The number of studies that show that partial immunization via available HPV (human papillomavirus) vaccines is not only insufficient at reducing overall HPV infection rates; the vaccines actually cause rarer, more lethal types of HPV to sweep in and the net effect could be devastating increases in HPV-related cancers.
Here I review the biomedical research studies that show that type replacement is real, and that vaccination against the more common types may be, sadly and ironically, expected to cause INCREASES in HPV-related cancer.
The first study is CDC’s own study, in which they show no net change in HPV infection rate (considering all types) after HPV vaccines were introduced medical practice:
Markowitz LE et al., 2016 Prevalence of HPV After Introduction of the Vaccination Program in the United States. Pediatrics. 2016 Feb 22. pii: peds.2015-1968.
That study concluded that type replacement did not occur because their univariate analysis of individual types showed no individual type with a significant increase. However, because the vaccines do clear the vaccine-targeted types, the lack of change in overall infection rate shows that type replacement must be occurring.
The second study is by Fisher et al. (2016), which specifically found that high-risk HPV types replacing the vaccine-targeted types. They wrote “the percentage of non-vaccine HR-HPV types was higher than expected, considering that eight HPV types formerly classified as ‘low-risk’ or ‘probably high-risk’ are in fact HR-HPV types.
Fischer et al 2016: Shift in prevalence of HPV types in cervical cytology specimens in the era of HPV vaccination. Oncol Lett. 12(1):601-610.
A third study is that by Guo et al., (2015) that also clearly found evidence of type replacement occurring as a result of HPV vaccination:
“The prevalence of high-risk nonvaccine types was higher among vaccinated women than unvaccinated women (52.1% vs 40.4%, prevalence ratio 1.29, 95% CI 1.06–1.57), but this difference was attenuated after adjusting for sexual behavior variables (adjusted prevalence ratio 1.19, 95% CI 0.99–1.43). HPV vaccination was effective against all 4 vaccine types in young women vaccinated after age 12. However, vaccinated women had a higher prevalence of high-risk nonvaccine types, suggesting that they may benefit from newer vaccines covering additional types.”
Guo et al., 2015. Comparison of HPV prevalence between HPV-vaccinated and non-vaccinated young adult women (20-26 years) American Association for Cancer Research Meeting, Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; 2015. Abstract nr 844
A fourth study is that by Mollers et al., who wrote
“…our findings do suggest that clustering differs among HPV types and varies across risk groups.”
and
“The ecological niche could also be taken through type replacement, which refers to the possibility that elimination of HPV16 and HPV18 could lead to an increased transmission of nonvaccine types. For this to occur, antagonistic interactions are required between vaccine types and those not included in the vaccine (8, 9). Type replacement has been observed following vaccination against other pathogens (e.g., Streptococcus pneumoniae) (10) and is plausible whenever genotypically diverse pathogen strains compete for the same hosts.”
A study of Italian women also considered type replacement and wrote that “an accurate post-vaccine surveillance is necessary to early detect a possible genotype replacement”
There are other studies that show type replacement. While some studies may show no type replacement, negative results do not take precedence over positive results. At best, one could say that the science is unsettled. However, CDC’s own study showed no net change in HPV infection rate, and studies now from the US, Germany, Italy and the Netherlands all support the same conclusions: there is evidence for grave concern over the adequacy of HPV vaccines: while the vaccine-targeted types are cleared, the hundred or so that can replace them across the sexually active population includes pathogenic types that may be more lethal than those targeted by the vaccines.
The statistics on the types that are said to be known to cause the most cancers are potentially misleading, because there is an inverse relationship between the ability of pathogen to cause disease (morbidity) and death (mortality). If you count numbers of cases, yes, HPV-16 appears to be high-risk. But the low-frequency types may be even HIGHER risk – which would explain why they are low-frequency.
The study from Germany (Fisher et al., 2016) is definitive, and we have our answer: HPV type replacement is real, and is caused by partial vaccination against an oncogenic virus group.
