Some regions have higher rates of HPV infections. In one province in South Africa, 74.6% of women have HPV.
HPV6 and HPV11 account for most genital warts.
HPV16 and HPV18 account for about 70% of cervical cancer.
Types 31, 33, 45, 52, 58 account for about another 20% of cervical cancer.
Current Gardasil prevents nine strains of HPV (HPV-16, 18, 31, 33, 45, 52, 58, 6, and 11) -- the ones that cause about 90% of cervical cancer.
The lifetime risk of cervical cancer is 1 in 152 in the United States. It is higher in countries without widespread screening programs; for instance, it is 1 in 40 in South Africa.
The lifetime risk of anal cancer 1 in 500 in the United States.
According to "The Role of HPV E6 and E7 Oncoproteins in HPV-associated Cervical Carcinogenesis",
"The abilities of high-risk HPV E6 and E7 proteins to associate with the tumor suppressors p53 and pRB, respectively, have been suggested as a mechanism by which these viral proteins induce tumors."According to " Genome-wide analysis of HPV integration in human cancers reveals recurrent, focal genomic instability",
"Whole-genome sequencing revealed HPV integrants flanking and bridging extensive host genomic amplifications and rearrangements, including deletions, inversions, and chromosomal translocations."And according to "APOBEC-Mediated Cytosine Deamination Links PIK3CA Helical Domain Mutations to Human Papillomavirus-Driven Tumor Development",
"we have uncovered a critical role for APOBEC-mediated mutagenesis in HPV-driven tumor development"For much more, see Google Scholar.
The FDA reviewed the clinical trial results for safety and efficacy, and approved Gardasil for use against cervical cancer and genital warts in women in 2006, and against anal cancer in anyone aged 9 through 26 in 2010.
Since fainting is possible after any vaccination, patients should sit for 15 minutes after being vaccinated.
The shot often hurts for a few days. A study on tolerability which emailed questionnaires to 3552 girls after each dose found that about 1 in 8 respondants said they experienced pronounced pain, stiffness, or swelling that started within 3 days and lasted about 1 to 5 days.
About 1 in 100,000 people may have an allergic reaction to the vaccine. Most recover without incident.
The lifetime risk of contracting cervical or anal cancer (1 in 152 and 1 in 500, respectively) is much higher than any of the serious risks indentfied so far with the vaccine.
See hpv.kegel.com/safety for more info on hpv vaccine safety.
Recent research indicates that two doses given six months apart may suffice if given by age 13. As a result, the UK is switching to a two-dose schedule.
The United States is considering this change as well, but will probably stick with the three-dose schedule until about 2016.
According to Merck,
"Gardasil is contraindicated in individuals with hypersensitivity, including severe allergic reactions to yeast, or after a previous dose of Gardasil."
According to Glaxo,
"You should not get Cervarix if you have or have had an allergic reaction to a previous dose of Cervarix, or an allergy to any of the ingredients in Cervarix (listed below)."
The proposed new test starts off by checking for HPV16 and HPV18 individually, as those are the two highest risk strains. It also checks for all other high risk strains as a group. It doesn't check for low risk strains, which is fine, as they generally don't cause cancer.
Here's how the test is supposed to be used:
"In women 25 years and older, the cobas HPV Test can be used as a first-line primary cervical screening test to detect high risk HPV, including genotyping for 16 and 18. Women who test negative for high risk HPV types by the cobas HPV Test should be followed up in accordance with the physician's assessment of screening and medical history, other risk factors, and professional guidelines. Women who test positive for HPV genotypes 16 and/or 18 by the cobas HPV Test should be referred to colposcopy. Women who test high risk HPV positive and 16/18 negative by the cobas HPV Test (12 Other HR HPV positive) should be evaluated by cervical cytology to determine the need for referral to colposcopy."In other words, if it finds the highest risk strains (HPV16 or 18), your doctor will have you get a colposcopy; if it finds other high risk HPV, your doctor will give you a Pap test.
