Human papillomavirus (HPV) is a small double-stranded DNA virus that commonly infects humans on every continent–so common in fact that nearly every sexually active person will be infected with HPV at some point in their life. Most of the time, the infections cause no symptoms and go unnoticed, aka asymptomatic.

The virus has been around since ancient times, and since then has evolved into over 300 types of HPV.

Some HPV strains are associated with common skin warts, and others genital warts.

Over 90% of HPV infections are cleared by the immune system within 12-24 months post-infection.

HPV and Cancer

A very small fraction of HPV infections persist or progress under certain conditions (associated with reduced immune function, such as HIV-positive status or long term oral contraceptive use) and after several decades become cancer.

It’s interesting to me that it’s a more favorable option to give every single person a series of 3 shots capable of serious reactions, from syncope and tonic-clonic movements and other seizure activity to death, than actually targeting at risk groups and education on prevention via reduction in risk factors.

 “Infection is not sufficient by itself to cause cancer, on the basis of the observation that most infected women resolve their HPV infection and do not develop cervical cancer.” (source) 

According to the CDC, about 10% of women with HPV infection on their cervix are at risk for cervical cancer (however that doesn’t suggest 10% of women actually get cervical cancer).

Like many cancers, a dysfunctional immune response is often the reason why cancer forms from an exposure, when exposure alone is not sufficient to cause cancer.

 “The immune responses detected in healthy volunteers, possibly as a result of previous viral clearance are either absent or dysfunctional in patients with low grade CIN, high grade CIN, or cancer.” 

source:  Crosbie et al. (2013). Human papillomavirus and cervical cancer. The Lancet

Risk Factors For Cervical Cancer

The fraction of women who develop cervical cancer are more likely to have certain risk factors, such as:

• Immune system deficiency (HIV-positive, transplant recipients)
• Herpes, chlamydia, syphilis infection
• Long term oral contraceptive use
• Smoking
• Low socioeconomic status
• Not getting routine pap smears
• Exposure to DES in utero (diethylstilbestrol) Read about DES here.

Cervical Cancer Mortality Data

The rate of death from cervical cancer has dropped steadily since the 1940s, when George Nicholas Papanicolaou created the Papanicolaou test, commonly known as the Pap smear, which revolutionized the early detection of cervical cancer. 

Countries with high screening rates have effectively and safely reduced the incidence and mortality of cervical cancer.

Japan, for example, has a much lower screening rate than other comparable income nations. While Japan’s screening rate rose from 37.7% in 2010 to 43.7% in 2019 among women aged 20-69 years, it is still low compared to other countries such as the United States (72.6%), UK (74.4%), and Korea (51.9%). 

Low screening rates affect the incidence and mortality of cervical cancer, because it allows pre-cancers to transition into cancers without detection and intervention.

In the United States, the current mortality rate of cervical cancer is 2.2 per 100,000 women.

Cervical cancer makes up 0.7% of all cancer deaths.

 Prevention 

HPV is spread through direct contact with an infected wart, or through sexual encounters, such as vaginal, oral and anal sex. The best way to prevent an STD is to not have sex. The second best way is to have sex with the same partner (and verify neither of you have an STD).

 Avoid Oral Contraceptives 

Women who have used oral contraceptives for 5 or more years have a higher risk of cervical cancer than women who have never used oral contraceptives. The longer a woman uses oral contraceptives, the greater the increase in her risk of cervical cancer. A 2003 Lancet study found a 10% increased risk for less than 5 years of use, a 60% increased risk with 5–9 years of use, and a doubling of the risk with 10 or more years of use.

There is some evidence that stopping oral contraceptives will reduce the elevated risk associated with long term oral contraceptive use.

 Micronutrients 

Micronutrients (e.g. carotenoids, vitamin C and folate) are thought to have a protective effect to cervical cancer by promoting the regression of low grade squamous intra-epithelial lesion (SIL). Some components of fruits and vegetables have been suggested to be protective too.

For example, in a 2003 study by Hernandez, et al, authors found:

 Riboflavin and thiamin from food sources, vitamin B12supplements, and total (food and supplements) folate displayed inverse, dose-responsive associations with high-grade SIL (HSIL). Riboflavin from food sources and total folate also demonstrated inverse, dose-responsive associations with low-grade SIL (LSIL). The odds ratios for LSIL and HSIL were reduced by 50–90% for the highest compared to the lowest levels of intake of these nutrients. 