UPDATE:
Mesher et al. (2016) [Population-Level Effects of Human Papillomavirus Vaccination Programs on Infections with Nonvaccine Genotypes EID Journal Volume 22, Number 10—October 2016); conducted a meta-analysis of nine studies focused on the questoin of type replacement. It is notable that their meta-analysis did not include results from any of these studies, nor were these studies cited as part of the background of available knowledge. In fact, they reference HPV type replacement as a “theoretical concern”, even after the empirical studies review here had been published that demonstrated type replacement as a fact. It is noteworthy that “EID Journal” is an online publication outlet hosted by the US CDC, and the study included authors from the CDC, whose own study had demonstrated type replacement via no net change in overall infection rates after HPV vaccines came to market (Markowitz et al., 2016).
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I have no words, my daughter aged 11 had her first vaccine followed by the remaining course, at age 16 she was diagnosed with primary ovarian failure and not one person could explain why, this was in Scotland United Kingdom
Heidi, terribly sorry to hear about your daughter’s serious problems after HPV vaccination. There are several papers about that very thing observed after HPV vaccination. See https://www.ncbi.nlm.nih.gov/pubmed/23902317 and https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4528880/
You write
Type replacement is denied by the CDC, even though their own data show it occurs. It, in my opinion, completely guts any rationale for HPV vaccines as currently formulated: https://jameslyonsweiler.com/2016/06/29/high-risk-hpv-type-replacement-follows-hpv-vaccination/
That I thought was well established for everything from Pneumococcal vaccine to HPV, CDC denial notwithstanding
Take the premise that as 70% of cervical cancers are due to 16/18 strains so the vaccine will prevent 70% cases of cancers.
But there are 100 strains of HPV and if these two strains are prevented, other strains will take its place.
There is NO proof that vaccination reduces cancer.
This is because cancer may take 40 years to develop.
So the look at early surrogate markers like CIN2.
(Many CIN2 will not become cancer but that is the only proof they have that the vaccine does something).
They say vaccine reduces CIN2 from 16/18 virus so it will reduce cancer later.
But they examine for CIN2 with 16/18 NOT CIN2 from all causes
‘If we examine CIN2+ due to all strains of HPV we can see where 16/18 CIN2 decreases, other strains increase and total CIN2 is more after vaccination than before.
Castellsague and colleagues (2011) showed that in their cohort, there were only 3 who had CIN2+ with vaccine type viruses in the vaccinated group, compared to 8 in the placebo group.
However non-vaccine type CIN2+ increased to 13 in the vaccinated compared to 4 cases in the placebo group.
The end result of vaccination was as follows
(Vaccine group) Vaccine group CIN2 =3 + Non vaccine CIN2 = 13
Total = 16 cases of CIN2
(Placebo group) Vaccine group CIN2 = 8+ Non vaccine CIN2 = 4
Total = 12 cases of CIN2
The paper of Castellsague is here
http://www.nature.com/bjc/journal/v105/n1/full/bjc2011185a.html?foxtrotcallback=true
Results from a prospective cohort study of young Japanese women showed that the profile of type-specific HPV infection was changed after initiation of HPV vaccination in Japan. In this study, HPV screening and type-specific HPV testing were performed on 2493 Pap test specimens collected from Japanese women aged 20 to 21 years during the period covering 2014 to 2017. HPV type-specific infection in different birth cohorts, 1993 to 1994 (prior to organized HPV immunization in the 12-16 year age group) and 1994 to 1997 (following organized HPV immunization in the 12-16 year age group) was determined. For the years 2014 to 2017, HPV vaccination rates were 28.6%, 74.8%, 76.7%, and 80.0%, respectively (P 2/3 of all cervical cancer cases worldwide so the premise was that as 70% of cervical cancers are due to 16/18 strains the vaccine will prevent 70% cases of cervical cancers but it appears that other high risk types are moving in. Type 58 was also not found in a gardasil 9 analysis by corvelva https://www.corvelva.it/it/speciale-corvelva/vaccinegate-en/initial-results-on-gardasil-9-chemical-composition.html