Chapter 5: Human Papillomavirus

For Public Health

Key points

This chapter provides general guidance for vaccine-preventable disease surveillance, describing the disease background/epidemiology, case investigation and reporting/notification, disease case definitions, and activities for enhancing surveillance, case investigation, and outbreak control for human papillomavirus.

HPV, illustration

Background

Authors: Ruth Stefanos, MD, MPH; Julia W. Gargano, PhD; Rayleen M. Lewis, PhD; Virginia Senkomago, PhD, MPH; Troy D. Querec, PhD; Elizabeth R. Unger, MD, PhD; Lauri E. Markowitz, MD

Genital human papillomavirus (HPV) is the most common sexually transmitted infection in the United States.12 An estimated 13 million persons are newly infected every year, and the annual direct medical costs of HPV are estimated to be $9.01 billion.3 Although the vast majority of HPV infections cause no symptoms and are self-limited, persistent HPV infection can cause cervical cancer in women as well as other anogenital cancers, oropharyngeal cancer, and anogenital warts in men and women.4

HPV is epitheliotropic, i.e., infection is restricted to epithelial tissues. More than 200 HPV types have been identified, including approximately 40 that preferentially infect the genital mucosa.567 HPV types that infect the genital mucosa are categorized according to their epidemiologic association with cancer.6 According to the International Agency for Research on Cancer (IARC), twelve HPV types (16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, and 59) have sufficient evidence of carcinogenicity in humans based on their association with cervical cancer (classified as high-risk types), and several types are classified as probably or possibly carcinogenic.6 High-risk types can cause low-grade cervical cell abnormalities and high-grade cervical cell abnormalities that are precursors to cancer, and cancers.689 Nearly all cervical cancers are attributable to high-risk HPV types,10 and approximately 70% of cervical cancer cases worldwide are caused by types 16 and 18.11 HPV 16 infection is also responsible for most cases of other HPV-attributable anogenital cancers, such as cancers of the vulva, vagina, penis, and anus, as well as cancers arising in some oropharynx sub-sites.6 Non-high-risk HPV types, including types 6 and 11, can cause genital warts, benign or low-grade cervical cell changes, and recurrent respiratory papillomatosis (RRP).12

Among the cancer outcomes of HPV infection, invasive cervical cancer has been considered the most important worldwide, with an estimated 662,301 new cases and over 300,000 attributable deaths in 2022.13 Though the vast majority of women with high-risk HPV infection do not develop cancer, persistent infection with a high-risk HPV type is widely recognized as the primary causative factor (necessary but not sufficient) for development of cervical cancer.141516

Disease description

Most HPV infections are transient and asymptomatic. More than 90% of new HPV infections, including those caused by high-risk HPV types, become undetectable within 2 years; HPV usually becomes undetectable in the first 6 months after infection.14151718 Based on recent studies, a consensus has emerged that loss of detection of HPV could be due to viral latency or low viral load infection that is below the detection threshold of the assay used, rather than true clearance of infection as previously thought.192021 Persistent infection with high-risk HPV is the most important risk factor for HPV-attributable diseases including precancers and invasive cervical cancer.141516

Many aspects of the natural history of HPV are poorly understood, including the role and duration of naturally acquired immunity after HPV infection. The risk for persistence and progression to precancer varies by HPV type as well as host factors. HPV 16 is more likely to persist and progress to cancer than other high-risk HPV types.2223 The usual time between initial HPV infection and development of cervical cancer is decades, but more rapid progression can occur. The median age at diagnosis for cervical cancer in the United States is 50 years.24

Introduction and increased use of Papanicolaou (Pap) screening and treatment of precancers before they progress to cancer during the past decades reduced the incidence of and mortality from cervical cancers before introduction of HPV vaccination.2526 The incidence of cervical cancer had decreased from 13.9 cases/100,000 in 1975 to 6.4 cases/100,000 in 2007 and mortality rates decreased from 5.6 deaths/100,000 to 2.4 deaths/100,000 over that same period.27

