HPV Transmission and Acquisition

Although the link between sexual activity and cervical cancer was noticed as long ago as the mid-19th century, it was not until 1974 that the first publications noting histological similarities between condyloma HPV and CIN I were published. Since then, the natural history of HPV has become more clearly defined.

^{(Reference: Arnheim 2005; Walboomers et al 1999)}

Women

Any woman who is sexually active is at risk of HPV infection. Infection with HPV is easily transmitted via genital skin-to-skin contact and does not depend on penetrative intercourse. Condoms do not fully protect women from HPV infection.

Every woman is at risk of infection with oncogenic HPV types.

It is estimated that up to 80% of people will acquire an HPV infection in their lifetime (Baseman and Koutsky 2005; Ho et al 1998; Brown et al 2005), and up to 75% of those infections will be with an oncogenic type of HPV (Peto 2004; Cushieri 2004).

Persistent oncogenic HPV infection may develop into cervical cancer, but only in some cases. The lifetime risk of a woman developing cervical cancer is approximately 3.7% (Goldie et al 2003). It has been estimated that for every 1 million women who are infected, approximately 10% (100,000) will develop pre-cancerous cervical cell changes (cervical dysplasia) and, of these, approximately 8% (8000) will develop early cancer confined to the outer layers of the cervical cells (carcinoma in situ [CIS]). Of these women, 20% (1600) will go on to develop invasive carcinoma (McIntosh 2000).

(Reference: Ferlay et al 2004)

If infection could be prevented by vaccination of the female population, this would not only be cost effective (Taira et al 2004) but also have an enormous impact in preventing the oncogenic HPV infections that can lead to the development of cervical cancer. The addition of vaccination to a well-established screening programme could reduce the lifetime risk of invasive cervical cancer by up to 66%. It could also reduce the incidence of pre-cancerous squamous intraepithelial lesions, thus decreasing the number of women diagnosed with a positive cervical screening result (Goldie et al 2004).  Together, these HPV types account for approximately 50% of cases of HSIL (CIN II/CIN III) (Clifford et al 2003).

Men

The role of men in carrying, transmitting and infecting women with HPV, and how this leads to the development of cervical and other cancers, is only beginning to be understood. Until now, it has been assumed that a similar proportion of men as women are infected with HPV. The absence of data on HPV in men is partly due to the lack of a validated method for sampling HPV DNA from male genitalia and also the possible lower motivation for such a test compared with women (Schiffman and Kjaer 2003).

Some investigators have observed a difference between the genders; it was found that after adjustment for sexual behaviour, the incidence and persistence of HPV 16 in the serum of women was higher than in men (Thompson et al 2004). The sexual behaviour of men (eg, number of previous partners), however, correlated with the risk of their female sexual partners developing cervical cancer (Castellsagué et al 2003).

There is some suggestion that circumcised men have a lower prevalence of HPV and that their female partners are at lower risk of developing cervical cancer than those with uncircumcised male partners (Castellsagué et al 2002). More rarely, men may become the victim of their own HPV, as infection increases the risk of developing penile and anal cancers (Castellsagué et al 2003).

There are currently studies underway on the natural history of HPV in men, for example, a longitudinal-cohort study of HPV infection among women in Hawaii, to investigate the natural history and incidence of genital HPV infection in a multi-ethnic cohort of heterosexual men (Hernandez 2005).