e18065 Background: Recent evidence suggests an association between oral microbiome diversity with oral HPV infection, the precursor of HPV-associated oropharyngeal cancer. There is significantly higher prevalence of HPV-associated oropharyngeal cancer in White (70.2%) than Black individuals (46.3%). Black individuals are significantly less likely to develop HPV-associated oropharyngeal cancer, which has better prognosis than HPV-negative disease. We examine racial differences in oral microbiome diversity to explore potential biological underpinnings for the racial differences seen in HPV-associated head and neck cancer. Methods: We analyzed differences in oral microbiome diversity in 3775 Black & White participants from the National Health and Nutrition Examination Study (NHANES) cycles 2009-2012. Oral rinse samples were 16S rRNA amplicon-sequenced (V4 region) and diversity metrics were calculated using QIIME1. Four alpha diversity measures, reflecting the richness and/or evenness of a single participant’s sample, were calculated: observed number of ASVs, Faith’s Phylogenetic Diversity, Shannon-Wiener index, and Inverse Simpson index. Three beta diversity measures, reflecting the dissimilarity between pairwise samples, were calculated: unweighted UniFrac, weighted UniFrac, and Bray-Curtis. A survey-weighted generalized linear model was fitted to assess associations between alpha diversity and combined self-reported race and oral HPV status. Principal coordinate analysis and permutational multivariate analysis of variance tested for differences in microbial community composition by combined race/HPV status. Results: Weighted medians of alpha diversity were significantly different by race and HPV status [Kruskal-Wallis: Observed ASVs (p<0.001); Faith’s Phylogenetic Diversity (p<0.001); Shannon-Wiener (p<0.001); Inverse Simpson (p=0.005)]. Black/HPV-positive participants exhibited significantly greater alpha diversity, for all four alpha diversity measures, compared to White HPV-negative participants (p < 0.01). Black/HPV-negative participants also showed significantly greater alpha diversity compared to White/HPV-negative participants (p < 0.01), but not for Inverse Simpson index. Significant differences in microbial community were identified by race and HPV status for Bray-Curtis (BC: R 2 =0.32%, SE R 2 =0.020%, p<0.001) and Unweighted UniFrac (R 2 =0.55%, SE R 2 =0.029%, p<0.001) distances, but not Weighted UniFrac (R 2 =0.26%, SE R 2 =0.017%, p=0.8). Conclusions: Microbial diversity differences by race and HPV status may contribute to racial differences in HPV-associated head and neck cancer. While the mechanism of these differences is unclear, microbial diversity represents a modifiable risk factor that could inform interventions to supplement or disrupt the microbiome.
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