Based on the most recent estimates during 2018–2022, an estimated 11,100 new cervical cancer cases per year were attributable to HPV in the United States.28 This number does not include incidence of cervical precancers, for which surveillance data are not collected nationally. However, abnormal lesions and precancers related to HPV are common, with estimates of nearly 200,000 women diagnosed per year.29 In addition to the burden of cervical precancers and treatment costs, treatment for cervical precancers may have adverse effects on pregnancy outcomes.3031

In the United States, prior to vaccine implementation HPV was detected in about 90% of cervical cancer samples collected from several cancer registries.32 From the same study, HPV was also detected in varying proportions of HPV-associated cancers occurring at non-cervical sites. Using data from that study, the numbers of HPV-attributable cancers have been estimated. During 2018–2022, it was estimated that 39,300 cancers per year were attributable to HPV (Table A1).28 Among non-cervical site cancers, the largest proportion attributable to HPV were anal cancers (91%), followed by vaginal cancers (75%), oropharyngeal cancers (70%), vulvar cancers (69%), and penile cancers (63%).32 Among HPV-attributable cancers, oropharyngeal squamous cell carcinomas (SCC) were the most common; from 2018–2022, there were an estimated 13,600 among males and 2,400 among females annually.28 During 2018-2022, rates of HPV-associated oropharyngeal SCC were higher among males (9.2 cases/100,000) than females (1.7 cases/100,000). Rates of anorectal SCC were higher among females (2.7 cases/100,000) than males (1.4 cases/100,000).33

Anogenital warts typically develop approximately 2–3 months after HPV infection (almost all caused by types 6 or 11); however, not all persons infected with HPV types 6 and 11 develop anogenital warts.123435 Anogenital warts should be assessed by a clinician and can be treated, although warts may regress spontaneously or recur.36

HPV (primarily types 6 or 11) can also cause RRP, a rare disease that is characterized by recurrent warts or papillomas in the respiratory tract, most commonly in the larynx.12 RRP is usually diagnosed by a specialist based upon clinical and pathologic evaluation. RRP is divided into juvenile onset (JORRP) and adult onset (AORRP) conditions based on age at symptom onset. JORRP is believed to result from vertical transmission (mother to baby) of HPV at the time of delivery; the age of diagnosis is usually younger than 5 years.373839 A multicenter registry including patients with JORRP from 22 US clinical centers demonstrated that the clinical course of JORRP is highly variable and associated with extensive morbidity, requiring a median of 4.3 annual surgeries to remove papillomas, preserve vocal quality, and maintain an open airway.37 The age distribution of AORRP is reported to be bimodal with peaks in the third and sixth decades of life; acquisition of HPV that leads to AORRP is often presumed to be through sexual transmission.40

Screening and treatment

No treatment is required for asymptomatic HPV infection; instead, treatment is directed at the HPV-associated conditions.36 Current treatment options for precancers, cancers, and anogenital warts vary by the severity of disease and the anatomical location as described below. Routine screening for early detection of cervical cancer and precancer is recommended. Screening is also recommended for early detection of anal precancer among certain groups.4142

Anogenital warts

Anogenital warts are usually diagnosed by visual inspection, although biopsy may be helpful in some cases. The primary objective of treatment is removal of the wart and amelioration of symptoms, if present. The appearance of warts also can result in substantial psychosocial distress, and removal can relieve cosmetic concerns. In most patients, treatment results in resolution of the wart(s). Untreated, anogenital warts can resolve spontaneously, remain unchanged, or increase in size or number. Because warts might spontaneously resolve, an acceptable approach for some persons is to forego treatment and monitor for spontaneous resolution within one year. Available therapies for anogenital warts might reduce, but probably do not eradicate, HPV infectivity. Whether the reduction in HPV viral DNA resulting from treatment reduces future transmission remains unknown. Detailed treatment guidelines have been published.36 Treatment of anogenital warts may be guided by considerations such as wart size, number, anatomic site, patient preference, cost of treatment, convenience, adverse effects, and clinician experience.

