Timaca...please inform the good Doctor Montoya (at Stanford) about this study...what anti-viral would he prescribe? To those of you not familiar, Dr. Montoya conducted a study using VALCYTE (not Valtrex) to treat high IgG viral titers.
On the other hand...CMV is NOT the cause of Mono...EBV is:
When "mono spot" or heterophile test results are negative, additional laboratory testing may be needed to differentiate EBV infections from a mononucleosis-like illness induced by cytomegalovirus, adenovirus, or Toxoplasma gondii. Direct detection of EBV in blood or lymphoid tissues is a research tool and is not available for routine diagnosis. Instead, serologic testing is the method of choice for diagnosing primary infection.
This could be the reason many of us have HBP issues!!!!
Peace, Love and Wellness, JRW
[ 05-17-2009, 11:04 AM: Message edited by: JRWagner ]
Posts: 1414 | From Ny, Ny | Registered: Oct 2002
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1Bitten2XShy
Unregistered
posted
Thanks for this very interesting link!
The past 3 months I have had high BP, years and years of normal, even low end normal. I am now on BP meds much to my chagrin.
Just in April did I test very positive for CMV...and put on Valtrex for 2 months to see what it does.
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sparkle7
Frequent Contributor (5K+ posts)
Member # 10397
posted
I don't understand this -
"Viruses have the ability to turn on human genes and, in this case, the CMV virus is enhancing expression of renin, an enzyme directly involved in causing high blood pressure," says Crumpacker.
When the scientists inactivated the virus through the use of ultraviolet light, renin expression did not increase, suggesting that actively replicating virus was causing the increase in renin.
Then it says -
"This suggests that further research needs to be directed at viral causes of vascular injury. Some cases of hypertension might be treated or prevented by antiviral therapy or a vaccine against CMV."
----
If they can inactivate the virus with UV light.... why isn't that form of treatment being studied? (ie: UV blood irradiation)
Posts: 7772 | From Northeast, again... | Registered: Oct 2006
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Marnie
Frequent Contributor (5K+ posts)
Member # 773
posted
INavctivating an enzyme called HMG Co A reductase shuts down the cholesterol pathway which IS one of the pathways Bb takes
to build its cell walls. This is KNOWN...Kegg pathways.
Mg INactivates HMG Co A reductase, but Bb "sees to it" that Mg levels dive at the outset of this disease and continue to spiral down.
Bb triggers the displacement of Mg in the cells it infects. So long Mg...not enough to help ATP transfer phosphates...
It wants/needs Na!!!
***Bb is using Na-ATPase to make its ATP and NaCl for motility.***
WE need Mg to do this in our MITOCHONDRIA:
ADP -> ATP -> ADP -> ATP. (Which actually involves 2 phosphate transfers, not one...either direction.)
Getting Mg back IN the cell is problematic since Bb is triggering the influx of NaCl and Na is more "reactive" (will combine with acids to make hydrogen) than Mg (or Ca) is.
ATP drives Mg back in the cells, where, in high enough quantity, can displace Na (and even Zn).
Bb is robbing 2 phosphates from serine to make glutamic acid which it then "eats" (metabolizes) to make GABA. The channel that opens is the chloride channels = fast inhibition = GABA A and GABA C (chloride channels). GABA B is NOT a chloride channel and it needs 2 helper G proteins to work = Gi/Go...in sequence.
Bb is using those 2 phosphates, stolen from serine to make glutamic acid-> GABA A and C in order to get NaCl to go in the cell.
Since glutamic acid is released simultaneously with acetylcholine, the temporary rise in glutamic acid might halt the release of acetylcholine...which is what we KNOW happens i.e., Bb's "toxin" inhibits acetylcholine release.
It's toxin is, incidentally a zinc metalloproteinase.
EDTA is far too dangerous.
Bb's Osps (outer cell wall proteins) are composed of this:
"Phospholipids are an important component of bacterial membranes. Borrelia burgdorferi differs from many other bacteria in that
it contains only two major membrane phospholipids: phosphatidylglycerol (PG) and phosphatidylcholine (PC)."
The temporary increase in glutamate (halts acetylcholine release) is broken down to GABA opens the *chloride channels* = GABA A and GABA C (which is what Frontline for dogs, blocks) and in goes "reactive" NaCl followed by CaCl in attempt to activate Bb's PKC (calcium ACTIVATED protein kinase) which Bb is inhibiting.
Say "hi" to the TRPM8 channel which is active in cancer. In goes NaCl and CaCl ("de-icers")...
But...Bb has a gene to EXPORT Ca 'cause it does NOT want Ca IN the cell 'cause calcium could ACTIVATE PKC (calcium activated protein phosphate (= Kinase) transfer...which would ALLOW phosphate transfers to "happen".
Bb has a PKC INHIBITOR. That is the absolute WORSE thing about it.
Your cholesterol level is up because HMG CoA reductase is NOT being inactivated because Bb has driven your INTRAcellular Mg level waaaaaaaaaaaay down.
High cholesterol...don't worry...there are much much worse things that WILL happen.
This is an incredibly DANGEROUS pathogen.
Sorry, I am being very honest and blunt because I am so angry.
I KNOW this can be stopped.
Posts: 9424 | From Sunshine State | Registered: Mar 2001
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JRWagner
Frequent Contributor (1K+ posts)
Member # 3229
posted
Thanks again Marnie!
Peace, Love and Wellness, JRW
Posts: 1414 | From Ny, Ny | Registered: Oct 2002
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