According to the FDA review packet, the new test finds more cancer using fewer colposcopies than does current standard practice.
Also, when cervical cancer screening finds an HPV-caused lesion, it has to be surgically removed to prevent the cancer (by cutting, freezing, or burning). Screening finds about 300,000 cases of HSIL (CIN2/CIN3) annually in the US, leading to approximately half a million LEEP procedures each year. Women vaccinated when they were age 9-14 have about 55% lower risk of CIN2 or CIN3 and thus about 55% lower risk of needing surgery to prevent cancer.
See also "Prophylactic HPV Vaccines: Current Knowledge of Impact on Gynecologic Premalignancies" by Diane Harper, which points out
"While Pap testing is effective, there still remain five specific challenges. First, screening must be done repeatedly over most of the woman's lifetime. Second, false negatives can occur; 30% of women developing cervical cancer having had a history of normal cytology screens (Sawaya and Grimes, 1999). Third, abnormal cytology causes much anxiety for many women (Rogstad, 2002). Fourth, for those women whose screening leads to a diagnosis of CIN 2/3, treatment with loop electrosurgical excision procedure (LEEP) can lead to an increased risk in subsequent pregnancies of preterm delivery, low birthweight infants, premature rupture of membranes, and operative delivery at a rate of 70-300% increase (Arbyn et al., 2008). Lastly, there is no lifetime protection from future HPV infections from her natural infection, leaving a woman at a 3-12 fold increased risk of other anogenital cancers about 10 years later (Edgren and Sparen, 2007)."(Note: that paper also contains a much lower estimate of what portion of HPV-caused cancers are noncervical (12% vs. 55%). The difference may be explained in part by our greater knowledge since then of the role of HPV in throat cancer.)
Four studies have checked Gardasil's protection at six, eight, nine, and 10 - 12 years, respectively; each study found Gardasil was still protecting.
The newer but very similar Gardasil 9 vaccine has been shown to protect at least six years so far, and a single booster shot restores full immunity.
Two studies have checked Cervarix's protection at 9.4 and 10 years, found no new persistent HPV 16/18 infections in vaccinated women during that time, and estaimated that vaccinating before age 25 gives lifelong protection against HPV 16 and 18.
None of these studies has found when the vaccines really wear off yet, but long-term studies are continuing, and eventually we may know how long it lasts.
Booster shots are not currently recommended, but the CDC's "HPV Vaccine Q&A" says "If protection from HPV vaccine doesn't last as long as it should, then the Advisory Committee for Immunization Practice would review the data and determine if a booster should be recommended."
There is evidence HPV vaccines work as a booster 4, 5, and 8.5 years after vaccination.
See also "Long-Term Studies of Quadrivalent HPV (qHPV) Vaccine Effectiveness", "The Efficacy and Duration of Vaccine Protection Against Human Papillomavirus - A Systematic Review and Meta-analysis", and "Review of Data on Duration of Protection after HPV Vaccination, Advisory Committee on Immunization Practices, June 23, 2016"
"Determinants of prevalent human papillomavirus in recently-formed heterosexual partnerships: A dyadic-level analysis" found
Dyads that always used condoms with previous partner(s) were 27% (95% CI: 9-42%) less likely to have HPV.
"Condom use and the risk of genital human papillomavirus infection in young women" found
In women reporting 100 percent condom use by their partners, no cervical squamous intraepithelial lesions were detected in 32 patient-years at risk, whereas 14 incident lesions were detected during 97 patient-years at risk among women whose partners did not use condoms or used them less consistently.
Girls vaccinated by age 14 had about 75% fewer abnormal results at their first pap test as their unvaccinated peers... but girls vaccinated by age 15 were only half as well protected.
And vaccinating by age 13 is even more effective.
