New Study: HPV Vaccine and Evidence of Herd Immunity or Type Replacement?

By Norma Erickson, President

 

HPV Vaccine: Herd Immunity?

 

Medical professionals rely on studies published in medical journals to keep abreast of new developments in their field. What happens when published studies raise more questions than answers? Where does that leave trusting medical consumers?

On July 12, 2012, Australia became the first country in the world to formally offer taxpayer sponsored HPV vaccines to their young men. HPV vaccines have been advertised as ‘cervical cancer’ vaccines. Boys obviously do not have a cervix, so how do you ‘sell’ males on the idea of a three shot series of the most expensive vaccine on the market?

Miracle of miracles – almost immediately press reports begin to come in from around the world about a new study that supposedly demonstrates evidence of HPV vaccinations providing protection to the unvaccinated population. What an outstanding way to convince boys it is their duty to protect those around them.

Unfortunately, none of the articles reporting this ‘miraculous’ development provide a link to the actual study so a person can check for themselves. So much for responsible journalism!

“Vaccine-Type Human Papillomavirus and Evidence of Herd Protection After Vaccine Introduction,” by Jessica A. Kahn, MD, MPH, et al., was accepted for publication in April 2012 by the medical journal Pediatrics, but will not be formally published until August.¹

Historically, academic ‘experts’ paid directly or indirectly by the industry have cherry-picked populations with a high prevalence rate of HPV infections or cervical cancer to generate a set of data. They extrapolate the ‘scientific’ data obtained from irrelevant populations to promote a vaccine with questionable value or an analytically inaccurate HPV test for use in the general population.

In 2001, a group of employees of the National Cancer Institute, a major patent holder and financial beneficiary of HPV vaccines, did just that when they used a population with an extremely high cervical cancer rate in a subpopulation of Costa Rica during development of the HPV ‘cancer’ vaccine and an HPV test for cervical cancer screening.² Then they helped expedite approval of HPV vaccines and an inaccurate HPV test through the Food and Drug Administration to be used in populations with little threat of cervical cancer progression.

In their most recent study, Jessica A. Kahn and her coauthors have done the same thing by using a cherry-picked subset of African American women with an extremely high rate (68.3%) of HPV infection for a statistical analysis to justify wide spread implementation of the HPV vaccination policy through so called “herd protection.” The authors conveniently ignore the fact that most American women under the care of gynecologists in private practice have a less than 10% HPV infection rate even when the most sensitive nested PCR amplification is used for detection. They also ignore the fact that African American women usually carry different strains of HPV viruses than women from other ethnic backgrounds.³

It is well known that test results obtained in a population with high disease prevalence rates cannot be extrapolated to a population with a low prevalence of the disease. These authors knowingly misapply their statistical data to support this “herd protection” hypothesis as if HPV infection had become a contagious disease like influenza in the classrooms of all high schools throughout the world.

It is unfortunate that their opinion, supported by public funding, is published in the official journal of the American Academy of Pediatrics as a continued medical education material to influence the practice of the pediatricians, policy-makers and health authorities.

This is particularly true when a careful reading of Khan et al.’s article reveals the following points:

1. Vaccine-type HPV infections reportedly decreased by 21.9% in vaccinated participants; but vaccine-type HPV infections also showed a decrease of 14.8% in the unvaccinated group when compared to the data from 2006-07. These changes are especially remarkable given that many participants were sexually experienced, presumably exposed to HPV, and only 1 HPV vaccine dose was required to be considered “vaccinated” in this analysis.
2. The authors should know there are 3 subtypes of HPV-18, namely the European, the Asian-American and the African subtypes.⁴ In the U.S., 91% of the HPV-18 isolates from white women are reported to be of the European and Asian-American variants, and 64% of the HPV-18 isolates from African American women belong to the African variants.⁵ The production of the Gardasil^® HPV-18 VLPs uses the HPV L1 gene from the SW756 cell line⁶ which carries an African subtype of HPV-18.⁴ Therefore, any “herd protection,” even if conveyed to a subset of African American women by Gardasil^® vaccination, cannot be automatically extrapolated to other races or ethnicities.
3. Why do the authors of the study consider one shot of Gardasil^® to give the participants vaccinated status when the recommended dose is a series of three injections? If one shot is enough, is three too many?
4. The study utilized the Roche Linear Array for HPV typing. According to World Health Organization documentation, only 8 of 17 datasets in a worldwide survey using the Roche Linear Array assay reported a 100% proficiency result in HPV genotyping.^{7 (table 2)} In 7 of the 17 testing sets, false positive HPV types were detected by the Roche Linear Array assay.^{7 (table 3)} This information brings the entire study into question.
5. The authors of the study state, “the overall HPV prevalence increased “modestly” between the two studies.” How can this happen if the vaccine provides herd immunity?