Authors concluded:

 “This investigation provides evidence that thiamin, riboflavin, folate, and vitamin B12 may play a protective role in cervical carcinogenesis.” 

The 2010 observational study Dietary factors and in situ and invasive cervical cancer risk in the European prospective investigation into cancer and nutrition study investigated whether “some dietary factors could be involved as cofactors in cervical carcinogenesis.” The authors tracked 299,649 women for 9 years and found:

 “We observed a statistically significant inverse association of ISC [invasive squamous cervical cancer] with a daily increase in intake of 100 g of total fruits (HR 0.83; 95% CI 0.72–0.98).”  

A 2010 study looked at compounds in green tea and its effects on cancer cells in vitro. The authors of Green Tea Compound in Chemoprevention of Cervical Cancer demonstrated:

 “the ability of two green tea polyphenols (EGCG and polyphenol E) to inhibit the proliferation of HPV-immortalized and HPV-positive cancer cells, through cell cycle arrest at the G0/G1 phase.”  

More recently, the 2020 study The Preventive Effect of Dietary Antioxidants on Cervical Cancer Development reviewed relevant research and found:

 “The intake of vitamins A and D and carotenoids may inhibit early cervical cancer development. The intake of folate may prevent or inhibit HPV infection rom progressing to various grades of CIN. The intake of vitamins C and E may widely inhibit the process of cervical cancer development. Polyphenols are often used in cases of cervical cancer in combination chemotherapy and radiation therapy. Regarding nutrients, different antioxidants may have differing abilities to intervene in the natural history of cervical diseases associated with HPV infection. Regarding foods, the intake of both vegetables and fruits containing multiple vitamins may widely suppress cervical cancer development.” 

It’s clear across all cancers that having a healthy diet filled with whole foods including a variety of fruits and vegetables is protective against cancer.

 Condoms 

Condom use has been shown to reduce the risk for HPV infection and HPV-associated diseases (ie. genital warts and cervical cancer.)

The 2003 study “Condom Use and Human Papillomavirus in Men” found:

 In the highest HPV exposure risk category (ie, men with no steady sex partners), those who reported always using condoms in the 6 months before study entry were about 50% less likely to become newly infected with any HPV types in the 12-month follow-up period, compared with men who never used condoms (adjusted hazard ratio [HR], 0.54; 95% confidence interval [CI], .31–.95).  

However, it’s important to understand that condoms do not cover every place HPV could be, for example, the testicles, or a wart that may be on the outside of the vaginal area or penis.

 Vaccination 

Vaccination is intended to prevent infection with specific strains of HPV which have been associated with some cervical cancers. The vaccines indirectly and theoretically would prevent the “infection” that takes 20 or longer years to turn into cancer.

Gardasil 9 targets HPV types 6, 11, 16, 18, 31, 33, 45, 52, and 58.

The vaccine is recommended for:

• Females and males ages 11 or 12 years (can start at age 9 years)
• Persons ages 13 through 26 years who have not been adequately vaccinated when younger

According to the CDC:

 The 9-valent HPV vaccine protects against HPV types 16 and 18, which cause about 66% of cervical cancers and most other HPV-attributable cancers in the United States, and five additional cancer-causing types, which account for about 15% of cervical cancers. It also protects against HPV 6 and 11, which cause most anogenital warts. 

However, there is some uncertainty about the effectiveness of the HPV vaccines in preventing cancer because the first vaccine was introduced in 2006, thus the oldest women vaccinated with HPV are still quite young and have not aged into the peak cancer age. For example, if a 12 year old was vaccinated in 2006, they would be 29 years of age today. While researchers and physicians will pitch that the vaccines “prevent cancer” there is little actual data to support the statement.

For example, this 2021 study which claims “We observed a substantial reduction in cervical cancer and incidence of CIN3 in young women after the introduction of the HPV immunisation programme in England, especially in individuals who were offered the vaccine at age 12–13 years” still only examined person years of women ages 20 years to younger than 30 years and used surrogate end points like CIN 3 to estimate risk reductions. Cervical cancers have been going down since the 1940s so for us to determined whether a reduction in CIN 3 is due to routine screenings, other lifestyle changes, increased awareness, or vaccination, needs to be properly teased out, as well as true observation of cervical cancer. HPV vaccination was introduced in 2008 in the UK, so the women were still younger than when cervical cancers are typically diagnosed. In other words, these women may go on to develop cancer or they may not if they exhibit more health seeking behavior than the woman who typically is diagnosed with cervical cancer.