Since the virus can be transmitted by just touching an infected area, you don't have to have "sex" to catch it. Two studies found between 2% and 46% of young women already had HPV by the time they first have intercourse. You can even catch HPV from open-mouth kissing. So even kids whose parents don't consider them sexually active are at risk.
Virginity pledges don't seem to protect against STDs such as HPV, either; see "After the promise: the STD consequences of adolescent virginity pledges" (full text).
"Under assumptions of lifelong vaccine immunity, the vast majority of published cost-effectiveness analyses have suggested that targeting pre-adolescent girls (ages 12 or younger) with an HPV-16/18 vaccine is very attractive in the context of current screening."
Long story: "CDC HPV Vaccine Information for Young Women" says
Ideally females should get the vaccine before they become sexually active and exposed to HPV. Females who are sexually active may also benefit from vaccination, but they may get less benefit. This is because they may have already been exposed to one or more of the HPV types targeted by the vaccines. However, few sexually active young women are infected with all HPV types prevented by the vaccines, so most young women could still get protection by getting vaccinated.
"Prevalence of HPV After Introduction of the Vaccination Program in the United States" found
"Within 6 years of vaccine introduction, there was a 64% decrease in 4vHPV type prevalence among females aged 14 to 19 years and a 34% decrease among those aged 20 to 24 years."
"Human Papillomavirus Prevalence and Herd Immunity after Introduction of Vaccination Program, Scotland, 2009-2013" found fully vaccinated women had about a third as many vaccine-type infections as nonvaccinated women.
"Reduction in Human Papillomavirus Vaccine Type Prevalence Among Young Women Screened for Cervical Cancer in an Integrated US Healthcare Delivery System in 2007 and 2012-2013" found
"In 2012-2013, vaccine-type HPV prevalence was significantly lower among those who initiated vaccination <19 years (adjusted prevalence ratio, 0.1; 95% confidence interval, 0.1-0.3)"
"Fall in Human Papillomavirus Prevalence Following a National Vaccination Program" says
"HPV genoprevalence in women aged 18-24 years attending family planning clinics in the prevaccine period (2005-2007) was compared with prevalence among women of the same age group in the postvaccine period (2010-2011). ... The prevalence of vaccine HPV genotypes (6, 11, 16, and 18) was significantly lower in the postvaccine sample than in the prevaccine sample (6.7% vs 28.7%; P < .001), with lower prevalence observed in both vaccinated and unvaccinated women compared with the prevaccine population (5.0% [adjusted odds ratio, 0.11; 95% confidence interval, 0.06-0.21] and 15.8% [adjusted odds ratio, 0.42; 95% confidence interval, 0.19-0.93], respectively)."
We already knew from clinical trials of Gardasil that it prevents about 80% of genital warts when given before exposure to HPV. Now, several studies have measured how effective it is in real world national immunization programs. For instance:
In areas that began strong vaccination programs in 2007, the effect of vaccination is already showing up in the general population. Figure 5.2 of the Victorial Cervical Cytology Registry 2014 report says that, since vaccination started, HSIL has fallen by 50% in the under-25 age group and by 25% in the 25-29 age group. (The decline began in 2009 for those under 25, in 2013 for those 25-29, and may have started declining in 2014 for those aged 30-34.)
(The 2015 VCCR report is not yet out, but here's a sneak peek of a key graph, courtesy of this tweet.)
Since CIN2 and CIN3 are treated by surgically removing part of the cervix, an operation that carries risks of complications, women will directly benefit from this reduction.
Since about 50% of untreated CIN3 progresses to cervical cancer, preventing CIN3 is quite likely to prevent some cervical cancer. And since about half of all cervical cancer in the US occurs in women who haven't been properly screened, this is true even in countries with screening programs.
