Chronic Fatigue Syndrome (CFS) is known as a “diagnosis of exclusion,” a disease with non-specific symptoms that can only be considered when all other reasonable diseases have been ruled out. Because there are no known proven causes of CFS, it’s impossible to design a test for the disease, and there is no defined treatment strategy. And yet, the CDC estimates that more than one million Americans have CFS, and patient groups are desperate for research into the origins of the disease.
Medical desperation begets controversy, and that’s what kicked up again this week with the publication Tuesday of a second report linking CFS to a mouse retrovirus. The research – which found DNA from the murine leukemia virus (MLV) family in more than 86 percent of CFS patients vs. only 7 percent of controls – would be interesting in and of itself. But the paper is the latest salvo in a scientific battle that has raged in the last year over the connection between CFS and viruses, exposing the modern balance between the slow crawl of research and the urgent desire of patients for information in the Internet age.
The first paper to link CFS with a mouse retrovirus was published last year in Science, creating a stir in the media and hope for CFS patients hungry for an explanation and a cure. But several subsequent studies failed to replicate the original finding, leading many to question whether the original experiments had been contaminated by mouse DNA or were simply not conducted properly. The controversy moved beyond the battlefield of scientific journals when the study’s senior author, Judy Mikovits, began to aggressively push the link between the retrovirus and CFS and other diseases – a saga recapped in an article earlier this summer by our friend Trine Tsouderos at the Chicago Tribune.
The new article, published by scientists from the FDA, NIH, and Harvard, gives conditional support to Mikovits’ original findings, detecting similar (but not identical) viral DNA in blood samples from CFS patients. The new study’s methods, which included extreme measures to ensure that no mouse DNA contamination could occur, were praised by many in the field. But the stench of controversy remained, as the paper only came out after being delayed two months while the authors reassessed their findings in light of yet another paper that failed to detect virus. CFS patient groups, who had received leaked word of the positive findings, cried foul over the delay.
But the publication of the new article may only kick up the debate’s intensity. The article’s authors very strongly stressed that their research was not proof that the virus causes CFS – an alternate explanation is that CFS renders patients vulnerable to viral infection. But the number of CFS patients jumping the gun and trying anti-retroviral drugs (usually designed for use in HIV patients) before clinical trials may only increase with the new publication. The desperate need of such patients for a treatment is paradoxically an argument for slow, careful research – and a cauldron for a scientific storm.
Another case study in the ramifications of journal publication timing was seen this week in the research on oil-eating bacteria rapidly digesting the Gulf of Mexico spill, which published only days after research that said the “oil plume” created by the spill was not going away. The best place for monitoring the navel-gazing of science journalists is the Knight Science Journalism Tracker, and they had a very interesting discussion on the topic of reporting such scientific messiness.
Those looking for a science project to do at home (or on their next Phish tour): How to Make Glowsticks. Warning: carcinogenic ingredients.
University of Chicago Associate Professor of Medicine Imre Noth talks to Tribune columnist Mary Schmich about idiopathic pulmonary fibrosis, the disease that caused the death of Schmich’s mother. ScienceLife talked to Noth in May about a recent study that attempted to use Viagra to treat IPF, and its promise for future treatments.