Mood music for this post: Messages by Xavier Rudd
So much contentiousness from people who are essentially on the same side! Let’s assume the worst case for the moment, that RRM is right. XMRV doesn’t pan out for the Blood Working Group or Lipkin. Where does that leave us? Where does that leave RRM, who has an affected loved one? Anyone arguing their points here is personally invested. So, hypothetically, XMRV is dead, a lab contaminant, and not as good at infecting live humans as it is at infecting human cells in tissue culture, so not a direct threat. Then what? Does it get put to bed again? That’s already happened a few times in the last 40 years. We still have millions of sick people for whom a retroviral etiology makes more sense than anything else. As a clinician, it is the best we’ve ever had as a model to develop an approach to treatment. Quite a lot is known about what similar viruses do in animals. Why don’t they spend the money to do the definitive deep sequencing we need rather than a couple of million dollars, and a bunch more time, to see whether a few scientists can do the same thing reproducibly? What if they don’t? While new babies are born with it and new people go down with it.
Andrew Mason’s excellent work is an important signpost. It suggests the likelihood of human infection with more than one family of retroviruses. If it’s true that retroviruses have been introduced through vaccines, then it would be expected to encompass more than murine retroviruses, as the cells used come from different phylogenetic orders. This is the frontier of future medicine. It changes the playing field. Or should. Once allowed into mainstream thought it will inform not only every facet of healthcare, but will illuminate genomics and evolutionary theory.
With passage of time, it becomes increasingly apparent how naive I was when all this began with respect to the pace of science. Max Planck said, “Science progresses one funeral at a time.” I am coming to terms with the fact that the glacial pace of progress means it will probably be too late for me and many others. For now, the best I can do as a clinician is to keep my patients as comfortable as possible while they are under siege, until the cavalry finally appears over the hill. It’s been a long time coming.
The model I’ve written about for the last year and a half, and outlined in the last post, is the most workable we’ve had for an explanation and approach to the neuroimmune illnesses, now rampant in some of our families. Many talented people have identified pieces of the puzzle over the years, measuring downstream effects of particular tributaries, each adding to the rushing river of illness. The fact that it isn’t one virus fits well with the clinical diversity, though I still maintain that, with respect to the chronic fatiguing illnesses, the various syndromes tend to converge over time into a rather clinically homogenous whole. Different paths to a similar place.