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XMRV --- contamination from vaccine creation?

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http://treatingxmrv.blogspot.com/2011/03/cover-up-and-contamination-theories.html

My guess is that passing lots of human tissue through mice and then culturing in the laboratory for now more than four decades produced the conditions to enable a very unlikely event- by giving it many chances to occur. A probable place for this to have happened was in the creation of live attenuated virus vaccines where virus is made less virulent with multiple passes through animal cells in tissue culture. The earliest live polio vaccine was made by Koprowski using Swiss albino mouse brain cells. The first dose was administered to a child in 1950. He also used monkey kidney cells which were implicated in passing SV40 to humans. Albert Sabin's live polio vaccine was produced from attenutated virus obtained from Koprowski.Mouse cells and the cells of other species have also been used over the years in the creation of other vaccines. Some vaccines, including attenuated Measles and Mumps in the MMR, are grown on duck and chick embryo cells. Domestic fowl have endogenous retroviruses, avian leukosis viruses (ALVs or ASLVs), that do very similar things to the gammaretroviruses. Recombination events are involved in pathogenicity and they can infect the cells of other species in tissue culture. XMRV requires the XPR1 receptor to infect cells. The XPR1 receptor is ubiquitous in mammalian cells. Lab mice are resistant by virtue of XPR1 polymorphisms. The alpha retroviruses use a receptor called TVB. TVB is a tumor necrosis factor receptor that is most likely the avian homolog of a TRAIL (TNF-related apoptosis-inducing ligands) receptor. Here is a paper about the receptor: A Fifteen-Amino-Acid TVB Peptide Serves as a Minimal Soluble Receptor for Subgroup B Avian Leukosis and Sarcoma Viruses. Knauss. The abstract contains the following sentence: "This peptide was sufficient not only for binding to ASLV-B but also for activating viral entry into mammalian cells that lacked the cognate viral receptor."Here are two recent papers that should be giving someone pause, but there is no evidence that anything is changing in the status quo at the CDC. Head in the sand or worse?

Endogenous retroviruses as potential hazards for vaccines. Miyazawa

Isolation of an Infectious Endogenous Retrovirus in a Proportion of Live Attenuated Vaccines for Pets. Miyazawa

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Dr. Deckoff- (who is XMRV positive) raises the question of whether the

whole autism epidemic might have been avoided if the CDC had paid attention to

the DeFrietas retrovirus back in the 90s. I don't see scientists buying in yet,

because the main take-home message from the CROI conference (just last week) is

that XMRV was created in a laboratory in 1996 or later and that positive XMRV

tests are positive because of contamination from those laboratory creations.

That's the message most scientists will be receiving. The CDC is safe to bury

its head (or worse) for a while longer! There are some very persistent people

researching and blogging and treating, so the reprieve may be short. I hope so.

Betty

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http://treatingxmrv.blogspot.com/2011/03/cover-up-and-contamination-theories.htm\

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> My guess is that passing lots of human tissue through mice and then culturing

in the laboratory for now more than four decades produced the conditions to

enable a very unlikely event- by giving it many chances to occur. A probable

place for this to have happened was in the creation of live attenuated virus

vaccines where virus is made less virulent with multiple passes through animal

cells in tissue culture. The earliest live polio vaccine was made by

Koprowski using Swiss albino mouse brain cells. The first dose was administered

to a child in 1950. He also used monkey kidney cells which were implicated in

passing SV40 to humans. Albert Sabin's live polio vaccine was produced from

attenutated virus obtained from Koprowski.

>

> Mouse cells and the cells of other species have also been used over the years

in the creation of other vaccines. Some vaccines, including attenuated Measles

and Mumps in the MMR, are grown on duck and chick embryo cells. Domestic fowl

have endogenous retroviruses, avian leukosis viruses (ALVs or ASLVs), that do

very similar things to the gammaretroviruses. Recombination events are involved

in pathogenicity and they can infect the cells of other species in tissue

culture. XMRV requires the XPR1 receptor to infect cells. The XPR1 receptor is

ubiquitous in mammalian cells. Lab mice are resistant by virtue of XPR1

polymorphisms. The alpha retroviruses use a receptor called TVB. TVB is a tumor

necrosis factor receptor that is most likely the avian homolog of a TRAIL

(TNF-related apoptosis-inducing ligands) receptor. Here is a paper about the

receptor: A Fifteen-Amino-Acid TVB Peptide Serves as a Minimal Soluble Receptor

for Subgroup B Avian Leukosis and Sarcoma Viruses. Knauss. The abstract contains

the following sentence: " This peptide was sufficient not only for binding to

ASLV-B but also for activating viral entry into mammalian cells that lacked the

cognate viral receptor. "

>

> Here are two recent papers that should be giving someone pause, but there is

no evidence that anything is changing in the status quo at the CDC. Head in the

sand or worse?

>

> a.. Endogenous retroviruses as potential hazards for vaccines. Miyazawa

> b.. Isolation of an Infectious Endogenous Retrovirus in a Proportion of Live

Attenuated Vaccines for Pets. Miyazawa

>

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