See Does the Vaccine Prevent Cervical Cancer? below.

Currently in the United States there is one licensed HPV vaccine: Gardasil 9.

Definition of Cervical Cancer

Pap smears look for what is called cervical dysplasia, a precancerous condition in which abnormal cells grow on the surface of your cervix. Another name for cervical dysplasia is cervical intraepithelial neoplasia, or CIN. 

Cervical intraepithelial neoplasia (CIN) is classified on a scale from one to three.

• CIN 1: Refers to abnormal cells affecting about one-third of the thickness of the epithelium.
• CIN 2: Refers to abnormal cells affecting about one-third to two-thirds of the epithelium.
• CIN 3: Refers to abnormal cells affecting more than two-thirds of the epithelium.

CIN 1 cervical dysplasia rarely becomes cancer and often goes away on its own.

CIN 2 and 3 are more likely to require treatment to prevent cancer.

Invasive cervical cancer is cancer that has spread from the surface of the cervix to tissue deeper in the cervix or to other parts of the body.

Not every abnormal pap smear is indicative of cancer. Many women can have an abnormal pap and it’s not because of HPV or cancer. During pregnancy, hormones can cause a woman to have an abnormal pap, which return to normal after the pregnancy.

How HPV Was Associated With Cancer

In the 1970s, President Nixon declared a war on cancer, and federal funding ($100 million) was allocated to cancer research. There were many scientists who jumped into the water on cancer and viruses and one of them was Harald zur Hausen. While Researchers Ian Frazer and Jian Zhou at the University of Queensland have been accorded priority under U.S. patent law for the invention of the HPV vaccine’s basis, the VLPs, it was Zur Hausen who identified the strains of HPV thought to be responsible for cervical cancer. Zur Hausen won a Nobel Prize for his part, but he also has patents. 

In 1983, in a scientific paper written by Durst, Zur Hausen et al., (prior to this Hausen was unsuccessful in his attempts to tie herpes simplex virus to cervical cancer) papillomavirus DNA was detected in a cervical carcinoma and they named the unidentified virus HPV 16.

The researchers examined cervical cancer samples to determine the presence of this DNA, and in a German sample of 18 patients, 61% were positive HPV 16. Then they looked at 23 cancer biopsy samples from Kenya and Brazil, and only 34% contained this DNA. Vulval and penile cancer samples were positive for type 16 DNA  28% and 25%, respectively. They concluded that type 16 is associated with certain malignancies but also:

“It is a common feature of malignant conversion after papillomavirus infection that it appears to require additional interaction with initiating events.”

Later in this paper authors write:

“The regular presence of HPV DNA in genital cancer biopsy samples does not per se prove an etiological involvement of these virus infections, although the apparent cancer specificity of HPV 16 is suggestive of such a role. Their biological significance as well as the proposed interaction with initiating events (2) certainly requires further investigation.”

A year later, Zur Hausen and his team identified another new HPV strain: they named it type 18. Then they looked back at their earlier samples of cervical cancer and found that 25% (9 out of 36 biopsies) from African and Brazilian patients, and 15% (2 out of 13) of cervical cancer biopsies from German patients.

In 1987 Hausen headed another research paper, this one titled “Human papilomavirus infections in women with and without abnormal cervical cytology.” The study looked at 9,295 pap smears and looked for these HPV DNAs in normal and abnormal pap smears, in the various CIN stages, as well as advanced cervical cancer.

Overall, 94% of female patients had normal smears.

Of the 8,755 women with normal smears: 9% were positive for HPV DNA (highest in the age group 15-50 (10-13%).

Of all smears:

• 2% (162) showed signs of mild of moderate dysplasia (cervical intraepithelial neoplasia CIN 1 or II)
• 1% (120) had carcinoma in situ (CIN III)
• 1% (62) had an invasive carcinoma. Most invasive cancer smears came from patients aged 55-80 years.

When CIN and invasive carcinoma patients were combined: 35-40% were HPV positive.

Authors write:

We detected HPV DNA in only 40% of smears from invasive cancer patients. An obvious explanation for this discrepancy [alluding to Southern Blots producing different results] is that the method we used was less sensitive than Southern blot hybridisation.”

