Some regions have higher rates of HPV infections. In one province in South Africa, 74.6% of women have HPV.
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.
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.
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.)
A trial of Cervarix in 437 women shows that vaccine still works after 9.4 years. (More details about the study as of 8.4 years.)
So far, none of the studies has found when the vaccines really wear off, but long-term studies are continuing, and eventually we may know how long it lasts.
Booster shots are not currently recommended, but if it turns out that protection wears off after ten years, that may change. There is some evidence Gardasil works as a booster after 5 years and after 8.5 years.
"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.
"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.
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.
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.
Both the US and Australia have done studies to measure what percent of girls and women have HPV before and after the vaccine was introduced.
The United States has recommended vaccinating girls since 2006. A study of the National Health and Nutrition Examination Surveys from 2003 to 2010 said
Results: Among females aged 14-19 years, the vaccine-type HPV prevalence (HPV-6, -11, -16, or -18) decreased from 11.5% (95% confidence interval [CI], 9.2-14.4) in 2003-2006 to 5.1% (95% CI, 3.8-6.6) in 2007-2010, a decline of 56% (95% CI, 38-69). Among other age groups, the prevalence did not differ significantly between the 2 time periods (P> .05). The vaccine effectiveness of at least 1 dose was 82% (95% CI, 53-93).
Conclusions: Within 4 years of vaccine introduction, the vaccine-type HPV prevalence decreased among females aged 14-19 years despite low vaccine uptake. The estimated vaccine effectiveness was high.
Australia has been actively vaccinating girls since 2007. "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).
In Denmark, about 80% of girls born since 1993 have been vaccinated. A study of all girls born in Denmark from 1989 to 1999 found
The relative risk of GWs among girls who had received at least 1 dose of vaccine compared with unvaccinated girls was 0.12, 0.22, 0.25, and 0.62 for those born in 1995-1996, 1993-1994, 1991-1992, and 1989-1990, respectively (P for trend <.0001). No GWs occurred among vaccinated girls in the youngest birth cohort (1997-1999).
Conclusions: The strong, highly significant reduction in the occurrence of GWs among vaccinated girls indicates an early and marked population effect of the national HPV vaccination program and may forecast a similar effect on cervical precancerous lesions.
For more data, see HPV and Warts.
We already knew from clinical trials of Cervarix and of Gardasil that HPV vaccines, when given before exposure to HPV, are 85%-100% effective against CIN3 caused by HPV16 and HPV18. Now, three studies have measured how effective they are in real world national immunization programs:
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.
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"
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).
It has completed stage 3 clinical trials, and Merck has applied for FDA approval. It was discussed at the February 2014 meeting of the CDC's ACIP (see slides). The FDA might vote in early 2015 on whether to approve it. After that, it will take the ACIP a few months to issue recommendations, and up to two years for health plans to cover it.
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 is near approval.
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.
According to "Human papillomavirus type distribution in invasive cervical cancer and high-grade cervical lesions: A meta-analysis update",
Combined HPV16/18 prevalence among ICC cases was slightly higher in Europe, North America and Australia (74-77%) than in Africa, Asia and South/Central America (65-70%). The next most common HPV types were the same in each continent, namely HPV31, 33, 35, 45, 52 and 58...By that estimate, the current vaccine should prevent about 75% of cervical cancer in North America, and about 67% of cervical cancer in South America.
Not coincidentally, the upcoming nonavalent (nine-strain) HPV vaccine adds protection for types 31, 33, 45, 52, 58, and will prevent the strains that cause about 90% of cervical cancer worldwide.
"Human papillomavirus genotypes in high-grade cervical lesions in the United States" found
"Among 4,121 CIN2+ cases reported during 2008-2009 in 18- to 39-year-old women ... Compared to non-Hispanic whites, HPV 35 and 58 were significantly more common in non-Hispanic blacks (14.5% vs 4.2%; 12.3% vs 3.4%) ... For CIN3, HPV 16 or 18 was present in 71.4% of specimens from non-Hispanic whites compared with 50.4% in non-Hispanic blacks and 54.6% in Hispanics...
