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and HPV16 Coinfection May Contribute to the Development of Cervical Cancer

Overview
Journal Virulence
Specialty Microbiology
Date 2024 Feb 21
PMID 38380669
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Abstract

Persistent human papillomavirus HPV infection is a necessary but insufficient condition for cervical cancer. Microorganisms are crucial environmental factors in cancers susceptibility and progression, recently attracting considerable attention. This study aimed to determine the infection status and relationship between high-risk HPV (HR-HPV) and lower genital tract infectious pathogens in cervical cancer and its precursors. From a retrospective and a prospective cohort analysis, () dominated the pathogens isolated from cervical discharges, and an isolation rate uptrend has been shown recently. HPV16 and 's coinfection rate gradually increased with the severity of cervical intraepithelial neoplasia. The adhesion and invasion abilities of the isolated to HPV16-positive SiHa cells were evaluated . The TCGA database and cervical tissues samples analysis showed that IL-10 was upregulated in cervical cancer. IL-10 expression levels increased in tissue samples with the severity of cervical cancer and its precursors with HPV16 and coinfection. Although no significant changes in IL-10 production were observed in the co-culture supernatant, we hypothesized that Treg immune cells in the tumour microenvironment might be responsible for the local IL-10 upregulation, according to our data showing Foxp3 upregulation and an upward trend with the cervical intraepithelial neoplasia grading to cancer and tumours with and HPV16 coinfection. Our data provide insights into the possible role of in cervical cancer progression and suggest that the application of HPV and screening programs may be an effective strategy to relieve the burden of cervical cancer and its precursor lesions.

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