I die. That's what you do not seem to understand about ME and CFS. This makes me wonder if you know about these diseases. It is deeply insulting to argue that ME patients should wait 10, 20, 30, 40, 50 years without understanding of the disease and a cure. If I had died during the initial acute viral onset (I was admitted to hospital) at least I would have been spared the last 30 intolerable years. Many HIV patients took their own lives as their health deteriorated as they found the suffering intolerable. ME patients are finding their own suffering intolerable.

Science isn't personal, we can't make sense of it by referencing our own experience, and certainly emotional appeals lead no where. At no point did I argue that research should be delayed. There is a finite amount of money going into research. Effective lobbying for increased funding and for best directed funding, requires the capacity both to understand the science and to make rational choices about what directions to support. HGRVs have the potential to be a perpetual mirage which M.E/CFS affected people could spend the next decade funding and lobbying on behalf of, without any sound reasoning as to why a useful result should come from that research. Emotional appeals to justice or suffering or whatever do not open up effective vistas of research, in fact usually the opposite. One of the things us 30 year veterans can do is bring a degree of philosophical perspective to these discussion yes on current form we will not get better before we shuffle off this mortal coil but: we have survived 20+ years without much in the way of medical intervention and one can either take a gloomy medicine has abandoned us view or one can described it as survival in the face of adversity, Id say the latter was the more progressive choice.

IVI