A team of scientists released long-awaited evidence Monday that a virus may be playing a role in chronic fatigue syndrome.
The researchers, from the National Institutes of Health, the Food and Drug Administration and Harvard Medical School, analyzed blood samples that were collected 15 years ago from 37 patients with chronic fatigue syndrome. Most of the subjects — 32, or 86.5 percent — tested positive for a virus known as a murine leukemia virus-related virus, the researchers found. In contrast, tests on 44 healthy blood donors detected evidence of the virus in only three of the subjects, or 6.8 percent.
While providing evidence that a virus may play a role in the mysterious condition, the researchers said the findings, published in the Proceedings of the National Academy of Sciences, are far from proving that the virus causes the syndrome.
But the findings are being hailed by advocates for chronic fatigue syndrome patients, such as the CFIDS Association of America. The head of that group, Kim McCleary, says the findings are a potentially important step toward finding the cause of the condition and possibly developing treatments, as well as dispelling the notion that the condition is psychological.
One million to 4 million Americans are thought to have the syndrome, which causes prolonged and severe fatigue, body aches and other symptoms. Over the years, many viruses have been linked to the syndrome, only to end up as dead ends.
But in 2009, Judy Mikovits and colleagues at the Whittemore Peterson Institute in Reno, Nev., published a paper in the journal Science. The paper reported that many syndrome patients appeared to be infected with a little-known virus called the xenotropic murine leukemia virus-related virus, or XMRV. XMRV is a retrovirus, which is the same type of virus as the AIDS virus. It has also been found in some prostate cancer patients.
But four other groups, including a team at the federal Centers for Disease Control and Prevention in Atlanta, failed to duplicate the findings in other patients, raising deep suspicions that this was yet another wild goose chase.
The recent findings will probably revive interest in the virus. The virus detected in the new study does not appear to be exactly the same one the Reno group found, but it is closely related. In addition to detecting evidence of the microbe in an overwhelming majority of the stored blood samples, the researchers found evidence of virus in fresh blood samples from seven of eight of the patients, indicating that the infection persists. Harvey Alter of the NIH, who helped conduct the study, says there also were indications that the virus had evolved slightly over time, which is what would be expected from a retrovirus.
The paper’s publication was delayed because of questions about whether the findings could have been the result of laboratory contamination. That prompted the researchers to conduct additional tests to try to rule that out, and rumors that the research was being suppressed.
But in an editorial accompanying the paper, the journal’s editor said that the additional studies were important to validate the findings.
Some researchers continue to question whether the scientists have ruled out contamination. And many researchers urged great caution in rushing to any conclusions.
But the scientists say they are confident that they ruled out laboratory contamination. They are not sure why they found evidence of the virus in syndrome patients while others failed. They speculated that there could be a variety of explanations, including that they tested a better-defined group of patients or perhaps that the virus is only found in patients in some geographical areas.
In a commentary accompanying the study, Andrew Mason of the University of Alberta in Canada and colleagues said that one of the next steps might be to try testing antiviral drugs on chronic fatigue patients in a carefully designed study.