The discovery of mouse virus fragments in cells from people with chronic fatigue syndrome has reinforced earlier claims that they may cause the condition.

The origins and even the existence of chronic fatigue syndrome have been widely debated for many years. Some claim that its symptoms, including cramps, listlessness and lethargy, have psychological causes, but the search for an infectious agent has continued.

The latest findings have revived speculation that mouse viruses may be responsible for the condition – although four earlier studies have failed to find traces of such viruses in samples from patients.

Confusingly, the gene fragments identified in the new study are not from the same strain of mouse virus – the xenotropic murine leukaemia virus-related virus (XMRV) – identified as a possible cause a year ago.


Instead, Shyh-Ching Lo of the Food and Drug Administration in Bethesda, Maryland, and colleagues found that blood samples from 32 of 37 people with chronic fatigue syndrome contained “polytropic” murine leukaemia virus-related fragments, compared with only three of 44 healthy blood donors.

Versatile virus

The crucial distinction is that XMRV won’t infect mouse cells – despite being a variant of a virus that originated in mice – whereas the “polytropic” variant is equally capable of infecting mouse cells and cells from other animals, including humans.

“The message is that murine leukaemia viruses, whether XMRV or polytropic MLVs, are strongly associated with the cases of chronic fatigue syndrome tested by us and the cases tested last year by the Whittemore Peterson Institute [in Reno, Nevada],” says Harvey Alter of the National Institutes of Health in Bethesda, Maryland, and the senior author of the new study.

Alter says that just as there are several viruses that cause similar symptoms of hepatitis, so there may be several MLVs causing chronic fatigue syndrome.

Repetition problem

The other puzzle is why four other studies published over the past year drew a blank when they hunted for traces of MLV-related viruses in blood from patients.

Bill Switzer of the Centers for Disease Control and Prevention, who headed one of the four studies, says that a recent quality-control trial has ruled out differences in the testing procedures as a possible explanation. Several labs, including Lo’s, all received identical samples to test. “All the labs had the same results, so it’s not the assays,” says Switzer.

Another possibility is that mouse viruses vary from place to place. This might explain why no mouse viruses have yet been found in European patients.

Myra McClure of Imperial College London, who headed one of the two British studies that failed to identify the virus, says that Lo and his colleagues could have done two further tests that would have strengthened the evidence that the patients’ cells contained live, infectious viruses.

By growing patients’ cells in the lab alongside healthy cells, Lo’s team could have proved that the virus could cross-infect uninfected neighbouring cells. Also, they could have screened blood for antibodies to the mouse viruses, which also would have shown that the viruses were infectious. “It would have been more reassuring to have those results too,” she says.

Journal reference: Proceedings of the National Academy of Sciences, DOI: DOI: 10.1073/pnas.1006901107