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:

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.

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):

#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] 

#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. 

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] 

#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]

Where does this leave the average medical consumer? Unfortunately, it leaves them with the following unanswered questions: