Behind every vaccine is an assumption. That HPV causes cervical cancer, that cervical cancer causes death, and that a vaccine can effectively interfere with this linear relationship is the assumption to be examined in this article. Cervarix is a vaccine recommended to girls beginning as early as 9 years old, intended to protect against HPV strains 16 and 18 upon completion of a 3 dose series. It is an aluminum-containing product, with notable "immunogenicity".
A new GlaxoSmithKline (GSK) funded study published in the Journal of Infectious Diseases has revealed that HPV infection, resulting in naturally acquired human papilloma virus (HPV) antibodies, reduces the risk for new infection and cervical abnormalities linked to cancer in non-HPV vaccinated subjects.
In addition to this startling finding – additional GSK-funded research from this year revealed that the HPV vaccine may not protect women against high-grade squamous intraepithelial lesions, dysplasias.
If, in fact, the HPV vaccines do not work as widely advertised, and natural HPV infectious exposures actually protect against the progression of HPV linked cervical changes to cancer, then taken together, both these findings challenge the most fundamental assumptions within vaccine science (aka vaccinology), and render highly dubious the oft repeated rhetoric that natural HPV infection is juggernaut –like deadly force the best defense against which are universal immunization campaigns.
HPV Infection Protects Against New Infection and Cervical 'Premalignancies'
The groundbreaking new study titled, Risk of newly detected infections and cervical abnormalities in women seropositive for naturally-acquired HPV-16/18 antibodies: analysis of the control arm of PATRICIA, analyzed data from the non-vaccinated control arm of the Papilloma Trial against Cancer in Young Adults (PATRICIA), to ascertain whether natural HPV16 and HPV18 antibodies reduced the risk for new HPV infection and/or cervical abnormalities over a 300 day period. A total of 16,656 women were included in the study's control arm (8,193 women in the HPV16 analysis and 8,463 women in the HPV18 analysis), with none of the women being administered the HPV vaccine.
It should be noted that this is one of the first studies to look at the natural history of HPV infection and immunity, as well as one of the first studies to show the validity of using the control arm data from vaccine efficacy trials. The control arm did, however, receive three doses of the Hepatitis A vaccine. As there are no vaccine studies in existence using a true non-vaccinated control group, the natural incidence of a disease, as well as the true risks of a vaccine cannot be effectively assessed.
The study found that the presence of natural antibodies against HPV16, considered one of the most malignant of the over 120 unique types identified, lowered the risk for newly detected infection and a type of abnormal pap smear result known as ASC-US+ or 'atypical squamous cells of undetermined significance'. The same protective effect was found for natural HPV18 antibodies, only to a lesser extent.
While the presence of HPV antibodies (seropositivity) overall was not associated with the development of the so-called cervical 'premalignancy' known as CIN1+, i.e. cervical intraepithelial neoplasia grade 1 or higher, those with the highest antibody levels at baseline had a significantly reduced risk of developing CIN1+ compared to women without detectable HPV antibodies (seronegative women).
Given that the entire justification for vaccination is based on the observation that surviving natural exposures to infectious challenges results in lasting immunity, this finding is not that surprising. HPV is no doubt one of countless infectious challenges the body's elaborate and highly effective adaptive immune system countermands, often subclincally/asymptomatically . Even the authors of the study acknowledged: "Naturally acquired antibodies can remain detectable for at least 4 to 5 years, albeit at much lower levels than those induced by vaccination." Given the outcomes demonstrating protective efficacy of these lower levels of antibodies, questions may be raised about other elements of the immune system at play in successful pathogenic defense.
The study brings to the fore three major realizations:
- Vaccine science is in its infancy, as we are still elucidating the role of antibodies, natural or synthetically stimulated. As we discussed in a previous article under the heading 'Beyond Antibodies,' the vaccine-inducible increase in antibody titers (often called "efficacy") does not ensure antibody-antigen affinity, the only likely relevant proxy measurement of real world vaccine effectiveness; furthermore, the entire antibody-centered view of vaccine effectiveness has been called into question by a recent study, including the following three well-known problems with the antibody-driven model:
- evidence of exposure without illness
- antibody production with subsequent infection
- lack of antibody production with illness.
The authors reference the acquisition of identifiable antibodies in only 50-70% of women infected with HPV-16 or 18. What is happening in the rest of the cases? The authors suggest that those with previous infection but without antibodies may have mounted a cell-mediated response that also conferred protection not assessed in this study (or acknowledge to be relevant by vaccine manufacturers). This is tacit acknowledgement of the biochemical individuality that underlies immune response, rendering a reductionist one-size-fits-all model inappropriate for preventive medicine.
2. It appears there is a correlation between antibodies related to infection and protection from dysplasia (cellular abnormalities) rather than infection progressing definitively to cancer. The commonly held notion that naturally transmitted HPV infection and subsequent elevation of antibody titers is a disease process that leads inevitably to tissue pathology and possibly precancer or cancer, rather than an instance of the immune system effectively meeting the HPV viral challenging and responding with an appropriate antibody response, conferring lasting immunity, is debunked by this new study. Clearly, natural infection not only prevents reinfection, but even reduces the risk of HPV's potential induction of dysplastic cellular changes associated with cancer.