"Decreasing Trends in Cervical Cancer Incidence among Young Women (15-34 Years) in the United States during the Human Papillomavirus (HPV) Vaccine Era" said
"Cervical cancer incidence among young women 15-24 years of age was stable during 2000-2006 from 9.5 in 2000 to 9.1 in 2006, but decreased from 6.9 in 2007 to 5.3 in 2013 (annual percentage decrease [APD] 5.7, 95% confidence interval [CI] 1.1-10.2, significantly different from the APD during 2000-2006).""Trends in cervical cancer incidence in younger US women from 2000 to 2013" found similar results.
Studies of the effect of national vaccination programs continue. We should see something noticable at least by the time the first group of girls to be vaccinated hits age 27 or so. (That's because cervical cancer rates jump to high levels at about that age.) That should happen about the year 2022.
One of the researchers in the long-term followup studies of Cervarix says:
" [with] the country-wide, population-based Finnish Cancer Registry... We have >= 80% power to provide data on vaccine efficacy against CIN3 in 2014, against ICC in 2022 and against other HPV- associated cancers in 2024"See also his paper "Ten-year follow-up of human papillomavirus vaccine efficacy against the most stringent cervical neoplasia end-point -- registry-based follow-up of three cohorts from randomized trials", which is starting to see a few cases of cancer in the control group already.
In the real world, when given to the average young woman aged 15 to 26, the vaccine is less effective because (a) many of these women have already been exposed to HPV, and (b) about 30% of cervical cancer is caused by types of HPV that the vaccine doesn't target.
At age 11-12, and even as late as age 14, most girls have not yet been exposed to HPV. Thus vaccinating at ages 11-12 should provide nearly 100% protection against HPV16/18, and about 70% protection against CIN3 caused by any type of HPV.
Women aged 16-26 may have already been exposed to HPV16 or HPV18; for these women, the vaccine was less effective (about 20% at four years, but more as time went on).
The new vaccine targets nine strains of HPV (HPV-16, 18, 31, 33, 45, 52, 58, 6, and 11) -- the ones that cause about 90% of cervical cancer, higher than the 70% of the current vaccine.
In clinical trials, it reduced biopsies for and treatments for cervical abnormalities from HPV 31/33/45/52/58 by 97% and 87%, respectively (see page 21 of the ACIP presentation).
It was approved by the FDA in December 2014, and recommended by the CDC in February 2015.
The current vaccines are based on the L1 major capsid protein, which is different for each strain. One promising one is based on the L2 minor capsid protein, which is much less variable. See for example "VLPs Displaying a Single L2 Epitope Induce Broadly Cross-Neutralizing Antibodies against HPV", "A Universal Virus-Like Particle-based Vaccine for HPV: Longevity of Protection and Role of Endogenous and Exogenous Adjuvants", and "Efficacy of RG1-VLP Vaccination against Infections with Genital and Cutaneous Human Papillomaviruses".
Vaccination after LEEP procedures has been reported to cut the risk of reinfection by about half. See "Is vaccination with quadrivalent HPV vaccine after loop electrosurgical excision procedure effective in preventing recurrence in patients with high-grade cervical intraepithelial neoplasia (CIN2-3)?" and "Effect of the human papillomavirus (HPV) quadrivalent vaccine in a subgroup of women with cervical and vulvar disease: retrospective pooled analysis of trial data".
One team found that, among HPV-positive women, those with abnormal pap smears and those with persistent HPV infections were less likely to eat papaya or oranges every week than those without.
Another study found that, among HPV positive women, those who cleared their HPV infections were more likely to eat vegetables every day than those who didn't.
"Cross-protective efficacy of two human papillomavirus vaccines: a systematic review and meta-analysis" found only slight protection for HPV types not targeted by either vaccine, so one would not expect current vaccines to have much impact on high risk strains beyond HPV-16 and 18.
This seems to be borne out by two studies of what has happened to the prevalence of HPV types after the introduction of national vaccination programs.
In England, after two to four years of national Cervarix vaccination, among a representative sample of 16-18 year old sexually active girls (65% of whom had been fully vaccinated), HPV-16 and 18 declined by about two thirds, other high-risk types as a whole were roughly unchanged, and HPV-6 and 11 increased by about a third.
