In a normal state, the healthy female vagina harbors over 200 types of microorganisms, with more than 95% dominated by lactobacilli and a small number being opportunistic pathogens. Lactobacilli are referred to as the "guardians of the vagina," playing a crucial role in maintaining a healthy vaginal environment and preventing the proliferation of pathogenic bacteria. On the other hand, Trichomonas vaginalis is an anaerobic parasitic flagellated protozoan, and the inflammation it causes is known as trichomonas vaginalis infection (TV). Increasing research indicates a close association between vaginal infections and the persistent infection of Human Papillomavirus (HPV), as well as the progression of cervical cancer.

To comprehensively understand the interaction between HPV and TV, Kelvin Stefan Osafo, at Fujian Maternity and Child Health Hospital (the first author), has reviewed the harm caused by TV and HPV co-infection on cervical and vaginal epithelia. The article titled "Exploring the interplay between Trichomonas vaginalis, Human Papillomavirus, and the microbiota" was published in "Gynecology and Obstetrics Clinical Medicine," with Professor Sun Pengming as the corresponding author.

Fig.1 Diagram of Trichomonas vaginalis Structure

The adhesion of Trichomonas vaginalis to cervical cells is influenced by the types of lactobacilli; specifically, Lactobacillus gasseri inhibits the adhesion of strong strains of Trichomonas vaginalis. Following a TV infection, there is an increase in bacteria associated with CST IV. Bacteria linked to Bacterial Vaginosis (BV) can act as pathogens, enhancing the adhesion of Trichomonas vaginalis to host cells. Additionally, Gardnerella vaginalis in the vagina can form a persistent biofilm, aiding Trichomonas vaginalis in attaching to vaginal and cervical epithelial cells—resulting in persistent trichomoniasis (treatment failure or drug resistance).

Fig.2 Graphical representation of the association between Trichomonas vaginalis and the microbiota. The figure shows normal epithelia with a normal mucus barrier and lactobacilli. In the presence of trichomonas vaginalis, CST IV bacteria increases. In the presence of CST IV bacteria, the mucus barrier is overpowered easily allowing the T. vaginalis to attach to the epithelial cells leading to inflammation of the cells.

In TV patients, the HPV infection rate is 17.65%, with the onset age predominantly concentrated between 20 and 39 years old. Although most HPV infections can resolve within 1-2 years after infection, external factors and variations in the immune system can affect HPV clearance. Research has found that trichomonal vaginitis can increase host inflammatory responses, heighten cervical epithelial injuries, and accelerate the invasive effects of HPV on the cervix, consequently leading to an increased HPV infection rate. Co-infection of Trichomonas vaginalis and HPV can elevate the risk of cervical intraepithelial neoplasia (CIN2+) and the occurrence of cervical cancer.

Fig.3 Graphical representation of the co-infection of trichomonas vaginalis and HPV and the associations with the microbiota. During the infection of T. vaginalis, CST IV bacteria increases, the mucus barrier is decreased, and as found by Hinderfield et al.,2019,54 tight junctions of the cells are weakened enhancing paracellular permeability making it easier for co-infection of T. vaginalis and HPV. During the co-infection, CST IV bacteria increase. The co-infection of TV and HPV leads to an increase in the risk of cervical lesions.

Based on the above research findings, it is recommended that women with trichomonal vaginitis undergo early screening and treatment for HPV, with joint treatment for their partners, to reduce the risk of cervical cancer. Additionally, maintaining the balance of the vaginal microbiota may indirectly contribute to the conversion from HPV-positive to HPV-negative status.

Reference:

1.      Osafo, Kelvin & Lin, Wenyu & Dong, Binhua & Sun, Pengming. (2023). Exploring the interplay between Trichomonas vaginalis, Human Papillomavirus and the microbiota. Gynecology and Obstetrics Clinical Medicine. 3. 10.1016/j.gocm.2023.10.002.

2.      https://mp.weixin.qq.com/s/c6Vihgkz-xDsqonex0giJA