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One of the most common sexually transmitted diseases is human papillomavirus (HPV) infection that affects around 80% of sexually active women. Although most of the women clear HPV infection, individuals with inadequate immune responses develop persistent infections which lead to premalignant lesions such as high-grade cervical intraepithelial neoplasia (CIN-III), with high potential to progress to cervical carcinoma. Based on molecular and epidemiological data, high risk papillomaviruses (hrHPVs) are now recognized as etiologic agents of cervical carcinoma, although some additional events are required [1, 2].

Chlamydia trachomatis genital tract infections are prevalent worldwide (Stamm 2008), with 92 million new chlamydia cases occured every year: 3–4 million new cases occur every year in the US, 5 million in Western Europe, and 16 million in Sub-Saharan Africa (World Health Organization 2001; Weinstock et al., 2004). Chlamydia prevalence has been reported to range from 3%–7% among asymptomatic populations in men, and in women range from 3.0% in the general population to 9.5% among university students (World Health Organization 2001; Stamm 2008; Patel et al.,. 2008; Forhan et al., 2009; Imai et al., 2010; Satterwhite et al., 2010).

Although essential for the transformation of cervical epithelial cells, HPV is not sufficient, a number of other cofactors and molecular events being also incriminated (Woodman et al., 2007). Cervical HPV infection is a sexually transmitted disease which occurs in women short time after beginning the sexual life. In young women, the disease is usually transient, its prevalence decreasing around 30 years (de Sanjose et al., 2007). A second peak of infection is found in older women and is superposed to the peak of cervical cancer incidence (Anton et al., 2011). Near 40 of the more than 140 HPV types identified so far can infect the cervix (Bernard et al., 2010). Differences in carcinogenicity of cervix specific HPV types are partially related to the expression of the E6 and E7 oncogenes which, among other functions, interfere with tumour suppressor proteins p53 and pRb, respectively (Sinal et al., 2005). By these interactions viral oncogenes abrogate the mechanisms of cell-cycle control and apoptosis.