Our findings confirm that an increased risk of HPV infection is strongly associated with a young age at first intercourse, and with an elevated number of sexual partners as would be expected for a sexually transmitted viral infection.
Epidemiological studies have demonstrated the role of other sexually transmitted infectious agents in the pathogenesis of cervical cancer, but knowledge about the specific role of these pathogens in the natural history of HPV infection is limited. There are several mechanisms by which these co-infections may act, such as direct genotoxicity, but probably the most likely biologic mechanism is the induction of cervical inflammation leading genotoxic damage through oxidative metabolites . An association between cervical cancer and C. trachomatis has been established . In fact, C. trachomatis infection may increase susceptibility to HPV causing microabrasions or alterations of epithelial cells thus facilitating the entry of virions. Some reports have suggested that concurrent C. trachomatis infection can reduce host ability to resolve HPV infection: chronic cervical inflammation seems to influence the HPV persistence through a raised production of free radicals and a reduction of host cell-mediated immunity [2, 10]. C. trachomatis infection induces a shift in the immune response and the unresolved infections have been associated with a humoral (T helper cell type 2) immune response, whereas cellular (T helper cell type 1) immune response is important for the clearance of HPV lesions. Therefore, the modulation of cervical immune response by C trachomatis may influence the clearance of HPV lesions .
Our data showed, in HPV positive patients, particularly in HR HPV positive women, an increased C. trachomatis infection rate; this result may suggest more accurate screening for C. trachomatis in HPV positive patients with an atypical cytology. Since both pathogens are co-variables related to sexual behaviour, probably they synergize in inducing cervical epithelium alterations [3, 23].
An increased infection rate of U. urealyticum in HPV positive group was also observed, but a significant association was found only with high density cervical presence. The biological role of U. urealyticum infection in the HPV outcome was not previously clarified, but high level of U. urealyticum seems to be a cofactor in the development of HPV related cervical dysplasia . It is tempting to speculate that the presence of U. urealyticum may play a role both in initiating cellular anomalies and in viral persistence. It was reported that Mycoplasma infections cause in vitro chromosomal changes and cell transformation throughout gradual progressive chromosomal loss and translocations . Robertsonian chromosome translocation has been identified in the presence of Mycoplasma infections .
Previous researches have produced conflicting results regarding the role of bacterial vaginosis as cofactor in the development of cervical intraepithelial neoplasia . Thus, although bacterial vaginosis may have an influence in acquisition of genital infections, its role into HPV acquisition and persistence remains to be clarified . Moreover, to date the only prospective study on bacterial vaginosis and HPV infection, showed that both infections occur simultaneously  and suggested that the presence of HPV may have an influence in the vaginal flora. In our findings, bacterial vaginosis is not statistically associated with HPV infection, even if alterations of vaginal flora tend to be more common among HPV positive than HPV negative women (8.6% vs. 5.2% respectively).
This study evidenced also the lack of protective precautions against sexually transmitted infections, both in HPV positive and HPV negative women. Despite the use of condom is not reported to be highly effective in reducing HPV transmission [30, 31], counselling on sexually transmitted diseases (STDs) prevention use should be continued, for instance, to prevent C. trachomatis transmission.