In the United States, after zero to four years of national Gardasil vaccination, among a representative sample of 14-19 year old sexually active girls (about 32% of which had been fully vaccinated), HPV-16, 18, 6, and 11 declined by about half, and there were no other significant changes.
"Vaccine-type human papillomavirus and evidence of herd protection after vaccine introduction" reported
the prevalence of high-risk, nonvaccine-type HPV increased 7.6% (48.6%-56.2%, P = .0038) for all participants, and the increase was significant (13.6%, P < .0001) for vaccinated but not for unvaccinated participants... A possible explanation for the finding that nonvaccine-type HPV prevalence increased in vaccinated but not in unvaccinated young women is that their risk for HPV may differ. Vaccinated versus unvaccinated girls did not differ in number of recent and lifetime sexual partners; however, they were more likely to be African American (84% vs 54%, P < .0001) and reported, on average, an earlier age of first sexual intercourse (mean = 14.6 vs 15.3 years, P = .0007), both of which have been associated with higher rates of HPV infection."
Vaccines covering more types of HPV are currently under develoment. In particular, a nonavalent vaccine was approved by the FDA in December 2014.
Further out, vaccines based on chimeric L1/L2 protein combinations (pubmed 23752042), L2 proteins alone, or L2-flagellin combinations may offer even wider coverage in the future.
A large recent study by S.Hariri et al (full text) measured which types of HPV were involved in cervical cancer vs. race. Here's its key finding (Figure 4b):
This shows that the current vaccine covers HPV types that cause about 80-90% of CIN3 in blacks, and about 90% in whites.
Dark is original vax (Gardasil), grey is added types in current vax (Gardasil 9).
"Taking into account the totality of the available information the PRAC concluded that the evidence does not support that HPV vaccines (Cervarix, Gardasil, Gardasil 9, Silgard) cause CRPS or POTS. The benefits of HPV vaccines continue to outweigh their risks."
As of July 2015, 80 cases have been compensated, and 82 have been dismissed without compensation.
Here's a table of cases where a case involving just the HPV vaccine was either settled or won.
"Introducing HPV vaccine and scaling up screening procedures to prevent deaths from cervical cancer in Japan: a cost-effectiveness analysis" (full text) estimated that vaccination and screening together reduced the lifetime risk of cancer to about half that of screening alone.
"Beyond cervical cancer: burden of other HPV-related cancers among men and women" said
In the United States annually (1998-2003), up to ... 4,753 noncervical cancers among men, and 4,128 noncervical cancers among women are potentially attributable to HPV infection. ... incidence rates for anal, oropharyngeal, and vulvar cancers have increased substantially in recent years.The vaccine has been reported to be effective against early stages of anal and vulvar cancer.
"Effectiveness of cervical screening with age: population based case-control study of prospectively recorded data" says
Cervical screening in women aged 20-24 has little or no impact on rates of invasive cervical cancer up to age 30.Accordingly, the UK does not screen women under 25 for cervical cancer. But a few women under that age do die of cervical cancer, and vaccination can prevent many of those deaths.
"Current studies do not support the hypothesis that multiple vaccines overwhelm, weaken, or "use up" the immune system. On the contrary, young infants have an enormous capacity to respond to multiple vaccines, as well as to the many other challenges present in the environment. By providing protection against a number of bacterial and viral pathogens, vaccines prevent the "weakening" of the immune system and consequent secondary bacterial infections occasionally caused by natural infection."
Long story: "Postlicensure Vaccine Safety Monitoring, 2006-2013 - United States" said
From June 2006 through March 2013, approximately 56 million doses of HPV4 were distributed in the United States... During June 2006-March 2013, the Vaccine Adverse Event Reporting System (VAERS) received a total of 21,194 adverse event reports occurring in females after receipt of HPV4; 92.1% were classified as nonserious. ... during the last 7 years, reporting patterns have remained consistent with the 2009 published summary of the first 2.5 years of postlicensure reporting to VAERS.i.e. there were 1674 serious reactions reported out of 56 million doses distributed. That's a reporting rate of serious reactions of .0029%, i.e. 3 in 100,000.