Cervical precancer

Persistent HPV infection can result in cervical precancer as well as invasive cervical cancer. With regular cervical cancer screening and appropriate follow-up, most cervical precancers can be identified and treated in time to prevent progression to invasive disease. Cervical precancers and invasive cancers are diagnosed based on the histology of tissues obtained with biopsy or excision, and these specimens guide further treatment decisions. Because precancers are asymptomatic, screening is the only way to detect them and changes in screening will impact detection.

Recommendations for cervical cancer screening in the United States are based on systematic reviews of evidence and evolve to reflect updated evidence and new technologies. Beginning in the 1950s, cervical cancer screening was endorsed by the American Cancer Society (ACS) and the National Cancer Institute (NCI) using the Papanicolaou (Pap) test (cytology).43 Increased understanding of HPV natural history and its role in cervical cancer in the late twentieth and early twenty-first centuries led to development of clinical HPV tests that received FDA approval in the United States for incorporation into cervical cancer screening.44 HPV tests were first used to triage equivocal Pap test results (e.g., atypical squamous cells of undetermined significance [ASC-US], see Abnormal screening tests and precancerous anogenital lesions section).45 In 2012, HPV tests were incorporated into routine screening guidelines for use as a co-test with a Pap test.4647 Subsequently, FDA approved some HPV tests for primary screening (i.e., HPV testing alone). HPV testing has a higher sensitivity than cytology but lower specificity. A follow-up test of some kind, cytology, specific type identification (extended genotyping), or immunohistochemical staining (dual stain), may be used to triage HPV positive patients, avoiding over-referral of women for further evaluation.48495051

In 2018, the United States Preventive Services Task Force (USPSTF) updated their recommendations on cervical cancer screening. The USPSTF recommends routine cervical cancer screening starting at 21 years of age, continuing through 65 years of age (Grade A recommendation: high certainty that the net benefit is substantial).49 Available screening tests include conventional and liquid-based cytologic tests (i.e., Pap tests) and testing for high-risk HPV. Pap testing is recommended every 3 years among 21–29 year-olds. Among 30–65 year-olds, women have 3 options: a Pap test every 3 years, a Pap test plus HPV test (i.e., co-test) every 5 years, or an HPV test alone (primary HPV test) every 5 years. The longer screening intervals for options incorporating HPV testing are because of the high negative predictive value of HPV tests. Updated USPSTF draft recommendations released in December 2024 preferentially recommend primary HPV testing and with no distinction between patient or clinician collected samples for women 30-65 years old; however, as of publication these recommendations remain in draft form and a subsequent update is in progress. Readers should consult the USPSTF website for the most current guidance.52 The American Cancer Society (ACS) differs in their guidance and preferentially recommends primary HPV testing beginning at age 25 years through age 65 years and screening interval depends on if the specimen was clinician or patient collected.5053 Currently, cervical cancer screening recommendations do not differ for HPV-vaccinated and unvaccinated women. ACS and USPSTF concur that women may be eligible to cease screening after 65 years of age based on results of prior screening tests.

