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What is HPV?

Human Papillomaviruses (HPV) consist of a very diverse group of over 150 viruses that can infect a variety of tissues in the body. Some types of HPV cause harmless skin warts, other HPV types cause genital warts, and a third group of HPV types can cause cervical, anal, or mouth and throat cancer.

Sexually transmitted HPV is the most common sexually transmitted infection worldwide.1,2 Before the HPV vaccine was introduced in 2008, an estimated 39.9 million females and 39.2 million males had an active HPV infection in the US, according to the National Health and Nutrition Examination Survey.3 More recently, in the US, 42.5% of adults aged 18-59 years had a genital infection with any HPV type, as measured between 2011 to 2014.4

Sexually transmitted HPV can be classified into low-risk or high-risk types.5,6 Low-risk HPV types – such as 6, 11, 42, and 44 – are associated with benign ano-genital and skin warts (or condylomata). High-risk HPV types can cause cervical cancer in females, and anal and oropharyngeal cancers in both females and males.5,6,7

Oropharyngeal refers to the mouth and the pharynx.
Ano-genital refers to the anal and genital regions.
Condylomata are raised growths on the skin – typically in the genital region – caused by HPV infection.

What are the common symptoms?

Though most HPV infections cause no symptoms, certain HPV types can lead to warts, precancerous lesions, or cancerous lesions.

Warts can have many shapes and sizes, and generally result from low-risk HPV infection.6,8 They are classified into non-genital and genital warts. Non-genital warts are transmitted through skin-to-skin contact and can be further classified into common warts, flat warts, plantar warts, and other warts. They are usually found on the hands or feet. Risk factors for non-genital warts are communal showers or locker rooms, handling meat, or immunosuppression. Common warts are typically caused by HPV types 1, 2, 4, 7, 27, and 57.9,10

Genital warts, also known as ano-genital warts or condylomata acuminata, are associated with low-risk, sexually transmitted HPV. These are most often caused by HPV types 6 and 11. They typically appear as raised or cauliflower shaped lesions. In males, genital warts usually appear on the penis, while in females, warts usually can be found on the labia, vaginal opening, or cervix.7,9

More than 10 sexually transmitted HPV types are considered high-risk, meaning that they can lead to cancer. HPV types 16 and 18 are the most common causes of cervical cancer.11 Although the most common form of HPV-related cancer is cervical cancer in females, both males and females infected with high-risk HPV strains can develop anal or oropharyngeal cancer. Penile cancer can also occur in males, though HPV infection is not the most common cause.9,11,12

Each year, there are approximately 530,000 new cases of cervical cancer diagnosed worldwide, and 270,000 cervical cancer related deaths,13 making cervical cancer one of the most common cancers for females.

 What are the causes?

Sexually transmitted HPV infection occurs through skin-to-skin contact. While the most common form of transmission is sexual intercourse, HPV infection can also be acquired through other routes, such as oral and anal sex. HPV infections can also be transmitted from mother to baby during birth.14

Risk factors associated with the development of HPV-associated cancer include an increasing number of sexual partners, a weakened immune system, young age at first sexual encounter, use of oral contraceptives, poor diet, and alcohol consumption.6,14

The ways in which HPV leads to cancer are complex. In general, HPV interferes with normal cell functioning, leading to uncontrolled and excessive growth.

It’s important to note that most HPV infections are cleared by the immune system, so 90% of HPV infections disappear within 1 or 2 years. In the remaining 10%, the infection persists, and these long-lasting infections are associated with an increased risk of developing cancer. Thirty years after initial infection, about half of these persisting infections with high-risk HPV strains will have led to cancer.6 The HPV types that cause cancer generally grow very slowly and result in few or no symptoms, which is why early detection of HPV-caused precancerous or cancerous lesions is so important.

How does this topic relate to my microbiome?

Unlike the gut microbiota, a healthy vaginal microbiota will often have low microbial diversity.15 HPV infection correlates with changes in the vaginal microbiome, with higher microbial diversity and fewer beneficial microorganisms. Studies show that HPV infection is associated with fewer Lactobacillus species within the vaginal microbiota, including L. crispatus, L. gasseri, L. iners, and L. jensenii. Additionally, HPV infection rates are higher among women with bacterial vaginosis (BV), whose vaginal microbiome often contains increased levels of microbes such as Sneathia species or Gardnerella vaginalis.15,16

Which diseases/topics are related to HPV?

The diseases or lesions associated with HPV include, in alphabetical order7:

  • Anal cancer
  • Anogenital cancers and precancers
  • Anogenital warts
  • Cervical cancer
  • Common warts
  • Epidermodysplasia verruciformis
  • Flat plane warts
  • Oral lesions
  • Oropharyngeal cancer
  • Plantar warts
This autosomal recessive inherited skin disorder is characterised by wart-like lesions that can appear on different parts of the body. It is a very rare inherited disease.

How can people take action?

