Chlamydia trachomatis and HPV co‐infections in HIV negative men from a multi‐ethnic area of Northern Italy at high prevalence of cervical malignancies

Abstract

Chlamydia trachomatis and HPV coinfections in the male population are often a disregarded issue. We performed a study to evaluate the prevalence of such infections in heterosexual HIV negative men from a Northern Italy multi-ethnic area at high prevalence for cervical malignancies. Urethral swabs (US) or first-voided urine were evaluated retrospectively from 1317 patients attending Sexually Transmitted Infections (STI) clinic and from 3388 outpatients attending private clinics. Informations about participants' demographic characteristics and attributes of C. trachomatis, including chronic infection, and HPV genotypes testing, were collected. Exact Fisher test, bivariate, and multivariate logistic regressions were carried out. The prevalence of C. trachomatis was 1.7% in the outpatients and 16.9% in the STI group (P < 0.0001) in which the highest frequency was observed in men of age ≤25 years. Among patients with C. trachomatis, asymptomatic HPV co-infection was detected in 33% of men from the STI clinic and in 2% of the outpatients. Out of all coinfections, 56% were due to single HPV, with a prevalence of 73% in young STI men. The distribution of HPV genotypes confirmed the increased circulation of LR-HPV42, HR-HPV51, HR-HPV52 and prHR-HPV82, and the decreasing of HR-HPV16. African nationalities and leucorrhea were significantly associated risk factors, while the regular condom use offered an effective protection. This study highlights the high prevalence of C. trachomatis and HPV asymptomatic co-infection in young HIV negative men attending the STI clinic, representing a reservoir of new HPV genotypes with potential oncogenic risk.

Human papillomavirus and Its Association with Other Sexually Transmitted Coinfection among Sexually Active Women from the Northeast of Brazil

“…Multiple STIs have the potential to influence HPV infection, although literature data report that C. trachomatis and T. vaginalis are among the main infections associated with HPV virus. Similarly, studies report that C. trachomatis contributes to the acquisition of high-risk HPV viruses; however, the present study did not observe an association between these two pathogens [ 7 , 20 – 22 ]. We suggested that there is a possible cooperation between multiple microorganisms, contributing to cellular microenvironment changes that facilitate HPV infection.…”

“…However, the microorganisms detected vary in each study. In women with HPV, the presence of coinfections by C. trachomatis , Ureaplasma urealyticum , Trichomonas vaginalis , and Neisseria gonorrhoeae are among the main STIs identified [ 7 , 8 , 17 , 22 , 24 , 28 ].…”

“…The presence of coinfections can reduce the immune system's ability to eliminate HPV infection, in addition to favoring the progression of cervical lesions through the unregulated expression of viral oncogenes [ 29 ]. STIs can also induce a chronic inflammatory process, promoting the secretion of immune mediators that increase the production of reactive oxygen species that can, consequently, lead to tissue damage and favor both the entry and performance of HPV viral oncogenes [ 7 ].…”

“…The relationship between HPV infection and other microorganisms plays an important role in the progression of cervical lesions to cancer [ 6 ]. Interactions between HPV and other microorganisms, such as Chlamydia trachomatis, Trichomonas vaginalis , and Neisseria gonorrhoeae , may contribute to the damages caused by HPV, as well as to persistent infection and cancer progression [ 7 – 9 ].…”

“…The main factor associated with the presence of coinfections is the chronic inflammation caused by these microorganisms, which can act as a promoter of carcinogenesis by inducing the occurrence of significant cellular and molecular changes. The proliferation, recruitment of inflammatory cells, and increased production of reactive oxygen species (ROS) during the inflammatory process can lead to damage and inhibition of DNA repair [ 7 ]. These changes induced by STIs make the cervical epithelium more susceptible to mutations by activating oncogenes, inactivating tumor suppressor proteins and, thus, facilitating the action of HPV in the induction of tumor lesions [ 7 , 10 ].…”