It's an interesting theory, but I wonder if contaminated vaccines were really the root cause behind CFS/ME, wouldn't science have established this causative relationship by now? If this retrovirus were the driving factor behind CFS/ME, one would think that at least a subset of patients would start to feel symptoms pretty soon after the vaccine had been given (at least those patients that already have co-infections). I don't believe this kind of reaction to a vaccine could happen without it becoming public knowledge.
To give an example, in 2009 a Vaccine called Pandemrix was introduced to Europe in order to treat the swine flu outbreak. Hundreds of thousands of people quickly got vaccinated in my country (Finland). Unfortunately, it turned out that this vaccine had a rare side effect, which would trigger narcolepsy in children with a certain genetic mutation. The occurrence of this was minimal (3.6 per 100 000), nevertheless, an investigation was launched by Finnish authorities and the link was established.
Based on above, if something like severe CFS/ME was triggered by vaccines in my country, and assuming that it's not as rare as the narcolepsy case above, I have little doubt that it would be public knowledge by now. Even if science was reluctant to investigate this, there would have been reports in newspapers about a subset of vaccinated people becoming sick with CFS/ME, just like there was in this much rarer narcolepsy case.
Perhaps this was not clear, but the hypothesis isn't claiming that outbreaks tend to happen at the point of vaccination. Contaminated vaccine lots would introduce smoldering, subclinical retroviral infections into the population. As shown by HIV and HTLV, most people don't show acute symptoms upon initial infection, and when they do the symptoms are rather general (fever, etc).
So no, I wouldn't expect many patients to descend into ME/CFS soon after vaccination (though that's not to say some don't, in particular as is reported with Hep B vaccine, since it can trigger acute immune activation).
However, once a retroviral contaminant (that resides in immune cells and proliferates via clonal expansion) had been introduced into the population, an "outbreak" of ME/CFS could emerge from an outbreak of any acute infection that triggers retroviral proliferation through immune activation (e.g. enterovirus, EBV, CMV, etc). Hence, while most of the population recovers from said acute infection, those with a smoldering retroviral infection have their immune systems sent into tailspin.
The ordering of events is important as well. Having an existing "co-infection" at the point of vaccine contamination wouldn't necessarily be problematic. Having latent retroviral infection at the point of acute immune activation via co-infection would.
The problem with looking primarily at enteroviruses/EBV/etc is that there is a gaping hole these hypotheses: why do the vast majority of people recover yet a small percentage descend into ME/CFS? At best, enteroviruses/EBV/etc are necessary but not sufficient. And they don't even appear to be necessary, given gradual onset cases and apparent variability in type of triggering infection. This hypothesis would fill that hole.
Not really, because for adults who develop ME/CFS in outbreaks of ME/CFS, because people move around, these adults would likely have grown up in a different part of the county, so where they were vaccinated as a child would have likely been a completely different geographic location to the outbreak; and furthermore, adults of different ages would have been vaccinated in different years or decades. So there would be no batch of vaccine common to those who develop ME/CFS in an outbreak.
There are numerous reasons why this is wrong or irrelevant:
Firstly, unless most outbreaks affected large percentages of the relevant populations, then movements of people wouldn't be problematic. Most outbreaks, esp the notable ones, appear to have been relatively small fractions of the population due to the fact that these outbreaks were only noticed by careful observation of clinicians who saw patterns emerge among patients.
Secondly, the outbreaks appear to have been most prevalent in the mid-1900s and petered out by the 1990s in inverse relation to increasing movements of population over time. To my knowledge there have not been many documented outbreaks in the past couple decades (though I'll leave it to those who like to invoke variants of "if XYZ were really happening, science would surely know!" to explain this apparent lack of recent outbreaks).
Thirdly, many outbreaks occurred in situations where people would have been similarly vaccinated: hospitals, schools, psych wards, small isolated communities.
Can you explain why you are only focusing on retroviruses? Is it because when government sponsored TV adverts warning about AIDS first appeared in the late 1980s, they created a sense of dread about retroviruses — a strong fear that has lodged in the collective psyche?
