I thought this was worth its own thread as it has important implications for the type of cells XMRV can infect and replicate in.
Apparently both Human and Mouse tetherin/CD317 and APOBEC restrict XMRV efficiently and there doesn't seem to be any viral accessory proteins that counteract these factors (like Vpu - an HIV-1 accessory protein). This is important as PBMCs and all hematopoietic cells express tetherin/CD317. If XMRV is an infective Human virus it's not likely to replicate in these cells. I also know that alot of prostate cancer cell lines don't express tetherin.
Susceptibility of xenotropic murine leukemia virus-related virus (XMRV) to retroviral restriction factors
http://www.pnas.org/content/107/11/5166.full
Apparently both Human and Mouse tetherin/CD317 and APOBEC restrict XMRV efficiently and there doesn't seem to be any viral accessory proteins that counteract these factors (like Vpu - an HIV-1 accessory protein). This is important as PBMCs and all hematopoietic cells express tetherin/CD317. If XMRV is an infective Human virus it's not likely to replicate in these cells. I also know that alot of prostate cancer cell lines don't express tetherin.
Susceptibility of xenotropic murine leukemia virus-related virus (XMRV) to retroviral restriction factors
http://www.pnas.org/content/107/11/5166.full
Xenotropic murine leukemia virus-related virus (XMRV) is a recently discovered gammaretrovirus that has been linked to prostate cancer and chronic fatigue syndrome. This virus is therefore an important potential human pathogen and, as such, it is essential to understand its host cell tropism. Intriguingly, infectious virus has been recovered from patient-derived peripheral blood mononuclear cells. These cells express several antiviral restriction factors that are capable of inhibiting the replication of a wide range of retroviruses, including other gamma retroviruses. This raises the possibility that, similar to HIV, XMRV may have acquired resistance to restriction. We therefore investigated the susceptibility of XMRV to a panel of different restriction factors. We found that both human APOBEC3 and tetherin proteins are able to block XMRV replication. Expression of human TRIM5?, however, had no effect on viral infectivity. There was no evidence that XMRV expressed countermeasures to overcome restriction. In addition, the virus was inhibited by factors from nonhuman species, including mouse Apobec3, tetherin, and Fv1 proteins. These results have important implications for predicting the natural target cells for XMRV replication, for relating infection to viral pathogenicity and pathology, and for the design of model systems with which to study XMRV-related diseases.