A molecular viewpoint of the intricate relationships among HNSCC, HPV infections, and the oral microbiota dysbiosis.

Abstract

HPV infection and the type of host microbiota play a role in the formation of HNCs. In contrast to other forms of OSCC, where the relationship between HPV and the cancer is less obvious, HPV-HNSCC is a particular type of oropharyngeal cancer. HPV has infected a stratified squamous epithelium, which includes the throat, mouth, anogenital tract, respiratory tract, and skin on the hands and feet. HPV DNA was found in high amounts in the saliva and gargle samples of patients with HPV-related HNSCC. It has been discovered that the specificity of oral mRNA (HPV) and HPV DNA identification varies from 23 % to 82 % in the identification of OPSCCs. The higher rate of HPV transmission through vaginal-oral compared to penile-oral sexual activity may be the reason for the difference in HPV-positive HNSCC patients between males and females. The researchers postulate that HPV-inactive tumours signify an advanced stage of HPV-positive HNSCC, which explains why there are racial disparities in gene expression that correspond to different disease progressions in Black and White patients. The increase of CD8+ T cells in the cancer microenvironment, linked to P16 activation, extends life expectancy in OSCC. tumour markers methylation caused by HPV and suggested using them as possible HNC biomarkers. Fusobacterium levels are much higher in patients with OSCC, while Actinobacteria phylum and Firmicutes are significantly lower. It also serves as a biomarker for notable variations found in Firmicutes, Actinobacteria, Fusobacteriales, Fusobacteriia, Fusobacterium, and Fusobacteriaceae. Therefore, based on this we evidence, we could investigate the role of oral microbiota as a maker for the HPV associated HNSCC.