Mr Towers, XMRV class viruses DO integrate into the same sites repeatedly

Full picture can be seen here ...

Gerwyn Morris, (26 February 2011) PA institute:

The authors are clearly not familiar with MLV viruses

MLV viruses have a preference for integrating within certain genes involved in the promotion or repression of tumours. A classic example would be PIM-1(1) or P53 (2) n-myc(3)is also a common integration site.
Thus mulv virus' display the propery of integrating into the same sites repeatedly.It is surprising that the authors have not researched into the subject. Hence the following section of the paper is completely incorrect

"With the exception of a single early publication on avian
sarcoma-leukosis virus, which was refuted by later work [10], sequencing studies of
thousands of retroviral integration sites have to our knowledge never identified exactly the
same site twice."

The following table demonstrates just how inaccurate the author's comments are. They illustrate the integration sites within genes of the class of virus to which xmrv belongs

BMC

The reader will note that the activity of these genes are all related to the development of cancer in humans

The authors are stating beliefs in the guise of fact.
They state that the sequences were unlikely to have been transfered into the DU125 cells from the patients examined without nothing but their biases as evidence.

Likewise they voice their belief that the other integration sites are probably caused by contamination despite failing to provide any evidence despite a rigorous effort to discover said evidence.

The integration of a mulv class virus into the PIM-1 gene leads to the overexpression of PIM-1(1).The degree of overexpression of PIM-1 correlates with severity of prostate cancer in humans(1)

I submit that patients with prostate cancer are entitled to anyone ,purporting to be scientists, investigating the link of XMRV to their condition limit themselves to publishing scientific evidence and not speculation in the guise of scientific evidence as is,sadly,the case here

references

(1)Wong KS, Li YJ, Howard J, Ben-David Y. Loss of p53 in F-MuLV 14induced-erythroleukemias accelerates the acquisition of mutational events that confers immortality and growth factor independence. Oncogene. 1999 Sep 30;18(40):5525-34.

2)Cuypers HT, Selten G, Quint W, Zijlstra M, Maandag ER, Boelens W, van Wezenbeek P, Melief C & Berns A. (1984) Cell 37: 141–150.

(3)van Lohuizen M, Verbeek S, Scheijen B, Wientjens E, van der Gulden H & Berns A. (1991) Cell 65: 737–752

Competing interests

none