A study in mBio this week shows that contrary to previous findings, new research proves there is no link between chronic fatigue syndrome and the viruses XMRV (xenotropic murine leukemia virus-related virus) and pMLV (polytropic murine leukemia virus). The authors say research that reported patients with chronic fatigue syndrome carried these two viruses was wrong and that there is still no evidence for an infectious cause behind chronic fatigue syndrome.
Chronic fatigue syndrome (CFS), also known as myalgic encephalomyelitis (ME), is a disabling condition in which sufferers experience persistent and unexplained fatigue as well as any of a host of associated problems, including muscle weakness, pain, impaired memory, and disordered sleep. Medical treatment for CFS/ME costs as much as $7 billion every year in the U.S. alone.
The possible causes of CFS/ME have been argued and researched for years with no success. Results from separate studies in 2009 and 2010 that reported finding retroviruses in the blood of patients with CFS/ME created a sensation among patients and the medical community and offered hope that a tractable cause for this disease had finally been found. Since then, other investigators have been unable to replicate the results of those studies, casting doubt on the idea that these viruses, XMRV and pMLV, could be behind CFS/ME.
Study co-author and director of the multi-site study, Ian Lipkin of Columbia University, says the National Institutes of Health wanted conclusive answers about the possible link. “We went ahead and set up a study to test this thing once and for all and determine whether we could find footprints of these viruses in people with chronic fatigue syndrome or in healthy controls,” says Lipkin. The study in mBio puts the speculation to rest, he says. Scientists were wrong about a potential link between chronic fatigue syndrome and these viruses.
“The bottom line is we found no evidence of infection with XMRV and pMLV. These results refute any correlation between these agents and disease,” says Lipkin.
The study authors recruited almost three hundred people, 147 patients with CFS/ME and 146 people without the syndrome, to participate. Researchers tested blood drawn from these subjects for the presence of genes specific to the viruses XMRV and pMLV, much in the way the earlier studies had done. But in this study, researchers took extraordinary care to eliminate contamination in the enzyme mixtures and chemicals used for testing, which may have been the source of viruses and genes detected in the earlier studies. XMRV and pMLV are commonly found in mice but there has never been a confirmed case of human infection with these viruses.
The authors of this study include many of the authors of the original papers that reported finding XMRV and pMLV in the blood of CFS/ME patients. This is an important point, says Lipkin, as their participation should lend credibility to the pre-eminence of these newer results over the flawed earlier studies, which offered a certain amount of false hope to the CFS/ME community.
Research on the causes of CFS/ME will continue, says Lipkin. “We’ve tested the XMRV/pMLV hypothesis and found it wanting,” he says. But, he says, “we are not abandoning the patients. We are not abandoning the science. The controversy brought a new focus that will drive efforts to understand CFS/ME and lead to improvements in diagnosis, prevention and treatment of this syndrome.”