Management of abnormal screening findings have shifted to a risk-based approach with guidance updated by the Enduring Consensus Cervical Cancer Screening and Management Guidelines Committee as the approved options for screening and triage continue to be developed.5154 The Enduring Guidelines process relies on a standing committee including broad representation of stakeholders from medical professional societies, patient advocacy groups, and federal agencies. Data on the follow-up (3- or 5-year) outcomes of women with specific screening and triage (follow-up testing) results is used to determine risk for precancer. The principle is that management of women is based on risk detected, regardless of specific methods of testing and triage. The approach was adopted to allow timely incorporation of knowledge about new screening and triage tests into guidance more rapidly than could occur through professional organizational guideline processes. Use of self-collected samples for primary HPV screening is one of the newest options approved by FDA and incorporated into Enduring Guidelines.55 In average-risk patients, clinician-collected cervical specimens are preferred, and self-collected vaginal specimens are acceptable. Management of results of self-collected specimens follows the risk-based approach of the Enduring Guidelines. For asymptomatic patients with a reassuring prior cervical cancer screening history, five-year intervals are recommended for negative clinician collected specimens, and three-year screening intervals are recommended for negative self-collected specimens. Management of positive self-collected test results varies based on HPV type detected, patient's prior history, and reflex and co-test results. ACS endorses these guidelines.53 HRSA supported Women's Preventive Service Guidelines updated the evidence review performed for the 2024 Draft USPSTF recommendations and also preferentially recommends primary HPV testing and supports the use of self-collected specimens.56 The American College of Obstetricians and Gynecologists (ACOG) endorses these guidelines.57 The impact of vaccination on risk will also need to be considered in the future.5158

The suggested nomenclature for the histology of precancerous squamous lesions in the anogenital tract has shifted from intraepithelial neoplasia (IN) terminology, graded 1, 2, or 3, to intraepithelial lesions graded as low or high grade, similar to that used for cytology. This move to standardize lower anogenital squamous terminology (LAST) was prompted by poor interrater agreement on CIN2 lesions.59 In LAST, high-grade squamous intraepithelial lesions (HSIL) include CIN3 and the subset of CIN2 lesions that are p16 positive with an immunohistochemical test. As CIN3 is the immediate squamous precursor to invasive cancer, it is recommended that designation of HSIL include the CIN nomenclature in parenthesis, HSIL (CIN2) or HSIL (CIN3). Precancerous cervical lesions include HSIL and adenocarcinoma in situ (AIS).

Anal cancer

The ANCHOR (Anal Cancer HSIL Outcomes Research) trial, a pivotal study, demonstrated that treatment of anal high grade squamous intraepithelial lesions was effective at preventing anal cancer among persons living with HIV.60 Following publication of those data in 2022, guidelines for anal cancer screening were updated. Guidelines for the Prevention and Treatment of Opportunistic Infections in Adults and Adolescents with HIV recommend anal cancer screening in special populations including men aged ≥35 years who have sex with men and have HIV, and people living with HIV aged ≥45 years. Screening is done with anal cytology alone or high-risk HPV co-testing.42 In combination with other data, the International Anal Neoplasia Society (IANS) also developed guidelines for anal screening in high risk groups including people who are living with HIV. Recommendations for screening are age and risk based.41

Treatment of cervical and other HPV-associated cancers

For invasive HPV-associated cancers, several treatment options are available including surgery, radiation therapy, and chemotherapy, alone or in combination depending on stage of disease.61626364656667 HPV-attributable oropharyngeal cancers have a better prognosis than those that are HPV negative, so HPV testing of oropharyngeal cancers is used in guiding therapy.68

Laboratory testing

Specimen collection

The Centers for Disease Control and Prevention (CDC) conducts HPV testing only for certain special studies and surveillance programs. Jurisdictions should not send specimens to CDC unless participating in a project with CDC.

HPV testing

HPV cannot be detected through conventional cell culture methods.

HPV infection of epithelial cells is associated with characteristic morphologic changes, and the presence of HPV may be suggested based on cytology or histology findings. However, definitive detection of HPV requires molecular testing of cells or tissue from the lesion. A wide variety of HPV assays are commercially available, most commonly relying on amplification methods (such as PCR) targeting varying numbers of HPV types and reporting results as type groups or individual types.

