people involved in finding XMRV in prostate tumor patients followed by
another article which I think talks about inhibiting XMRV replication
with interferon and RNaseL though I could be wrong as I haven't read
the articles, I just found them on pubmed. You can look for others on
pubmed by searching for 'XMRV', there's not too many of them.
******************************************
'A scientific journey through the 2-5A/RNase L system'
Silverman, RH.
Department of Cancer Biology, NB40 Cleveland Clinic, 9500 Euclid
Avenue, Cleveland, OH 44195, USA. silverr@ccf.org
Cytokine Growth Factor Rev. 2007 Oct-Dec;18(5-6):381-8.
Full text-
http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=3Dpubmed&pubmedid=
=3D17681844
Abstract-
The antiviral and antitumor actions of interferons are caused, in
part, by a remarkable regulated RNA cleavage pathway known as the
2-5A/RNase L system. 2'-5' linked oligoadenylates (2-5A) are produced
from ATP by interferon-inducible synthetases. 2-5A activates
pre-existing RNase L, resulting in the cleavage of RNAs within
single-stranded regions. Activation of RNase L by 2-5A leads to an
antiviral response, although precisely how this happens is a subject
of ongoing investigations. Recently, RNase L was identified as the
hereditary prostate cancer 1 gene. That finding has led to the
discovery of a novel human retrovirus, XMRV. My scientific journey
through the 2-5A system recounts some of the highlights of these
efforts. Knowledge gained from studies on the 2-5A system could have
an impact on development of therapies for important viral pathogens
and cancer.
****************************************
'An infectious retrovirus susceptible to an IFN antiviral pathway from
human prostate tumors'
Dong B, Kim S, Hong S, Das Gupta J, Malathi K, Klein EA, Ganem D,
Derisi JL, Chow SA, Silverman RH.
Department of Cancer Biology, Lerner Research Institute, Cleveland
Clinic, 9500 Euclid Avenue, Cleveland, OH 44195, USA.
Proc Natl Acad Sci U S A. 2007 Jan 30;104(5):1655-60.
Full text-
http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=3Dpubmed&pubmedid=
=3D17234809
Abstract-
We recently reported identification of a previously undescribed
gammaretrovirus genome, xenotropic murine leukemia virus-related virus
(XMRV), in prostate cancer tissue from patients homozygous for a
reduced activity variant of the antiviral enzyme RNase L. Here we
constructed a full-length XMRV genome from prostate tissue RNA and
showed that the molecular viral clone is replication-competent. XMRV
replication in the prostate cancer cell line DU145 was sensitive to
inhibition by IFN-=CE=B2. However, LNCaP prostate cancer cells, which are
deficient in JAK1 and RNase L, were resistant to the effects of IFN-=CE=B2
against XMRV. Furthermore, DU145 cells rendered deficient in RNase L
with siRNA were partially resistant to IFN inhibition of XMRV.
Expression in hamster cells of the xenotropic and polytropic
retrovirus receptor 1 allowed these cells to be infected by XMRV. XMRV
provirus integration sites were mapped in DNA isolated from human
prostate tumor tissue to genes for two transcription factors (NFATc3
and CREB5) and to a gene encoding a suppressor of androgen receptor
transactivation (APPBP2/PAT1/ARA67). Our studies demonstrate that XMRV
is a virus that has infected humans and is susceptible to inhibition
by IFN and its downstream effector, RNase L.
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