Authors still seemed inconclusive and looking for other co-factors:

“Only about 30% of women who were positive at the first examination remained positive in subsequent examinations in our study. Similarly, some patients who were negative at the first test became positive later. The most likely explanation for these conversions is fluctuations in virus production because the changes have also been noted with highly sensitive detection procedures (Gissniann L, Schneider A, unpublished). The factors discussed here suggest that our results probably underestimate the real rate of HPV infection by a factor of 2 to 3. However, careful validation studies with different methods of HPV analysis are needed to substantiate this possibility. The high prevalence of HPV again indicates that a papillomavirus infection is not the sole factor responsible for the transformation of normal cervical tissue to a malignant tumour. Other factors, perhaps those that interact with control mechanisms within the infected cell, may be required.”

A 1995 paper “Prevalence of Human Papillomavirus in Cervical Cancer: A Worldwide Perspective” sought to determine whether the association between HPV infection and cervical cancer is consistent worldwide and to investigate geographic variation in the distribution of HPV types.

More than 1000 specimens of invasive cervical cancer from 32 hospitals in 22 countries were screened for more than 25 types of HPV, and they found:

• HPV DNA detected in 93% of tumors
• HPV 16 present in 50% of specimens
• HPV 18 present in 14%
• HPV 45 present in 8%
• HPV 31 present in 5%

Their conclusions were that “most HPVs are associated with cancer, at least occasionally.”

Adverse Reactions

The safety of GARDASIL 9 was evaluated in seven clinical studies that included 15,703 individuals who received at least one dose of GARDASIL 9 and had safety follow-up.

Adverse reactions were solicited for 5 days after each injection of Gardasil 9. To read more about the Injection-Site and Systemic Adverse Reactions that occurred within 5 days of each vaccine dose, please refer to the FDA’s package insert.

Postmarketing Experience

Gardasil & Gardasil 9

• Gastrointestinal disorders: Vomiting
• Skin and subcutaneous tissue disorders: Urticaria
• Blood and lymphatic system disorders: Autoimmune hemolytic anemia, idiopathic thrombocytopenic purpura, lymphadenopathy.
• Respiratory, thoracic and mediastinal disorders: Pulmonary embolus.
• Gastrointestinal disorders: Pancreatitis.
• General disorders and administration site conditions: Asthenia, chills, death, malaise.
• Immune system disorders: Autoimmune diseases, hypersensitivity reactions including anaphylactic/anaphylactoid reactions, bronchospasm.
• Musculoskeletal and connective tissue disorders: Arthralgia, myalgia.
• Nervous system disorders: Acute disseminated encephalomyelitis, Guillain-Barré syndrome, motor neuron disease, paralysis, seizures, transverse myelitis.
• Infections and infestations: Cellulitis.
• Vascular disorders: Deep venous thrombosis

Autoimmune Disease and Gardasil

From the insert:

 “In all of the clinical trials with GARDASIL 9 subjects were evaluated for new medical conditions potentially indicative of a systemic autoimmune disorder. In total, 2.2% (351/15,703) of GARDASIL 9 recipients and 3.3% (240/7,378) of GARDASIL recipients reported new medical conditions potentially indicative of systemic autoimmune disorders, which were similar to rates reported following GARDASIL, AAHS control, or saline placebo in historical clinical trials.” 

However, it is extremely disingenuous to say this last part as the saline placebo group was combined with the AAHS control group, thus making it impossible to know the rate of autoimmune conditions with a true saline placebo.

This combining of two control groups, one who received an active ingredient, masks the adverse effects of the vaccine. Merck knew this and this will be argued in court, as countless women and men have suffered from lifelong chronic autoimmune diseases as a results of this vaccine and its aluminum adjuvant.

HPV Vaccine and Early Menopause

Case reports are often the first line of evidence and observational data. After the HPV vaccines were introduced there have been documented cases where young girls go into premature ovarian failure.

This 2014 case series documents premature ovarian insufficiency of three girls following HPV vaccination.

A 2022 paper found that the mean number of reported POF (premature ovarian failure) events significantly increased after the first HPV vaccine launch in 2006 with 22.2 POF cases/year up from 1.4 POF cases/year before the launch. PRR was 46.1 (95% confidence interval: 31.7–67.2) and sensitivity analyses yielded similar estimates.

Our study suggests the presence of a potential safety signal of POF associated with HPV vaccination, which may only be partly attributed to notoriety bias. Due to the well-known limitations of spontaneous reporting data, further investigations are warranted.

