They might NOT be giants.

Enrico Fermi was asked at least once what characteristics Nobel Prize winners in physics had in common.

His reply is revealing, "I cannot think of a single one, not even intelligence."

I hasten to add that this judgment should not be limited to either physicists or Nobel Prize winners. Intelligence is not an essential requirement for successful scientists. Some have it, some don't. Likewise originality among scientists is overrated. Far more published work is like Charles Darwin's detailed studies of barnacles than either his account of the Voyage of the Beagle or "On the Origin of the Species by Means of Natural Selection". (In fact his work on barnacles was far better than mediocre natural science.)

While there is an enormous range of intelligence, originality, energy and personalities among working scientists, most are like ordinary people who spend their lives going through the motions, expressing opinions as facts, drawing paychecks and fighting strenuously over prestige and perquisites. This is where the stereotypical conspiracy run by diabolical geniuses (Professor Moriarty? Lex Luthor?) falls apart. We have a case right at hand.

Had such a centrally directed conspiracy existed it would have known better than to introduce the idea that a dangerous human pathogen could have originated by accidental recombination in a laboratory, then gone undetected for 18 years. This is precisely what protesters in the 1970s debates feared research on recombinant DNA would unleash. Arguments made to placate them then were that such outcomes were extremely improbable, only took place under special circumstances, and would be avoided or detected (by measures put in place by responsible researchers) before the resulting pathogen entered the general population. With researchers currently testing themselves and numerous laboratories for contamination by a potential human pathogen those old assurances now ring especially hollow.

Even assuming the rhetorical cunning to circumvent this weakness, the argument that the recombination event could only take place in a laboratory because the genome fragments which recombined were only present in one strain of laboratory mouse should have been an obvious non-starter. If the genes are only found in such mice, they must not be older than that strain, and the virus responsible is likely to remain around in some biological reservoir. If they were only found in laboratory mice, the notion that the source for the genes is tied to humans would be hard to dispel.

The second try was to insist that the gene fragments were actually present both in other laboratory mice -- and in wild mice. The catch here is that while the specific mice where these were first noticed, and other laboratory mice, lack the XPR1 receptor which allows entry by both xenotropic and polytropic murine viruses, there are other species of wild mice which have these receptors, and can be infected by the recombinant virus. What appears wildly improbable on human time scales in a single mouse in the laboratory, is rather plausible in the billions(?) of such mice spread across south and east Asia.

Such small mammals often experience population explosions and crashes in response to changing conditions. Environmental stresses during population crashes drive infected survivors into new habitats, including close association with humans, who they might otherwise avoid. This is precisely how hantavirus jumped from mice to humans. Human crises like overpopulation, deforestation, famines and wars can multiply the probability of such events. Mass movements of people can then spread pathogens to much larger human populations. Such large movements have taken place in living memory, and major shifts in human populations are still taking place.

An argument against one specific pathogen has opened a whole new can of worms. That is not the least of the problems created by polemical use of this hypothesis.

Recombination of defective inserted provirus being carried passively in chromosomes takes place at virtually geological rates characteristic of host evolution, not rapid viral evolution. Starting with a replication-competent retrovirus similar enough to activate gene transcription, and incorporate the results in its own genome, makes improbable events much more likely, but the whole argument was created to get rid of the idea that any replication-competent retrovirus was active in the first place.

It also introduced the new technique of assuming ERV fragments could spontaneously recombine, then mutate into a more replication-competent form, which vastly expands the scope for spontaneous creation of new pathogens from old, forgotten ones both in laboratory animals and in the wild. A search for such possibilities is far easier to do in a computer database than in any living organisms. (And, why would anyone assume this will only be done, or not done, by your scientific allies?)

This brings up a new possibility. Why should nature, which need not use computer databases, wait for a virus to jump species if there are already replication-competent retroviruses in large numbers of humans with compromised immune systems? You might think this only applies to people in the third world with untreated HIV infections. (Following which you might naively assume you could prevent spread to Americans by introducing draconian border controls, which would still overlook the 50,000 or so still turning up in this country each year.) This ignores the largely unchecked spread of another retrovirus, HTLV-1, among IV drug users inside the U.S. (Protection of the blood supply in that case depends entirely on seroconversion. See below, concerning TB, for possible defects in this approach. Check also for a population with significant rates of MDR TB. The scale of these "natural experiments" should be compared to the scale of laboratory experiments.) Start with an active retrovirus already adapted to humans, and calculate all the possible ways this virus could incorporate HERV elements (or elements from coinfecting pathogens) to become a more dangerous pathogen in the same way that the origin of XMRV was modeled. How would you judge the probability? The most you could say is "it hasn't happened yet -- or at least we think it hasn't".

This is where the question of disease surveillance pops up. Don't we have such an active and effective surveillance system to warn us of any new retroviruses? Apparently not for gamma retroviruses.

If this had been so we would have known immediately that the reported XMRV virus was a fluke in 2006. Instead we find that eminent virologists found the idea quite plausible until some time in 2010.

(The time lag is very similar to the time lag for HIV, which discovery also had arguments about contamination, and suffered from misidentification of a lentivirus, comparable to equine anemia virus, as a delta retrovirus, similar to bovine leukemia virus. The differences between delta and lenti retroviruses are greater than the difference between gibbon ape leukemia virus (GALV) and any well-known murine leukemia virus (MLV). (What does this tell you about expert opinions on origins? Don't take my word for this, check the literature of that time.) The scientific, social and economic forces causing delay remain much the same as in that crisis. The victims are different, but, once again, stand accused of mental or moral failings which obscure the role of infectious disease. In the present case, the victims also fail to provide convenient clinical signs of chronic disease suitable for use in a 10 minute examination, or to conveniently drop dead to provide pathologists specimens.

