Background
Human papillomavirus (HPV)-driven oropharyngeal cancers (OPCs) are preceded by a long-term (decades) infections with high-risk (HR) HPV types. Previous studies have shown differences in the oral microbiota of patients with HPV-positive and HPV-negative OPCs. However, it remains unclear whether these changes occur in otherwise healthy people with oral HPV infections. Thus, we investigated the oral microbiome in sample of the general population with intermediate HPV infection.
Methods
Testing was conducted retrospectively on a subset of a previously established sample bank from the Oral Health Study (OHS). The OHS subset used in this study consisted of 128 oral samples (64 HPV-positive and 64 HPV-negative). PacBio HiFi Sequencing was performed at the Australian Genomic Research Facility (AGRF, Melbourne, Australia) using universal primers F27 and R1492 to amplify the entire 16S rRNA gene. Statistical analysis of alpha and beta diversity, as well as taxonomic composition (differential abundance testing), were used to determine differences between subject groups.
Results
We demonstrated (1) significant differences in the abundance of Streptococcus salivarius in oral HPV-negative males; (2) males with low-risk HPV had an increased abundance of several species and (3) decreased abundance of Streptococcus salivarius and Streptococcus parasanguinis. For women, (4) oral microbiome diversity (alpha diversity; Shannon Entropy) was significantly lower in HPV-positive subjects compared to HPV-negative subjects and (5) oral microbiome structure (beta-diversity) was significantly different between HPV-positive and HPV-negative subject groups.
Conclusions
The presence of intermediate oral HPV infection is associated with significant changes in the abundance of some commensal taxa, which differ between men and women. Our observations in females also suggest an association between HPV infection and altered community richness and structure. It is therefore possible that HPV infection, along with other factors, may contribute to carcinogenesis via dysbiosis of the oral microbiota.