HPV Vaccine During Pregnancy

According to its package insert:

 “there are no adequate and well-controlled studies of GARDASIL 9 in pregnant women. Available human data do not demonstrate vaccine-associated increase in risk of major birth defects and miscarriages when GARDASIL 9 is administered during pregnancy.”  

NONCLINICAL TOXICOLOGY 13.1

Carcinogenesis, Mutagenesis, Impairment of Fertility

“GARDASIL 9 has not been evaluated for the potential to cause carcinogenicity, genotoxicity or impairment of male fertility. GARDASIL 9 administered to female rats had no effects on fertility.”

Does The Vaccine Prevent Cervical Cancer?

A 2020 New England Journal of Medicine study HPV Vaccination and the Risk of Invasive Cervical Cancer  investigated whether HPV vaccination is associated with a reduced risk of invasive cervical cancer. They looked at over 1 million girls ages 10-30. Unsurprisingly, the youngest girls had the highest rates of vaccine uptake, whereas the oldest girls in the study had the lowest, as the vaccine was not introduced until 2006. Because more of the young girls who were vaccinated more often had lower rates of cervical cancer which is also expected as cervical cancer typically doesn’t show up until later in life, the study concluded:

 “Among Swedish girls and women 10 to 30 years old, quadrivalent HPV vaccination was associated with a substantially reduced risk of invasive cervical cancer at the population level.” 

Cancers of the cervix are most frequently diagnosed between the ages of 35 and 44 with an average age of diagnosis being 50 years. How do they know in a study that looks at women ages 10-30 years, that they won’t go on to develop cancer later? 

In this study, it’s easy to see that more of the highest vaccinated group in the study was born after 2000, and with followup until 2017, they are at most 17, whereas all of the group born prior to 1984 are unvaccinated and over 33 years of age.

Looking at the graph below, it’s easy to see that being diagnosed with invasive cervical cancer is still technically a rare thing. Most birth cohorts around 0.02% to as high as 0.09% of women are diagnosed. The 1975-79 cohort, 0.02% were diagnosed (all unvaccinated), whereas the next cohort, 0.06% of unvaccinated women and 0.07% of vaccinated women were diagnosed (which translates to a 27% increased risk for that cohort). The following cohort is, 0.09% of unvaccinated women and 0.02% of vaccinated women. These are statistically small numbers.

But still, the vaccinated birth cohort 1980-1984 had an incidence rate of 15.96 per 100,000 person years, compared to 9.35 for unvaccinated women.

Importantly, are they “adjusting”for sexual history, other STDS, oral contraceptive use, number of sexual partners? I don’t see where or if they are. 

Overall, it looks like there are other factors at play here…aka confounding variables, influencing these subtle shifts in diagnoses, which could be anything from healthy vaccinee effect, increased access to pap test screenings, smoking, long term oral contraception use, having a weakened immune system, chlamydia infection, other sexually transmitted diseases, multiple sex partners, etc.

It’s important we are capturing total cervical cancer in a given study, which we aren’t because we have to wait for these younger, “vaccinated” cohorts to age. We simply cannot predict the future, they can be just like that 1980 birth cohort and have a HIGHER rate of cervical cancer for all we know.

1. Was amorphous aluminium hydroxyphosphate sulfate adequately evaluated before authorisation in Europe?

“The EMA reports that AAHS was introduced without any prelicensure safety evaluation. The adjuvant is described by the company to be both physically and functionally distinct from all other previously used aluminium adjuvants. There is a need for rigorous evaluation of benefits and harms of the adjuvant AAHS.”

2. Human Papillomavirus Vaccination and Premature Ovarian Failure: A Disproportionality Analysis Using the Vaccine Adverse Event Reporting System

“Our study suggests the presence of a potential safety signal of POF associated with HPV vaccination, which may only be partly attributed to notoriety bias. Due to the well-known limitations of spontaneous reporting data, further investigations are warranted.”

3. Human papilloma virus vaccine and primary ovarian failure: another facet of the autoimmune/inflammatory syndrome induced by adjuvants

We documented here the evidence of the potential of the HPV vaccine to trigger a life-disabling autoimmune condition. The increasing number of similar reports of post HPV vaccine-linked autoimmunity and the uncertainty of long-term clinical benefits of HPV vaccination are a matter of public health that warrants further rigorous inquiry.