The lifetime risk of cervical cancer in the United States is about 1 in 152, or about 660 in 100,000.
So (if one trusts statistics from VAERS, which one should not do), the serious adverse reaction reporting rate from Gardasil is about 230 times lower than the lifetime risk of developing cervical cancer.
Looking at death: the reporting rate for death according to the 2009 summary was about 0.1 per 100,000. The lifetime risk of dying from cervical cancer in the United States is about 1 in 435, or about 230 in 100,000.
Again, the vaccine is safer, by a factor of 2300.
Previous surveys on hypothesized sexual activity changes after human papillomavirus (HPV) vaccination may be subject to self-response biases. To date, no studies measured clinical markers of sexual activity after HPV vaccination. This study evaluated sexual activity-related clinical outcomes after adolescent vaccination. ... Conclusions: HPV vaccination in the recommended ages was not associated with increased sexual activity-related outcome rates.See also
In May 2014, girls in Carmen de Bolivar in Columbia started fainting, and by September, the media was full of reports blaming the HPV vaccine. But the Minister of Health tweeted the results of a preliminary investigation which found
"... symptoms were also present in non-vaccinated girls"So it is likely that the Columbian girls were also suffering from conversion disorder. More news as it happens :-)
Both cases received quite a bit of media attention, and there was much speculation that the HPV vaccine might have been to blame. However, their autopsies showed that the British girl was killed by a pre-existing chest tumor, and the Milwaukee girl was killed by an overdose of benadryl. In neither case does the HPV vaccine appear to have been at fault.
The CDC says that as of March 2014, of the 96 reports of death received by VAERS, 47 reports had enough information to investigate, but none of them appeared to be caused by the vaccine. By contrast, the human papilloma virus kills about one person every 82 minutes in the United States. (You can read a few of their stories here.)
For more data, see HPV vaccine safety.
Fainting ("syncope") can occur especially during the first 15 minutes after any shot. You can hurt yourself if you fall when fainting; that's why everyone getting any shot should remain seated for 15 minutes afterwards.
Fainting can also be associated with seizures; a study of syncope and seizures after HPV vaccination found
"The reporting rate after 4vHPV vaccine for syncope and syncopal seizures was 7.8/100,000 and 2.6/100,000 doses distributed, respectively."
Seizures can also be triggered by the brief fever that sometimes follows immunization. According to "Childhood Febrile Seizures: Overview and Implications",
"Although the occurrence of febrile seizures in childhood is quite common, they can be extremely frightening, emotionally traumatic and anxiety provoking when witnessed by parents. During the seizure, the parent may perceive that their child is dying, but fortunately the vast majority of febrile seizures are benign."
Finally, there are seizures caused by genetic defects. A study of 23 children who developed epilepsy after vaccination identified underlying genetic causes in 65% of cases.
There are several problems with the papers by Little and Ward.
First: the authors have an axe to grind. They are pro-life activists; Dr. Little serves on the board of advisors of Family Life International, a Catholic group which claimed as in 2007 (and still claims today) that the vaccine promotes promiscuity and VD, which is not supported by the evidence. This should have been disclosed as a conflict of interest.
Second, the paper claims to have ruled out all causes other than Gardasil for the problem... but they didn't check (as far as I know) for the specific mutations estimated to account for 20%-25% of the risk for premature ovarian failure.
Third, premature ovarian failure happens in unvaccinated girls at a significant rate -- about one in ten thousand girls per year from age 15 up. If there are about 6 million 16 year old girls in the US, that paper predicts roughly 600 cases of premature ovarian failue per year among them -- with or without vaccination. So hearing about two or three girls with premature ovarian failure is not a sign of trouble; hearing about ten thousand might be.