Even clear signs may not be enough. Correspondents have given me reliable reports about a patient with advanced TB being given ECT for an assumed major depressive disorder, (with fatal results,) because their immune system was too far gone to produce antibodies on demand. In other cases patients with the copper ring on the surface of the eye characteristic of Wilson's disease were confined to mental hospitals. Just how clear does a sign of chronic disease need to be? But, this is a digression -- back to the main topic.)

We are told many researchers were not able to tell that their own laboratories were contaminated by a gamma retrovirus over a period of many years. The contaminant was present in cell lines, which are monocultures of identical human cells. (Take a moment to try to imagine where detection of a virus might be easier.) If this is true, what odds would anyone give me that there are at present no gamma retroviruses in the wild in humans, where they are harder to detect? What odds of being able to detect a new one resulting from recombination outside the laboratory, as described above, before it had infected millions of people? Considered as a test of our early warning system for novel human retroviruses this fiasco makes it clear the system is scarcely better today than it was 30 years ago.

The last time such a retroviral surprise happened the lag from the initial event to clinical recognition was about 70 years, and the body count necessary to provoke action was roughly the same as from a medium-sized war. That conflict has not ended.

In the current debacle, the only people who knew there could be no virus were those who had defined the disease out of existence. They knew they had defined the disease in such a way that evidence of viral infection was a condition for exclusion, as were other organic causes, (charitably assuming this definition defines any clinical entity whatsoever.) Testing was superfluous, and the logical short circuit ensuring this was so deeply hidden in published literature that only a determined critical reader could find it. This strategy has been remarkably effective when used against human adversaries, (like legislators who control budgets, and scarcely have time to read their own speeches before they deliver them,) but leaves abundant room for doubt that it offers any protection against viruses. We asked for a system which would protect us against new human retroviruses. What we got was a system which protects us from the discovery of new human retroviruses.

If the recombination argument is plausible in one case observed in a laboratory, so too is natural recombination in numerous situations where it cannot be observed. If overlooking a novel virus in a laboratory for 18 years is plausible there is strong reason to suspect huge gaps in surveillance. Selective attention to limited implications is strikingly prominent, as is a corresponding blindness.

This all sounds far less like the result of brilliant central planning than an emergent behavior of frightened people responding separately to any change which might impair their ability to go on doing the same things and drawing paychecks until they reach retirement.


I don't think XMRV is dead at all. I remember way back in the 80's when Gallo was swearing up and down that HIV was not the cause of AIDS, and all of a sudden, HIV became the accepted virus associated with AIDS. So I still don't think it's a dead issue yet. I do believe we are seeing smoke screens put up my researchers who stand to lose their funding if XMRV is accepted as a factor. So they will never admit if they do find it in testing.

But I'm really starting to lean more toward us all simply being vaccine victims. I've been studying alot of info on vaccines and what they really do to the immune system. They destroy it. All vaccines. They force the immune system to work in a completely unnatural way and it creates disease. I think they turned us all into walking timebombs. And some virus or other infectious agent that wouldn't normally make an unvaccinated person sick, triggers CFIDS/ME in a vaccine damaged individual if certain conditions are right at the time. And it can trigger it years after you've been vaccinated. Once they shoot you up, you are a walking timebomb. And that's why vaccine manufacturers are exempt from prosecution. They know all this. The vaccine industry is a fraud. The truth is out there, if you dig deep enough.
Hi Carrigon,

I continue to lean toward the idea that vaccination provokes a obvious response merely because it is an immune challenge which reveals a preexisting immune weakness.

A virus which infects cells of the immune system without killing them, then lies latent until a separate immune challenge causes clonal expansion of infected cells, has a very natural strategy which allows it to use the host cell's mitosis and the host organism's immune response to propagate itself in a situation where immune defenses are directed against another pathogen. When HIV kills host CD4 T cells it denies itself use of this strategy. This is probably because it is still fairly new at the game. The class of retroviruses we are looking for has been around for a long time, even if new strains keep appearing. A better adapted pathogen wouldn't make such mistakes. I am seriously considering the possibility that the reason some people died from TB at a time when everyone was exposed was an undetected retrovirus weakening immune response without killing hosts, which would have been far beyond the reach of medical technology until about 1980. Medicine would then have removed an opportunistic infection without fixing the underlying problem. Few seem to know that people infected with TB before streptomycin was developed in the late 1940s continued to die of the disease into the 1960s. Something else was wrong with their immune systems. Curing TB once it becomes established remains a struggle.

My feeling about what this episode reveals about current disease surveillance systems and chronic disease is similar to a sardonic comment remembered from the time of the Cuban missile crisis: "This concludes a test of the Emergency Broadcast System. This was only a test. Had this been a real emergency you would now be radioactive dust."
A paper on "Long-Term Infection and Vertical Transmission of a Gammaretrovirus in a Foreign Host Species" has just been published on PLoS. This describes a year of experimental results from infection of mus pahari with XMRV. The infection was established, though not through natural means, and was transmitted to at least one offspring, though the route of infection can only be guessed. In addition to detection in blood, tissue samples from vital organs were also used. Only 3 out of 8 infected mice showed proviral DNA at one year. There was some evidence of mutation in this DNA. Parallel infections in humans would not be easy to detect unless caught at a stage when patients were highly viremic.

This was a wild Asian mouse I had in mind in my blog post. I would feel more confident about statements that these wild mice lack active MLV infections, or any MLV ERVs which might recombine, if the name mus pahari could be definitely applied to a single species. At present we can't be sure just how many species and subspecies are covered by a single label, a strong indication of incomplete knowledge. Transmission of MLVs from fights with domestic mice when population crashes force stressed wild mice into the same territory seems plausible. Laboratory infection can be viewed as merely accelerating natural processes which are either slow or have low probability.

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