Sexually Transmitted Infections: Human Papillomavirus

Introduction

• Description: Infection by one or more subtypes (of the more than 100 known) of human papillomaviruses (HPVs) causes epithelial proliferations at cutaneous and mucosal surfaces. Some serotypes are associated with warty growths on the hands, feet, and other locations (including genital warts). Some high-risk serotypes are found in more than 99% of cervical cancers.

• Prevalence: Considered to be the most common sexually transmitted infection (STI) in the world. Approximately 20 million people (United States) are currently infected with HPV. At least 75% of sexually active people acquire genital HPV infection at some point in their lives. One study estimated that 64%–82% of adolescent girls were infected with at least one strain of HPV ( Table 73.1 ). By the age of 50 years, at least 80% of women will have acquired genital HPV infection. Approximately 6.2 million Americans acquire a new genital HPV infection yearly. HPV is responsible for >20,500 virus-related cancers in women each year. Immunization programs using currently available vaccines have resulted in a drop in the incidence of infection in many studies.

  Table 73.1

  HPV Serotypes and Common Clinical Conditions

  Disease	HPV Strain
  Anogenital warts	6 and 11 (90% of cases), 42, 43, 44, 55, and others
  Cervical cancer, vulvar squamous cancer	16 and 18 (70% of cases), 31, 33, 35, 39, 45, 51
  Bowen disease	16, 18, 31, 32, 34, and others
  Common warts	2, 1, 7
  Epidermodysplasia verruciformis	More than 15 strains
  Flat cutaneous warts	3, 10
  Focal epithelial hyperplasia	12, 32
  Oral papillomas	6, 7, 11, 16, 32
  Oropharyngeal squamous cell carcinoma	16 and others
  Plantar warts	1, 2, 4
  Respiratory papillomatosis	6 and 11

• Predominant Age: Reproductive age and beyond.

• Genetics: No genetic pattern to infection. The genetic characterization of the virus has led to the identification of those serotypes that are oncogenic.

Etiology and Pathogenesis

• Causes: Exposure to the double-stranded DNA HPV. More than 40 serotypes (of >100) are known to be sexually transmissible. Vertical transmission from mother to child during childbirth can occur and rarely results in laryngeal polyps (approximately 2/100,000 births). Papillomaviruses initiate infection in the basal layer of the epithelium and viral genome amplification occurs in differentiating cells. After infection, differentiating epithelial cells that are normally nondividing remain in an active cell cycle. This can result in a thickened, sometimes exophytic, epithelial lesion. The virus is released as cells exfoliate from the epithelium. Research indicates that HPVs produce proteins (designated E5, E6, E7) that interfere with tumor suppressor p53 proteins that arrest the cell cycle when there is DNA damage.

• Risk Factors: Direct contact with an infected individual; therefore, having multiple sexual partners or contact with a person with multiple sexual partners increases the risk. Viral persistence is more likely in those with reduced immunity and tobacco smokers. Other epidemiologic factors associated with the risk of cervical cancer include long-term use of oral contraceptives, coinfections such as chlamydia, parity, and nutritional factors.

Signs and Symptoms

• Most infections are asymptomatic and are spontaneously cleared (70% by 1 year and more than 90% within 2 years; median infection, 8 months)

• Persistent infections may be associated with warty growths at the site of infection (condylomata acuminata) and cellular changes associated with dysplasia or cancer (including cancers of the anus, vulva, vagina, cervix, and some cancers of the oropharynx).

• The incubation period required before symptoms appear is highly variable and varies from several weeks to years.

Diagnostic Approach