However, even if true, these results do not necessarily imply differential effectiveness of vaccine for the prevention of cervical cancer. Among oncogenic HPV types, vaccine type 16 has a higher potential to persist and cause cancer than most other types [25-27], and although not a direct measure of risk, data from the Guan et al study  corroborate the relative importance of HPV 16 and 18 for causing cervical cancer, even in regions where lower proportions of these types were found in high-grade lesions... "
A recent study by C Hoya et al claimed an even larger racial disparity for CIN2 lesions, but its results were based on a small sample size, only just barely reached statistical significance, and as the authors themselves said, may have been due to chance.
See also the CDC's page on cancer health disparities.
"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.
Long story: As of September 2011, about 40 million doses of Gardasil had been distributed in the US, and there were 71 reports of death; only 34 of these could be confirmed at all, only 23 of these reports look reputable and have no obvious cause, and there is no discernable pattern in the causes of death.
For more data, see HPV vaccine safety.
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."Human Papillomavirus Vaccine Increases High-Risk Sexual Behaviors: A Myth or Valid Concern" also found no evidence of sexual practices differing between vaccinated and non-vaccinated college women.
There are several problems with the paper 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 in the paper.
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. )
Long story: Newborn rats injected with the equivalent of the amount of Polysorbate 80 in about 60 doses of Gardasil were found to grow up to be sterile in one experiment in 1993.
Because this was such a high dose, given so early in life when the rats were still developing, it's very hard to say this means Gardasil is risky. Further studies would be needed to establish the level of risk with certainty.
This might need to be rexamined especially if the vaccine is considered for administering to younger children.
Long story: The Phase III trials of Gardasil enrolled thousands of healthy women, checked whether they had HPV at the start, vaccinated them, and then looked at how many of them went on to develop disease. There were two big studies: Study 13, and Study 15. Mostly they analyzed the data from women who didn't have HPV before vaccinating, but they also analyzed the data from women who very definitely had active HPV at the start of the study (about 293 women in Study 13, and 828 women in Study 15).
Because the vaccine works by preventing HPV infection, the expectation was that vaccination wouldn't have any effect on cancer rates.
Here are the results:
|HPV+ Women who developed CIN 2/3 or worse by end of study / total women|
|HPV+ at start of Study 13||31/156||19/137|
|HPV+ at start of Study 15||42/398||48/430|
When they looked closer at the data, they saw that the women who were HPV+ at start of Study 13 weren't randomized very well:
|Study 013 subgroup||Gardasil||Placebo|
|Current smoker at start of study||34.6%||31.4%|
|History of cervicovaginal infection or STD at start of study||35.9%||32.1%|
|Pap test with HSIL at start of study||6.5%||3.7%|
(See Tables 17, 18, and 20, and the conclusion on page 15, of the Phase 3 study summary.)
JapanIn June 2013, reacting to reports of adverse effects, Japan's health ministry announced that it would stop actively recommending it, pending investigation, but that the vaccine would continue to 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 Japanese government is now considering whether to resume active recommendation for HPV vaccination.
The vaccine is still recommended in Japan; see Hachinohe City Routine Immunization Schedule (Nov 2013), Vaccination Schedule Recommended by the Japan Pediatrics Society (Jan 2014), and Immunization Schedule, Japan 2014 (as of April 1, 2014)
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 The HPV Vaccination in Japan -- Issues and Options (CSIS, April 2014) as well as HPV vaccination programme in Japan (Lancet, Aug 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. Also, it 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. However, the vaccine itself is still approved in India, and appears on the IAP's 2013 recommended schedule of vaccination.
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.
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...On January 5th, 2013, I had the following email conversation with her:
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."
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 Dan Kegel
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