Sexually transmitted HPV infection can be prevented. Currently, HPV vaccines can prevent infections for the most common sexually transmitted high-risk HPV types associated with cancer, including most cervical cancers.5 Infection by HPV can also be prevented by consistent condom use.17

Regular screening can make a significant difference in preventing HPV-related cancer. The U.S. Preventive Services Task Force recommends screening for cervical cancer in women age 21 to 65.

  • Women age 21-29 should be screened with cytology (pap smear) every 3 years. HPV screening is not recommended in this group unless their pap smear results are abnormal or inconclusive.
  • Women age 30-65 should be screened with a combination of cytology and HPV testing every 5 years,18 though the new USPSTF recommendation includes stand-alone HPV testing every 5 years for women age 30-65.19


1. Loya, A., Serrano, B., Rasheed, F., Tous, S., Hassan, M., Clavero, O., … Alemany, L. (2016). Human Papillomavirus Genotype Distribution in Invasive Cervical Cancer in Pakistan. Cancers, 8(8), 72.

2. Wheeler, C. M. (2013). The Natural History of Cervical Human Papillomavirus Infections and Cervical Cancer. Obstetrics and Gynecology Clinics of North America, 40(2), 165–176.

3. Satterwhite, C. L., Torrone, E., Meites, E., Dunne, E. F., Mahajan, R., Ocfemia, M. C. B., … Weinstock, H. (2013). Sexually Transmitted Infections Among US Women and Men. Sexually Transmitted Diseases, 40(3), 187–193.

4. McQuillan, G. M., Kruszon-Moran, D., Markowitz, L. E., Unger, E. R., & Paulose-Ram, R. (2017). Prevalence of HPV in adults aged 18-69: United States, 2011-2014. Hyattsville, MD: US Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Health Statistics.

5. Markowitz, L. E., Dunne, E. F., Saraiya, M., Chesson, H. W., Curtis, C. R., Gee, J., … Centers for Disease Control and Prevention (CDC). (2014). Human papillomavirus vaccination: recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR. Recommendations and Reports : Morbidity and Mortality Weekly Report. Recommendations and Reports, 63(RR-05), 1–30.

6. Zandberg, D. P., Bhargava, R., Badin, S., & Cullen, K. J. (2013). The role of human papillomavirus in nongenital cancers. CA: A Cancer Journal for Clinicians, 63(1), 57–81.

7. Cubie, H. A. (2013). Diseases associated with human papillomavirus infection. Virology, 445(1–2), 21–34.

8. Dochez, C., Bogers, J. J., Verhelst, R., & Rees, H. (2014). HPV vaccines to prevent cervical cancer and genital warts: an update. Vaccine, 32(14), 1595–1601.

9. Doorbar, J., Egawa, N., Griffin, H., Kranjec, C., & Murakami, I. (2015). Human papillomavirus molecular biology and disease association. Reviews in Medical Virology, 25(10), 2–23.

10. Loo, S. K.-F., & Tang, W. Y.-M. (2014). Warts (non-genital). BMJ Clinical Evidence, 2014.

11. Crosbie, E. J., Einstein, M. H., Franceschi, S., & Kitchener, H. C. (2013). Human papillomavirus and cervical cancer. The Lancet, 382(9895), 889–899.

12. Grce, M., & Mravak-Stipetić, M. (2014). Human papillomavirus–associated diseases. Clinics in Dermatology, 32(2), 253–258.

13. World Health Organization. Cervical cancer.

14. Burchell, A. N., Winer, R. L., de Sanjosé, S., & Franco, E. L. (2006). Chapter 6: Epidemiology and transmission dynamics of genital HPV infection. Vaccine, 24(S3), S52–S61.

15. Mitra, A., MacIntyre, D. A., Marchesi, J. R., Lee, Y. S., Bennett, P. R., & Kyrgiou, M. (2016). The vaginal microbiota, human papillomavirus infection and cervical intraepithelial neoplasia: what do we know and where are we going next? Microbiome, 4(1), 58.

16. Kyrgiou, M., Mitra, A., & Moscicki, A.-B. (2017). Does the vaginal microbiota play a role in the development of cervical cancer? Translational Research, 179, 168–182.

17. Lam, J. U. H., Rebolj, M., Dugué, P.-A., Bonde, J., von Euler-Chelpin, M., & Lynge, E. (2014). Condom use in prevention of Human Papillomavirus infections and cervical neoplasia: systematic review of longitudinal studies. Journal of Medical Screening, 21(1), 38–50.

18. Vesco, K., Whitlock, E., Eder, M., Lin, J., Burda, B., Senger, C., … Zuber, S. (2011). Screening for Cervical Cancer : A Systematic Evidence Review for the U . S . Preventive Services Task Force. AHRQ Publication, 11–05156–E(86), 263.

19. Young, K. (2018). USPSTF: Stand-Alone HPV Testing Recommended as Cervical Cancer Screening Option.