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Review
. 2014 Apr;3(4):e.
doi: 10.1038/emi.2014.25. Epub 2014 Apr 9.

The saga of XMRV: a virus that infects human cells but is not a human virus

Maribel Arias  1 , Hung Fan  1
Affiliations
Review

The saga of XMRV: a virus that infects human cells but is not a human virus

Maribel Arias et al. Emerg Microbes Infect. 2014 Apr.

Erratum in

Abstract

Xenotropic murine leukemia virus-related virus (XMRV) was discovered in 2006 in a search for a viral etiology of human prostate cancer (PC). Substantial interest in XMRV as a potentially new pathogenic human retrovirus was driven by reports that XMRV could be detected in a significant percentage of PC samples, and also in tissues from patients with chronic fatigue syndrome (CFS). After considerable controversy, etiologic links between XMRV and these two diseases were disproven. XMRV was determined to have arisen during passage of a human PC tumor in immunocompromised nude mice, by activation and recombination between two endogenous murine leukemia viruses from cells of the mouse. The resulting XMRV had a xentropic host range, which allowed it replicate in the human tumor cells in the xenograft. This review describes the discovery of XMRV, and the molecular and virological events leading to its formation, XMRV infection in animal models and biological effects on infected cells. Lessons from XMRV for other searches of viral etiologies of cancer are discussed, as well as cautions for researchers working on human tumors or cell lines that have been passed through nude mice, includingpotential biohazards associated with XMRV or other similar xenotropic murine leukemia viruses (MLVs).

Keywords: XMRV; chronic fatigue syndrome; endogenous retrovirus; murine leukemia virus; prostate cancer; retrovirus.

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Figures

Figure 1
Figure 1
Generation of the XMRV genome by recombination. The two endogenous MLV parental proviruses present in nude mice, PreXMRV-1 and -2 are shown at the top of the figure. The larger boxes at either end represent the LTRs. PreXMRV-1 has mutations (‘X') in the gag (a 16 nt deletion) and pol (a single-nucleotide frame-shift) that render it incapable of encoding functional proteins, but the env coding sequences are intact. PreXMRV-2 has open reading frames for all three genes. The recombinations between PreXMRV-1 and -2 that generated XMRV are shown at the bottom of the figure. There are three single nucleotide substitutions and one insertion (*) that also occurred during development of infectious XMRV (the substitution in the LTR is present at either end of the provirus).
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