G
gerwyn morris
Guest
I'm talking about the German study Lack of evidence for Marine Lukaemia related virus in German prostate cancer patienrs.Hohn et al Retrovirology;Oct 2009,6:92
The initial study identificating XMRV in patients with prostate cancer with patients homozygous for the R462Q mutation was carried out by Urisman Et al Journal of Clinical Virology 2008 Nov 43 (3) 277-83.Crucially theu used full lengh viral genomic clones found XMRV in !% of STROMAL cells ajacent to the carcinoma.
The second American study by Schlarberg it al proceeds National Accademy Sciience USA Sep 8 2009,22;106 (38):16351-6 Epub
Found XMRV in !5% of EPITHELIAL cells of prostate cancer patients homozygous for the mutation again using WHOLE VIRAL CLONES------Bear with me this is important
A THIRD American study by Hong et al which also involved German centers again using whole viral cloens found a tenfound increase in XMRV tires in EPITHELIAL cells in prostatic cancer patients compared to stroma cells This study can be referenced
Hong et al American Microbiolocy Society .July 2009,p6995-7003 vol 83 No14
They also found That before cells can be infected with XMRV they must produce a particular receptor and even then transfection rates were as little as 7% This study is a third study to finf XMRV in prostate cancer unless I'm mistaken and seems to have slipped under the radar
The GERMAN STUDY PREPARED ITS SAMPLES IN SUCH A WAY THAT THEY COULD ONLY LOOK AT STROMA CELLS because they "Assumed" that this is where they would find the virus despite existing data showing tht only 1% of those cells would be infected
More crucially they used synthetic XMRV sequences containing GAG and elements upstream
If one consults nature reviews?microbiology volume5/Feb2007/131 the 5' cap end of the XMRV is essential for Ribosome binding before the GAG initiation sequence starts replicating.In other words the bit of the synthetic XMRV genome in the German study would have made replication very unlikely if not impossible.XMRV uses UTR and IRES sequences to replicate .All other proceedures used even smaller bits of the synthetic genome,unidentified culture cells and processes that would have mangled a weak vius like XMRV even if initially there
The initial study identificating XMRV in patients with prostate cancer with patients homozygous for the R462Q mutation was carried out by Urisman Et al Journal of Clinical Virology 2008 Nov 43 (3) 277-83.Crucially theu used full lengh viral genomic clones found XMRV in !% of STROMAL cells ajacent to the carcinoma.
The second American study by Schlarberg it al proceeds National Accademy Sciience USA Sep 8 2009,22;106 (38):16351-6 Epub
Found XMRV in !5% of EPITHELIAL cells of prostate cancer patients homozygous for the mutation again using WHOLE VIRAL CLONES------Bear with me this is important
A THIRD American study by Hong et al which also involved German centers again using whole viral cloens found a tenfound increase in XMRV tires in EPITHELIAL cells in prostatic cancer patients compared to stroma cells This study can be referenced
Hong et al American Microbiolocy Society .July 2009,p6995-7003 vol 83 No14
They also found That before cells can be infected with XMRV they must produce a particular receptor and even then transfection rates were as little as 7% This study is a third study to finf XMRV in prostate cancer unless I'm mistaken and seems to have slipped under the radar
The GERMAN STUDY PREPARED ITS SAMPLES IN SUCH A WAY THAT THEY COULD ONLY LOOK AT STROMA CELLS because they "Assumed" that this is where they would find the virus despite existing data showing tht only 1% of those cells would be infected
More crucially they used synthetic XMRV sequences containing GAG and elements upstream
If one consults nature reviews?microbiology volume5/Feb2007/131 the 5' cap end of the XMRV is essential for Ribosome binding before the GAG initiation sequence starts replicating.In other words the bit of the synthetic XMRV genome in the German study would have made replication very unlikely if not impossible.XMRV uses UTR and IRES sequences to replicate .All other proceedures used even smaller bits of the synthetic genome,unidentified culture cells and processes that would have mangled a weak vius like XMRV even if initially there
