This report claims two major conclusions (last paragraph of Abstract):(via the comments in the ERV blog)
1. XMRV replicates efficiently in prostate epithelial cells by downregulating A3G expression.
2. Our data suggest a novel mechanism by which retroviruses can counteract the antiviral effects of A3G proteins.
Neither conclusion is supported by the data.
First, some background. Many publications to date have shown that XMRV can be mutated by APOBEC3 proteins (A3A - A3G) present at various levels in human cells. Sequencing of the RNA genomes of XMRV viruses produced from particular human cells shows that some genomes are intensely mutated (hypermutated) while others show only background mutation rates likely due to errors in reverse transcription. Rates of hypermutation vary for viruses produced from different human cells, from almost none for XMRV produced by 22Rv1 prostate cancer cells (Paprotka et al., 2010), to ~25% for DU145 prostate cancer cells (Paprotka et al., 2010), to almost 100% for virus produced by human peripheral blood mononuclear cells (PBMC) (Chaipan et al., 2011). The results obtained for human PBMC clearly show that XMRV is not able to circumvent the effects of A3 restriction in human cells.
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Saturday, February 25, 2012
XMRV still not able to circumvent host restriction factors in humans
A Dusty Miller's comment to "Downregulation of APOBEC3G by xenotropic murine leukemia-virus related virus (XMRV) in prostate cancer cells"
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