For clinical applications, test results for specific sample collection methods matched to specific assays need to be validated against clinical outcomes and receive regulatory approval by the U.S. Food and Drug Administration (FDA). Most FDA-approved clinical HPV assays detect viral DNA; some assays detect viral mRNA from oncogenic HPV types.69 Currently FDA approved assays for cervical cancer screening or triage detect 14 types (HPV 16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 66, and 68). First generation assays reported pooled results as positive or negative for any of these types. With increased recognition of differing risk profiles among the HPV types, newer assays also provide separate results for HPV 16 or 18 and grouped or individual results for selected additional high-risk HPV types (extended genotyping).70 Currently, HPV assays used for anal cancer screening rely on those FDA-approved for cervical cancer screening, as no HPV assays are specifically FDA-approved for anal cancer screening, and assays that provide HPV 16-specific results are preferred.42 HPV testing does not distinguish between transient and persistent infection and does not indicate the presence of disease.

For epidemiologic and research questions using detection of HPV nucleic acid as an endpoint, assays that provide type-specific HPV results are important. There are many different sampling methods and assay formats that provide results on varying number of types. Surveillance and research assays are evaluated against analytic endpoints (i.e., detection of viral nucleic acid) rather than clinical disease endpoints and should not be used clinically. High analytic sensitivity and inclusion of types with limited clinical relevance yield results that are not necessarily predictive of disease requiring treatment.71 Research assays are conducted at government laboratories and academic centers, and experts from HPV reference laboratories worldwide have developed a manual to promote best practices and support standardization of HPV testing.72

In unvaccinated populations, serologic testing for HPV antibodies may be useful to determine past or current HPV infection.73 However, as HPV infection is confined to the epithelium and infected cells are shed before cell death, natural HPV infection results in minimal host immune response and not all those infected have detectable antibodies. Serologic assays are important in vaccine studies, comparing new vaccine formulations, novel methods of administration, or reduced dosing strategies.74 However, to date there is no immunologic correlate of HPV protection. Serologic assays are currently used only in research settings.

HPV vaccines

For specific information about the use of human papillomavirus vaccines, refer to the Child and Adolescent Immunization Schedule by Age for Healthcare Professionals, which provides general recommendations, including vaccine use and scheduling and contraindications and precautions.

Importance of surveillance

HPV infections are not nationally notifiable. This is because (1) most sexually active individuals will acquire at least one type of HPV infection at some point in their lives and infections usually clear or become undetectable, and (2) most infections will not have any associated clinical disease. However, special studies to monitor HPV infection and disease sequelae can help assess the impact of HPV vaccination. In addition to existing systems, new systems were established to monitor impact of HPV vaccination on early, intermediate, and long-term outcomes in the United States (see Enhanced Surveillance section).

Disease reduction goals

After the quadrivalent HPV vaccine was licensed in 2006, Healthy People goals regarding vaccination coverage were introduced. Healthy People 2030 includes an objective of 80% coverage with the recommended number of HPV vaccine doses for adolescents aged 13 to 15 years75 and also an objective to "reduce infections due to human papillomavirus (HPV) types prevented by the 9-valent vaccine in young adults."76 There is also a goal to "increase the proportion of females who receive a cervical cancer screening based on the most recent guidelines" with a target of 79.2% of women 21 to 65 years of age receiving screening (from a baseline of 75.0% in 2019).77 There are currently no goals for reduction of anogenital warts or RRP.

Case definitions

HPV infections and most HPV-associated conditions are not nationally notifiable. In contrast to other anatomical sites for which both carcinoma in situ (not yet invasive) and invasive carcinomas are reported to central cancer registries, only invasive cervical cancers are currently required to be reported. Cervical carcinoma in situ was reported in the past, but was discontinued, although some registries continued collection voluntarily. The explanations provided below are intended to describe classification of HPV-associated endpoints where surveillance is possible.

HPV infection

No national case-reporting system for HPV infections exists. Routine testing for HPV infection is not recommended; screening for high-risk types is clinically indicated in specific situations. For information on clinical indications for high-risk HPV testing, see Screening and Treatment section. For information on laboratory tests that can be used to detect HPV infections, see Laboratory Testing section.