The paper by Colafrancesco and Tomljenovic has similar problems; it lists a case of two sisters with premature ovarian failure. When two sisters both come down with a genetically linked disease, it's even more likely that a bad gene is the cause, but that was not mentioned in the paper.
So these case studies don't show that Gardasil is dangerous, they don't show that the four cases were not caused by a genetic problem, and they don't account for the fact that we don't know why the majority of cases of this problem occur with or without Gardasil.
( Thanks to Respectful Insolence for posting excerpts of the second paper. )
If you give newborn rats 0.1% of their body weight of one of the ingredients of Gardasil (see Newborn rats injected with polysorbate 80) there are problems, but that's about four hundred thousand times higher than the human dose by weight.
For problems common to all vaccines, you might want to test against a simpler placebo. One trial's placebo also omitted the aluminum adjuvant: "Safety and persistent immunogenicity of a quadrivalent human papillomavirus types 6, 11, 16, 18 L1 virus-like particle vaccine in preadolescents and adolescents: a randomized controlled trial." (alternate link) compared adverse events in Gardasil vs. a simpler placebo for 18 months after vaccination. (In all, 275 girls and 322 boys received the saline placebo.) It concluded "No serious vaccine-related adverse experiences were reported."
The clinical trial "Safety and immunogenicity of a 9-valent HPV vaccine in females 12-26 years of age who previously received the quadrivalent HPV vaccine." compared adverse events in Gardasil 9 vs. a saline placebo for 15 days post vaccination.
This rumor is a distortion of the studies required by the FDA before approving Gardasil.
Two big studies (Protocol 13, and Protocol 15) mostly looked at women who didn't have HPV before vaccinating, but they also looked at a few women who had active HPV infections at the start of the study (about 293 women in Protocol 13, and 828 women in Protocol 15).
Because the vaccine works by preventing HPV infection, the expectation was that vaccination wouldn't have any effect on cancer rates on these hpv-positive women. And that's exactly what they found in Protocol 15.
But in Protocol 13, it turned out that the HPV positive women were twice as likely to already have HSIL at the start of the test, before vaccination (6.5% vs. 3.7%). And not surprisingly, these women went on to have more cancer.
When you start with more precancer, you get more cancer, regardless of whether you later vaccinate.
(For data, see Tables 17, 18, and 20, and the conclusion on page 15, of the Phase 3 study summary.)
See also Does HPV vaccination increase cancer risk in carriers? at ask.metafilter.com
JapanAs of June 2012, Japan reported 75 serious reactions in 6,338,709 vaccinations with Cervarix, and 7 serious reactions in 530,826 vaccinations with Gardasil.. That's about 1 in 100,000.
In June 2013, reacting to a burst of reports of adverse effects in the media, Japan's health ministry announced that it would stop actively recommending it, pending investigation, but that the vaccine would continue to be administered free of charge. The investigation is now complete; "Summary of the Report on the Surveillance Results of HPV Vaccines" says "the available evidence was insufficient to suspend the marketing authorizations for the HPV vaccines." The Japan Society of Obstetrics and Gynecology demanded in August 2015 that the recommendation be resumed, and again in January 2017, but as of August 2017, it's still not being actively promoted.
According to "Effect on HPV vaccination in Japan resulting from news report of adverse events and suspension of governmental recommendation for HPV vaccination", vaccine initiation rates fell sharply as a result of the scare.
See also the excellent account at HPV Vaccination in Japan -- The Continuing Debate and Global Impacts (CSIS, April 2015; an update of The HPV Vaccination in Japan -- Issues and Options), as well as "HPV Vaccination Controversy in Japan, Rates Plummet to 1%" (July 2016) and "HPV vaccination programme in Japan" (Lancet, Aug 2013.)
