Two studies were published last week that showed no link between xenotropic murine leukemia virus-related virus (XMRV) and either chronic fatigue syndrome or prostate cancer.

The scientific journals consider the matter settled with these studies. In theirs new sections, Nature and PLoS ONE wrote about “the nail in XMRV’s coffin” and “The Final Chapter on XMRV and Prostate Cancer.”

Umm . . . good luck with that.

Actually, the link between XMRV and prostate cancer may be laid to rest fairly easily. That disease doesn’t seem to engender the same level of emotion about what causes it as CFS does, and certainly, if it’s a made up disease, it is made up by the screening guidelines. No one accuses men of prostate cancer being all in their imaginations.

For the link between XMRV and CFS, I would not be too surprised if rather than dying, it ends up being one of those unfortunate, undead beliefs, like the autism-vaccine link.

Notably, several of the questions at the press conference where W. Ian Lipkin and his team announced the lack of a link between centered on whether the connection might, in fact be there, but in places unseen by the scientists. Could it be in the other organs rather than blood? Could there be an interaction with host genotype? These are exactly the kind of possibilities that vaccine skeptics love to bring up about autism – and that are impossible to truly disprove. There is always some angle you haven’t looked at.

If the team around Lipkin meets with more success with truly laying the notion of a link between XMRV and CFS to rest than the autism–vaccine contingent, it may be not because of the quality of their data. Instead, the key may lie in the study’s second author Judy Mikovits, whose team published the original paper claiming a link.

Judy Mikovits has gone to some lengths to defend her theory and her data; at one point, she spent five days in jail for stealing lab equipment and data. She has lost her position at Whittemore Peterson Institute over her conduct in the aftermath of the study, and her affiliation on the paper is listed as “Mikovits Consulting.”

But unlike Andrew Wakefield, who first championed the link between vaccines and autism and has steadfastly refused to let the facts get in the way of his opinion, Mikovits was willing to rigorously test her own theory, along scientists who disagreed with her – and to let the data convince her that her original idea was wrong.

In one sense, this is what scientists do. But she is doing it well, and she deserves kudos for that.

But the movie’s tag line is also worth keeping in mind: “Nothing spreads like fear.”

Another round of alarming news has brought the real H5N1 back into the headlines in recent weeks. Experimental findings that it only takes a few mutations for the virus to become highly contagious via human-to-human transmission were deemed so dangerous that publication of the experimental details has been delayed, and there is currently a voluntary moratorium on H5N1 research.

But a study published today suggests that H5N1 infections are already more frequent, but milder, than the current WHO data indicates.

The WHO’s official count as of Feb. 22, 2012: There have been 586 humans infected with the H5N1 virus since 2003; 346, or 59 percent, of those infections have been fatal.

But the authors of the new paper, which appears in the Feb. 24, 2012 issue of Science, believe that the WHO’s stringent criteria end up missing most cases of H5N1.

Believe me, I am not trying to sneer at the WHO here. Public health organizations face a difficult task, needing to alert but not unduly alarm the public, encouraging prudence without panic. The WHO walks that line well.

But it is worth noting that the criteria for confirmed H5N1 infections make it unlikely that mild cases of H5N1 will be confirmed in the first place.

The new paper is a meta-analysis of prior studies that looked at serum antibodies to H5N1 as a way to estimate true rates of exposure to the virus. Such antibodies can identify people who have been exposed to H5N1 but are not counted in the WHO tally, because their case was too mild to meet WHO criteria ‑ or for them to seek medical attention at all.

Overall, those numbers tell a very different story than the official 586 cases. The best estimate for rates of exposure were in the range of 1 percent to 2 percent of the population, which, the authors said, would translate into millions of infected individuals.

Figuring out the true death rate is harder still than determining how many people have been infected with H5N1.

Even in the U.S., with its high rates of access to healthcare and mountains of medical records, figuring out how many people get infected with annual flu, and how many die from it, is an imprecise science. For one thing, not everyone with the flu goes to see a doctor. For another, flu deaths are indirect. The virus does its damage by weakening the body, especially the lungs, and the direct cause of death is most often pneumonia.

Such uncertainties are multiplied in the developing areas where new flu strains set out on their annual global trek, and where H5N1 has been circling in its animal reservoirs and popping out every now and then. Just like there appear to be many people who are infected with H5N1 without making it into WHO statistics, so there are undoubtedly people who have died of H5N1 without the medical community’s being any the wiser.

Still, even if the new paper had somehow managed to overestimate the number infections tenfold – which is hard to imagine, given that senior author Peter Palese is an extremely well-respected influenza researcher – then a death rate of nearly 60 percent would mean that there were hundreds of thousands of H5N1 deaths that have somehow gone unnoticed. This seems a lot less likely than the alternative possibility, namely, that H5N1 may not be as deadly as we think.