4. Detection of human papillomavirus (HPV) L1 gene DNA possibly bound to particulate aluminum adjuvant in the HPV vaccine Gardasil

“The results showed that all 16 Gardasil samples, each with a different lot number, contained fragments of HPV-11 DNA, or HPV-18 DNA, or a DNA fragment mixture from both genotypes. The detected HPV DNA was found to be firmly bound to the insoluble, proteinase-resistant fraction, presumably of amorphous aluminum hydroxyphosphate sulfate (AAHS) nanoparticles used as adjuvant. The clinical significance of these residual HPV DNA fragments bound to a particulate mineral-based adjuvant is uncertain after intramuscular injection, and requires further investigation for vaccination safety.”

5. A case-control study of quadrivalent human papillomavirus vaccine-associated autoimmune adverse events

“It was observed that cases with the SAAE outcomes of gastroenteritis (odds ratio (OR) = 4.6, 95% confidence interval (CI) = 1.3-18.5), arthritis (OR = 2.5, 95% CI = 1.4-4.3), systemic lupus erythematosus (OR = 5.3, 95% CI = 1.5-20.5), vasculitis (OR = 4, 95% CI = 1.01-16.4), alopecia (OR = 8.3, 95% CI = 4.5-15.9), or CNS conditions (OR = 1.8, 95% CI = 1.04-2.9) were significantly more likely than controls to have received HPV4 vaccine (median onset of SAAE symptoms from 6 to 55 days post-HPV4 vaccination).”

6. Systemic lupus erythematosus following human papillomavirus vaccination: A case-based review

“In this article, we provide a report of a case of SLE onset following HPV vaccination and a review of 11 similar cases. An analysis of 12 patients revealed that 7 cases of SLE developed between 3 weeks and 2 months post-vaccination.” 

7. Adolescent Premature Ovarian Insufficiency Following Human Papillomavirus Vaccination: A Case Series Seen in General Practice

Three young women who developed premature ovarian insufficiency following quadrivalent human papillomavirus (HPV) vaccination presented to a general practitioner in rural New South Wales, Australia. The unrelated girls were aged 16, 16, and 18 years at diagnosis. Each had received HPV vaccinations prior to the onset of ovarian decline. Vaccinations had been administered in different regions of the state of New South Wales and the 3 girls lived in different towns in that state. Each had been prescribed the oral contraceptive pill to treat menstrual cycle abnormalities prior to investigation and diagnosis. 

Since this group includes all prepubertal and pubertal young women, demonstration of ongoing, uncompromised safety for the ovary is urgently required. This matter needs to be resolved for the purposes of population health and public vaccine confidence.

8. The safety of human papilloma virus-blockers and the risk of triggering autoimmune diseases

The current HPVv are both effective and generally safe. However, it should be noted that autoimmune side effects have been reported in several studies. Further research should be done to understand the relationship between HPVv and autoimmunity.

9. Resolution of Harada disease-like uveitis after quadrivalent human papillomavirus vaccination: a case report

“This article describes a patient who developed Harada disease-like uveitis after quadrivalent human papillomavirus (HPV4) vaccination and experienced resolution without any systemic treatment.”

10. Case Report: Posterior Uveitis after Divalent Human Papillomavirus Vaccination in an Asian Female

“Although this case resembled Harada disease, we diagnosed it as vaccine-induced uveitis rather than coincidental autoimmune disease based on the rapid response to a short course of systemic corticosteroids. Because vaccine-induced uveitis is rare and difficult to distinguish from coincidental autoimmune disease, our case reminds eye care providers to be aware of the possible association between vaccination and a Harada-like reaction.”

11. Signal detection of human papillomavirus vaccines using the Korea Adverse Events Reporting System database, between 2005 and 2016

In this study, we found a total 97 signals of AE after HPV vaccination. Of these, 78 AEs were already present on the HPV vaccine labels of South Korea and the following 19 AEs were not listed: neuralgia, tremor, neuritis, depersonalization, axillary pain, personality disorder, increased salivation, peptic ulcer, circulatory failure, hypotension, peripheral ischemia, cerebral hemorrhage, micturition disorder, facial edema, ovarian cyst, weight increase, pain anxiety, oral edema, and back pain. 

12. Case report: Anti-GAD65 antibody-associated autoimmune encephalitis following HPV vaccination

Herein, we describe a 39-year-old woman who developed seizures and experienced a rapid decline in memory shortly after her first dose of the HPV vaccine. Cranial magnetic resonance imaging and cerebrospinal fluid analysis were performed, and the patient was diagnosed with anti-glutamic acid decarboxylase 65 (anti-GAD65) antibody-associated autoimmune encephalitis.