Abnormal Pap tests and precancerous anogenital lesions

Pap tests assess cells collected by scraping or brushing the surface of the cervix (exfoliative cytology). Abnormal Pap test categories are listed by increasing grade of severity for squamous lesions: atypical squamous cells of undetermined significance (ASC-US); low-grade squamous intraepithelial lesions (LSIL); ASC cannot rule out high-grade squamous intraepithelial lesion (ASC-H); and high-grade squamous intraepithelial lesions (HSIL). Categories for glandular lesions include atypical glandular cells (AGC), atypical glandular cells of undetermined significance (AGUS), and adenocarcinoma in situ (AIS). An abnormal cervical cancer screening test (Pap test and/or clinical HPV test) should prompt follow-up. Increasingly, HPV tests are used in screening algorithms. Those with results indicating sufficient risk (see cervical precancer screening section) are referred to colposcopy and areas of abnormality are biopsied. Histologic evaluation of the biopsy determines diagnosis and clinical management.

Anogenital and oropharyngeal cancers

The primary site and pathologic diagnosis of the cancers are coded using the International Classification of Diseases for Oncology, 3.2 (ICD-O-3.2).78

Anogenital warts

A diagnosis of anogenital warts is made based on visual inspection of the lesion(s). Although anogenital warts are not nationally notifiable at this time, a 1996 case definition was published based on a clinical description and laboratory criteria.79

Recurrent respiratory papillomatosis

A diagnosis of RRP is made based on the presence of wart-like lesions in any respiratory tract site, most commonly in the larynx, and histopathology demonstrating papillomas.1280

Reporting and case notification

Case reporting within a jurisdiction

In the United States, the burden of cervical and other HPV-associated cancers is measured by population-based cancer registries participating in the CDC's National Program of Cancer Registries (NPCR) and/or the Surveillance Epidemiology and End Results (SEER) program.81 Data are collected and analyzed at the state (central cancer registries) as well as national (NPCR/SEER) levels. Rates of HPV-associated cancers vary geographically; up-to-date incidence and mortality statistics on HPV-associated cancers can be visualized through a web-based tool.

Case notification to CDC

HPV infection and other HPV-associated clinical conditions are not nationally reportable or required by CDC. However, some states or jurisdictions have made certain HPV-associated conditions reportable. Contact your state or jurisdiction health department for reporting requirements in your area.

Enhanced surveillance

The primary goal of HPV vaccination is to prevent cervical cancers, other HPV-attributable cancers, anogenital warts, and RRP caused by vaccine-targeted HPV types. The primary purpose of surveillance for HPV infections and associated conditions is to monitor impacts of the vaccination program. Such surveillance poses many challenges: infection with HPV is relatively common, a high proportion of infections are asymptomatic and resolve spontaneously, and some HPV-attributable disease may not develop until many years after initial infection.

Surveillance data on HPV-associated cancers, including cervical cancer, are collected in two population-based central cancer registries—NPCR and SEER—which together collect data on cancers diagnosed in 100% of the US population.81 Data from the registries were used to assess the pre-vaccine burden of HPV-associated cancers and will be the basis for monitoring relevant cancers post-vaccine introduction. Data from cancer registries have shown declines in cervical cancer in young women for several decades due to cervical cancer screening and treatment.26 Continued and steeper declines in this age group in more recent years are likely due to a combination of both changes in screening recommendations and HPV vaccination impact.82 A birth cohort analysis found that cervical cancer incidence rates were lower among women who were age 18 or younger when HPV vaccination was introduced. Cervical cancer incidence was 54% lower in vaccine-eligible 1990-1999 cohorts compared with the non-vaccine eligible 1970-1979 cohorts (4.7 vs 10.2 cases per 100,000 women).83

Earlier evidence of vaccination impact has been observed on outcomes such as HPV infections, anogenital warts, and cervical precancers.84 A variety of activities have been established to monitor these endpoints in the United States as described below.

