I thought Cheney's point was that fish oil was more likely to oxidize. Have you heard of patients that improve with NT Factor (any particular brand)? It's expensive. (and I'm supposed to avoid soy which most of these products use. I do have the mito blockage, with hair dye maybe used once and benzene.)
I think they say viruses can also destroy the mitochondria (apoptosis?) as well as oxidative stress.
I brought up xmrv because of using lipid cell envelopes so I went back to trying to understand Gerwyn's hypothesis again. Do these CREB processes regulate mitochondria? Does it make any sense to you?
Would vegetable and fish oils not have the cholesterol that viruses might use? (assuming virus and methylation problems)
XMRV inserts into CREB gene, transcription start sites (Silverman 2007), can create insertional mutations (Silverman 2010).
Creb master gene regulator including sterols (lipodystrophy 2002)
On other threads generally say Viruses can cause mitochondrial disease. Herpes viruses can eliminate mitochondrial DNA (saffran 2007).
XMRV may travel with lipid rafts cell to cell like HIV
other gammaretroviruses like FLV cell envelopes create neurotoxins, and MULV?
use the cells envelope to create new virus envelope
Refs
An infectious retrovirus susceptible to an IFN antiviral pathway from human prostate tumor
Proc Natl Acad Sci U S A (2007) 0: .
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. and Integration of the cDNA copy of the viral RNA genome is essential for retroviruses to establish a productive infection (for reviews, see reference [12]). However, because of its nonspecific nature, retroviral DNA integration is inherently a
mutagenic event. Many retroviruses, especially members of the gammaretrovirus genus, can induce tumors as a consequence of
integrating their viral genome into the host cell chromosome and activating proto-oncogenes via promoter or enhancer
insertion, a mechanism referred to as proviral insertional mutagenesis [13]. XMRV is a member of the gammaretrovirus family,
and does not encode host-derived oncogenes [1]. Genome-wide analyses of XMRV integration sites in a human prostate cell line,
DU145, and prostate cancer tissues showed that XMRV integration favors gene-dense regions and genomic features frequently
associated with structurally open, transcriptional regulatory regions of a chromosome, such as transcription start sites, CpG
islands, and DNase hypersensitive sites [14]. The XMRV integration sites in prostate cancer tissues are further associated
with cancer breakpoints, common fragile sites, and microRNA genes.
FIDELITY OF TARGET SITE INTEGRATION, Silverman et al, 2010.
http://www.plosone.org/article/info:doi/10.1371/journal.pone.0010255
Gerwyn said : I have the hypothesis that XMRV does irs dirty work by causing the creb gene to malfunction.Untill this paper
there was no actual evidence that XMRV could affect the CREB gene in this way.Insertional mutagenesis is such a
mechanism.Xmrv can act as a duplication mutation or a deletion. Either way the proteins formed from CREB would be abnormal
and affect their regulatory function.
Increased insulin sensitivity despite lipodystrophy in Crebbp heterozygous mice. 2002
CBP enhances transcriptional activities via histone acetylation and the recruitment of additional co-activators such as SRC
(steroid coactivator)-1 (r The CBP protein (cAMP response element binding protein (CREB) binding protein) is a co-activator
for several transcription factors with a wide range of important biological functions, such as sterol regulatory element
binding proteins This study demonstrates that CBP may function as a 'master-switch' between energy storage and expenditure.
Herpes simplex virus eliminates host mitochondrial DNA, Holly A Saffran et al, 2007
http://www.nature.com/embor/journal/v8/n2/full/7400878.html
The Scientist: NewsBlog:
New non-drug fix for HIV?
Researchers are slowly establishing a connection between an extremely rare genetic disease and HIV -- and homing in on a
safe, non-prescription compound that could treat both.
Recently, James Hildreth at the Meharry Medical College School of Medicine in Nashville, Tenn., and his colleagues found
that cells affected by Niemann-Pick Type C (NPC), which disrupts cholesterol trafficking, were unable to release HIV,
suggesting these cells would not spread the virus.
These findings, published May 27 in the Journal of Virology, are rooted in a hypothesis Hildreth has explored for a long
time: that "cholesterol is somehow essential" to HIV, he said. For instance, HIV-1 relies on specialized structures known as
lipid rafts, which are rich in cholesterol, to infect new cells.
That line of thinking has led him to investigate whether a compound widely employed by the food and chemical industries
(and used as a drug solubilizer) which depletes cells of cholesterol could serve as a preventative agent -- or even a
treatment -- for HIV. And his growing body of evidence is suggesting the compound, known as cyclodextrin, might do just that.
