Gardasil: New Study Brings More Safety Questions to Light

Gardasil: New Study Brings More Safety Questions to Light

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Norma Erickson
Activist Post

Why were HPV-16 L1 DNA fragments detected in post mortem samples taken
six months after Gardasil vaccination and not the other vaccine-relevant
types? Dr. Sin Hang Lee, of Milford Hospital and Milford Molecular
Laboratory, may have provided an answer in his most recently published
paper entitled, "Topological
conformational changes of human papillomavirus (HPV) DNA bound to an
insoluble aluminum salt – A study by low temperature PCR."[1] His
findings suggest that non-B-conformational changes in HPV L1 gene DNA
fragments bound to the AAHS adjuvant may be genotype related, in other
words specific to HPV-16.

In September 2011, SaneVax Inc. informed the FDA that despite all claims
stating Gardasil contained ‘no viral DNA’ Dr. Lee had discovered there
were indeed fragments of HPV-11, HPV-16 and HPV-18 L1 DNA firmly
attached to Merck’s proprietary aluminum adjuvant in 100% of the samples
he tested, but all were lacking a region amplifiable by an MY09
degenerate primer.[2] The FDA was quick to confirm that Gardasil does
contain residual HPV L1 gene DNA fragments,[3] but that these fragments
posed no health risk. The FDA completely ignored a request for further
investigations put forth by the SaneVax Team.[4]

In light of the FDA statement corroborating Dr. Lee’s
previous findings, the presence of HPV DNA fragments of vaccine origin
in the bodies of recipients might be anticipated after intramuscular
injections of Gardasil. However, finding HPV-16 L1 DNA fragments in
post-mortem blood samples of a teenager who died six months after
completion of 3 Gardasil injections without finding any other
vaccine-relevant fragments was a surprise.[5] Obviously, further investigations were necessary.


At the request of SaneVax Inc., Dr. Lee agreed to use PCR amplification
followed by direct DNA sequencing to try and determine what was going
on. What he discovered is stated clearly in the conclusion of the above
referenced paper. It says:
<blockquote class="tr_bq">Naked HPV L1 gene DNA fragments bound to Al3+
in solid phase by ligand exchange have acquired a non-B-conformation.
The resulting topological conformational changes may affect a region
shared by many HPV genotypes, for example at the primer-binding site for
the degenerate MY09 primer, or may affect a region of a specific
genotype, for example at the degenerate MY11 primer-binding site of the
HPV-16 L1 gene DNA. DNA conformational changes induced by a particulate
aluminum-based adjuvant may have stabilized the residual HPV-16 L1 gene
DNA fragments in an injectable vaccine and prevented their enzymatic
degradation in a vaccine recipient.</blockquote>B-Conformation DNA

The
term ‘non-B conformation’ refers to any DNA conformations other than
the orthodox B-conformation right-handed Watson-Crick structure pictured
on the left. Conformational change may be induced by many factors such
as a change in temperature, pH, voltage, ion concentration,
phosphorylation, or the binding of a ligand. Conformational change can
be something as simple as a slight twisting, kinking, or knotting. Non-B
DNA conformations also include some of the more complex structures
referred to in the quotes below. Scientists have been studying non-B
conformation DNA as related to genetic disorders since the mid 1960s.[6]

Consider the following quotes from various peer-reviewed scientific papers (emphasis added):
<blockquote class="tr_bq">#1 “Recent discoveries have revealed
that simple repeating DNA sequences, which are known to adopt non-B DNA
conformations (such as triplexes, cruciforms, slipped structures,
left-handed Z-DNA and tetraplexes), are mutagenic.The mutagenesis is due to the non-B DNA conformation rather than to the DNA sequence
per se in the orthodox right-handed Watson-Crick B-form. The human
genetic consequences of these non-B structures are approximately 20 neurological diseases, approximately 50 genomic disorders (caused by gross deletions, inversions, duplications and translocations), and several psychiatric diseases
involving polymorphisms in simple repeating sequences. Thus, the
convergence of biochemical, genetic and genomic studies has demonstrated
a new paradigm implicating the non-B DNA conformations as the
mutagenesis specificity determinants, not the sequences as such.”[7] </blockquote><blockquote class="tr_bq">#2
“In 2004, Albino Bacolla and colleagues discovered that breakpoints for
gross deletions that cause a number of human diseases coincide with the
presence of non-B DNA structures (described below). These and later
studies have cemented the role of non-B DNA structures in human disease.
Because of the strength of these techniques and the compelling nature
of the results that were obtained, these concepts have been widely
accepted and extended by the biological and medical communities. </blockquote><blockquote class="tr_bq">This
and subsequent work have revealed that slipped structures, cruciforms,
triplexes, tetraplexes, and perhaps other non-B DNA structures,
including left-handed Z DNA, are formed in chromosomes and elicit
far-reaching genetic consequences via recombination/repair. Repeating
sequences, in their non-B conformations, cause gross genomic
rearrangements (translocations, deletions, insertions, inversions, and
duplications). These rearrangements are the genetic basis for
numerous human genomic diseases, including polycystic kidney disease,
adrenoleukodystrophy, follicular lymphomas, and spermatogenic failure.
At least 70 diseases fall into this category.”[8] </blockquote><blockquote class="tr_bq">#3 “Current genome-wide sequence analyses suggest that the genomic instabilities induced by non-B DNA structure-forming sequences not only result in predisposition to disease, but also contribute to rapid evolutionary changes, particularly in genes associated with development and regulatory functions.”[9]</blockquote>Where does this leave the average medical consumer? Unfortunately, it leaves them with the following unanswered questions:

• Once injected, how long will the HPV-16 L1 DNA fragments attached to aluminum remain in my body?
  
• Are the non-B conformation HPV fragments in Gardasil potentially harmful?
  
• Will the non-B conformation DNA fragments in Gardasil induce autoimmune disorders?
  
• Will the non-B conformation DNA get integrated in the genome causing mutagenesis and/or cancer?
  

The scientific community needs to investigate these potential risks
immediately. Medical consumers need to know the risks as well as any
potential benefits before they decide if Gardasil is right for them.

In the interest of public health and safety, the FDA needs to rescind
approval for Gardasil until satisfactory answers are provided to the
four questions above. The time for poke and hope is long since passed.
Medical consumers need proof this vaccine is safe.

Source:-
http://www.activistpost.com/2013/03/gardasil-new-study-brings-more-safety.html