The vaccine is still on the immunization calendar in Japan; see Vaccination Schedule Recommended by the Japan Pediatrics Society (October 2016), inoculation possible vaccine in Japan type (May 18, 2015) (japanese), Immunization Schedule, Japan 2014 (as of April 1, 2014), and Hachinohe City Routine Immunization Schedule (Nov 2013).
IsraelOn 3 September 2013, Israel considered cancelling their free school-based HPV vaccination program, but less than a week later, decided to go ahead with it. In September 2015, it was announced that boys will also receive the HPV vaccine in schools.
The HPV vaccine remains on the schedule of recommended vaccines.
IndiaOn 4 July 2008, India's DCGI approved Gardasil for use in India. In 2009, a demonstration project was started which immunized girls in two states. Antivaccination groups protested, and in 2010, responding to public pressure after seven deaths that turned out to be unrelated to the vaccine, India suspended the demonstration project.
The vaccine itself is still approved in India, and appears on the IAP's recommended schedule of vaccination for 2013 and 2014.
This story even came to the attention of Politifact in 2016.
FranceIn early 2014, antivaccine activists sent an open letter and petition charging that the vaccine was unsafe and ineffective, and Michele Rivasa (a MEP who thinks aluminum in vaccines is harmful) held a meeting on the topic. In response, 17 national societies of gynecologists, midwives, obstetricians, oncologists, and others released their own open letter and petition. There has been no change in the status of HPV vaccination in France; it still appears on the Calendrier des vaccinations 2014 dated 25 April 2014.
SpainThe HPV vaccine appears both on the Immunisation schedule of the Spanish Association of Paediatrics: 2015 Recommendations and official state vaccination calendars for 2015.
The information gives the impression that the vaccine is risky and experimental. The BFV tried in December 2013 to get the insurers to update their info, without results, so they have now lodged a complaint with the federal office for insurance.
I checked, and the information is indeed outdated, and furthermore was based on an incorrect translation of the old ECDC information.
"Duration of efficacy is key to the entire question. If duration is at least fifteen years, then vaccinating 11-year-old girls will protect them until they are 26 and will prevent some precancers, but postpone most cancers. If duration of efficacy is less than fifteen years, then no cancers are prevented, only postponed."She then wrote an article laying out her position in detail. (That article was written back when we thought 88% of all HPV-caused cancers were cervical cancer; according to the CDC, the current figure is 45%. Also, that article assumed that HPV vaccination only reduced abnormal pap smears by 10%, but a more current figure is 47.5%.)
More recently, she wrote
"US health policy preferences push achieving a high coverage rate of young women instead of relying on possible herd immunity from both sexes of a partially vaccinated population...and in April 2017, she wrote
A majority of adolescents appear to participate in long chain networks of relationships... Interruption by HPV vaccination may reduce this spanning network into smaller isolated groups, thereby preventing a majority of HPV infections... young men are responsible for infection propagation twice as often as young women. Perhaps... to see a more cost-effective reduction in HPV infections, we should turn our attention to targeting boys before high school entry."
"This series of vaccinations is highly likely to protect her from HPV infection until she enters the routine screening program... HPV vaccines reduce abnormal screening tests, colposcopies and excisions."On January 5th, 2013, I had the following email conversation with her:
In other words: she is a (very) cautious advocate for the vaccine, and has never said it should not be used.From: Dan Kegel To: Diane Harper Hi Dr. Harper, recently on TV you said "I looked at the fact that Gardasil doesn't last long enough to prevent cervical cancer..." ... I think you meant to say "We don't know yet whether Gardasil lasts long enough to prevent cervical cancer without a booster shot", right? From: Diane Harper To: Dan Kegel ... you are correct, I should be quoted as saying "We don't know yet whether Gardasil lasts long enough to prevent cervical cancer without a booster shot", So I do give you permission to print that in your blog!
Copyright 2013, 2014, 2015, 2016, 2017 Dan Kegel
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