Why not other types of virus? The only virus I am aware of that passed from animals to humans through vaccines is SV40, which is a polyomavirus, not a retrovirus. If you look at this list of pathogens that are associated with various chronic diseases, there are very few retroviruses in that list. You find lots of herpes family viruses in that list, lots of enteroviruses, parvovirus, and various bacteria; but very few retroviruses.
And if it is a retrovirus you are focusing on (or fearful about), why should it have been transmitted via vaccines? Why not transmitted via contact with animals, as HIV is thought to have crossed into humans? Or why not a retrovirus that has been present in the human species for many millennia, such as the HTLV retrovirus?
Anything can seem arbitrary from a standpoint of ignorance. You freely cite the consensus narrative versions of the XMRV and older retrovirus (e.g. DeFreitas) sagas without apparent understanding of how and why these associations arose and why many people are displeased with the questionable science propping up these narratives.
For one thing, XMRV was found while conducting a broad search for any and all known viral evidence. For another, once found, it was not seen as surprising or arbitrary. Researchers familiar with retroviral infections and the pathophysiology of ME/CFS have long noted how numerous aspects of ME/CFS point to retroviral involvement: depletion of NK cells, cytokine patterns, neurotoxicity of certain retroviral proteins, associations with rare cancers, explanation for the positive effects of B cell depletion (Rituximab), etc.
Here is a tangentially involved researcher expressing her dismay at this very idea: that all roads lead to Rome (retrovirus), yet Rome was prematurely and unscientifically decided not to exist.
But never mind, you're right. I'm interested in retroviral involvement because I saw a poster of HIV in the 80s and have been quivering in fear ever since.
In any case, if there were a retrovirus involved in ME/CFS etiology, the first thing to do would be to find that in ME/CFS patients. Later you can worry about where that retrovirus came from.
This sounds oddly like plea bargaining, like you have some pressing need to pre-vindicate vaccinations before even considering the hypothesis. Sure, there are numerous way to approach this, but the source of contamination is somewhat vital to the hypothesis.
Not discarded, but treated with caution, perhaps in part in case it generates another wave of retrovirus religious fervor in the ME/CFS community, like the high emotions surrounding the XMRV story. And as we know with previous retrovirus discoveries in ME/CFS patients, the initial findings may not pan out when further research is performed.
Unless he's published this data or in is in the process of publishing it, then by definition it has been discarded. You can rationalize it how you like, but science doesn't proceed by individuals acting as judge, jury and executioner, regardless their pedigree.
It is a good question.
I think part of the answer may be the way human beings think: they want a simple cause-and-effect relationship, like a specific virus that causes the specific disease of ME/CFS. So the idea that XMRV might be the singular cause of ME/CFS is attractive because of its simplicity.
In science, there is always the feeling that the answer ultimately will be a simple and beautiful one.
But when you have a situation where viruses like enterovirus and EBV appear to trigger ME/CFS now and then in some people, but not in general, then that creates messy complexity and a multifactorial etiology that is harder to fathom and understand. So maybe scientists are not attracted to researching that, because it seems messy, complex and ugly.
However, it could well be that there is a simple explanation. For example, it could be that ME/CFS only occurs when an enterovirus infection is able to break into certain tissue compartments, such as the brain, or such as immune organs like the thymus or spleen.
That might explain why Dr Chia has found that patients who are inadvertently given immunosuppressive corticosteroids during an acute enterovirus infection are at increased risk for developing ME/CFS: the immunosuppression may allow enterovirus to penetrate deeper into the body, and break into tissue compartments like the brain that it might not usually infected, thereby triggering ME/CFS.
I've never understood this insistence upon things being inherently and insurmountably complex. It's like giving up before even starting. Clearly there will not be a single cause/explanation for all people who fall under the vague ME/CFS umbrella. But there will necessarily be subsets who do share common causes that will appear "simple" once they are elucidated.
Understanding begets simplicity, due to the high level discernment of basic necessary and sufficient conditions. Nor does simplicity preclude complexity in underlying details: the hypothesis I've put forth allows for great complexity in that regard.
Furthermore, all "understood" diseases have simple high-level explanations: HIV=AIDS, etc. Do you run around proclaiming that these are "too simple" to be of any value? By your logic, HIV cannot cause AIDS because it's too simple.
Regarding Dr. Chia's observation about steroids,
this link discusses how steroids promote retroviral replication, in particular gamma retroviruses.