Efforts to monitor HPV vaccine impact on cervical precancer are on-going. A geographically varied 5-site population-based cervical precancer monitoring program has measured the incidence of HSIL (CIN grades 2 and 3) and AIS (collectively referred to as CIN2+) since 2008 (HPV-IMPACT); monitoring of cervical cancer has also been included. The program has demonstrated vaccine effectiveness and impact and has also demonstrated declines in CIN2+ attributed to vaccine types.858687888990 A statewide project in New Mexico has monitored the incidence of cases of CIN1, CIN2, and CIN3 since 2007; this system, which also conducts typing on lesions periodically and maintains a cervical cancer screening registry to monitor changes in screening practices, has documented declines in precancers overall and in those attributed to HPV types 16, 18, 31, and 33 in screened young women.919293

The National Health and Nutrition Examination Survey (NHANES) has been used to monitor the impact of vaccination on HPV prevalence; type-specific HPV prevalence was monitored in genital specimens from females in 2003 through 2018 and from males in 2013 through 2018.949596979899100 Monitoring was conducted in oral specimens in 2009 through 2016.101102 Monitoring of genital and oral specimens was reinitiated in NHANES in 2025. HPV prevalence has also been monitored in women undergoing cervical cancer screening at selected managed care organizations103 and among men who have sex with men through clinic-based studies.104105 Additional ongoing efforts include analyses of administrative medical claims data to monitor the impact of HPV vaccination on HPV-associated conditions, including anogenital warts and cervical lesions.106107 Trends in JORRP have also been monitored.39

Although CDC does not recommend collection of routine surveillance data on HPV-associated conditions other than cancer, such data may be useful in sentinel projects (i.e., HPV-IMPACT) within specific states or jurisdictions with sufficient resources to collect data and where standardized protocols are used. Within such settings, some jurisdictions have made conditions such as CIN2/3 (HSIL) and AIS reportable, which has facilitated complete case ascertainment.108

Appendix A.

Table A1. Number of HPV-Associated and Estimated Number of HPV-Attributable Cancer Cases per Year28

Table A1
Cancer site Average number of cancers per year in sites where HPV is often found (HPV-associated cancers) Percentage probably caused by any HPV typeA Estimated number probably caused by any HPV typeA
Cervix 12,287 91% 11,100
Vagina 889 75% 700
Vulva 4,370 69% 3,000
Penis 1,429 63% 900
AnusB 8,348 91% 7,600
— Female 5,726 93% 5,300
— Male 2,622 89% 2,300
Oropharynx 22,585 70% 16,000
— Female 3,809 63% 2,400
— Male 18,776 72% 13,600
TOTAL 49,908 79% 39,300
— Female 27,081 84% 22,500
— Male 22,827 74% 16,800

Data are from population-based cancer registries participating in CDC's National Program of Cancer Registries (NPCR) and/or the National Cancer Institute's Surveillance, Epidemiology, and End Results (SEER) Program for 2018 to 2022, covering 100% of the United States population.

To determine the cancers most likely to be HPV-associated, the following additional criteria were applied to the data:

  • All cancers were confirmed histologically.
  • Cervical cancers were limited by histology to carcinomas only.
  • All other cancer sites were limited by histology to squamous cell carcinomas only.
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National Center for Immunization and Respiratory Diseases (NCIRD); Office of the Director (OD)
  1. HPV types detected in study; most were high-risk HPV types known to cause cancer. (Saraiya M, et al. U.S. assessment of HPV types in cancers: implications for current and 9-valent HPV vaccines. J Natl Cancer Inst. 2016;107:djv086). Estimates were rounded to the nearest 100. Estimated counts might not sum to total because of rounding.
  2. Includes anal and rectal squamous cell carcinomas.
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