Consider the following data taken from the soon to be published article regarding this ‘modest’ overall increase in HPV infections. This chart is a representation of HPV prevalence changes discovered when the post-vaccination surveillance group of 2009-10 was compared to the pre-vaccination surveillance data from 2006-07:

HPV	All	Vaccinated	Non-vaccinated
Any Type	8.5% increase	9.0% increase	1.8% increase
High Risk Type	1.1% increase	5.2% increase	7.5% reduction
Vaccine Type (16/18/11/6)	18.3% reduction	21.9% reduction	14.8% reduction
High Risk Vaccine Type	14.2% reduction	17.8% reduction	12.0% reduction
Non-Vaccine Type	14.0% increase	15.2% increase	7.6% increase
Non-Vaccine High Risk Type	7.6% increase	13.6% increase	2.7% reduction

Why was there no statistically significant change in HPV infection rates among the unvaccinated participants? Does this mean that other types of HPV are taking over the role of the vaccine-suppressed HPV types in the vaccinated? If so, will the other types become more dangerous than the suppressed ones?

Does this mean the manufacturer targeted the wrong types of HPV for this population? Or, does it simply mean the vaccine doesn’t work?

Does this article provide evidence of herd immunity or potentially dangerous HPV mutation/type replacement?

Is this simply another example of the quality one can expect from industry sponsored ‘scientific studies’ destined to be blindly accepted and widely quoted to influence worldwide health policies?

This study raised far more questions than it answered. Medical consumers deserve better.

References:

1. Kahn JA, Brown DR, Ding L, Widdice LE, Shew ML, Glynn S, Bernstein DI. Vaccine-Type Human Papillomavirus and Evidence of Herd Protection After Vaccine Introduction. Pediatrics. 2012 Jul 9. [Epub ahead of print] http://pediatrics.aappublications.org/content/early/2012/07/03/peds.2011-3587.abstract
2. HPV co-factors related to the development of cervical cancer: results from a population-based study in Costa Rica. Hildesheim A, Herrero R, Castle PE, Wacholder S, Bratti MC, Sherman ME, Lorincz AT, Burk RD, Morales J, Rodriguez AC, Helgesen K, Alfaro M, Hutchinson M, Balmaceda I, Greenberg M, Schiffman M. Br J Cancer. 2001 May 4;84(9):1219-26.PMID: 11336474 [PubMed - indexed for MEDLINE] Free PMC Article Free textRelated citations
3. Dunne EF, Unger ER, Sternberg M, McQuillan G, Swan DC, Patel SS, et al. Prevalence of HPV infection among females in the United States. JAMA 2007; 297: 813-9.
4. Lurchachaiwong W, Junyangdikul P, Termrungruanglert W, Payungporn S, Sampatanukul P, Tresukosol D, Niruthisard S, Trivijitsilp P, Karalak A, Swangvaree S, Poovorawan Y.: Whole-genome sequence analysis of human papillomavirus type 18 from infected Thai women. Intervirology 2010, 53:161-166
5. Xi LF, Kiviat NB, Hildesheim A, Galloway DA, Wheeler CM, Ho J, Koutsky LA. Human papillomavirus type 16 and 18 variants: race-related distribution and persistence. J Natl Cancer Inst. 2006 Aug 2;98(15):1045-52.
6. Hofmann KJ, Neeper MP, Markus HZ, Brown DR, Müller M, Jansen KU. Sequence conservation within the major capsid protein of human papillomavirus (HPV) type 18 and formation of HPV-18 virus-like particles in Saccharomyces cerevisiae. J Gen Virol. 1996 Mar;77 ( Pt 3):465-8
7. http://jcm.asm.org/content/early/2012/04/19/JCM.00840-12.abstract