Cytokines and Markers of Immune Response to HPV Infection

Abstract

Cervical cancer is the third most commonly diagnosed cancer in women worldwide (Ferlay, Shin et al. 2010) and is a result of infection with cancer-causing types of human papillomavirus (HPV) (Bouvard, Baan et al. 2009). HPV is a very common infection, although in most circumstances, infection does not usually result in cervical disease (Trottier and Franco 2006). In fact, the natural history of HPV infection suggests that additional factors are required to drive progression from infection to the development of cancer. Most women are thought to clear their HPV infections within two years, but in approximately 10% of women, infection persists (Schiffman, Castle et al. 2007). Persistent HPV infection is, in effect, the strongest risk factor for progression to cervical precancer and cancer (Koshiol, Lindsay et al. 2008), and a dysfunctional immune response is likely to underlie the amplified risk that leads to HPV persistence and cervical cancer. Although efficacious prophylactic vaccines against the two types of HPV (16 and 18) that cause about 70% of cervical cancers (Munoz, Castellsague et al. 2006) are available, these vaccines are expensive, difficult to administer in poorer countries and will not protect women who have already been exposed to the virus (FUTURE II Study Group 2007; Hildesheim, Herrero et al. 2007) (Su, Wu et al. 2010). Thus, it is important to understand factors that predispose some women infected with a carcinogenic HPV infection to persist and progress.