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This study integrated transcriptomic data from in vitro GV infection experiments and a GEO dataset (GSE75132) of HPV16 persistence to elucidate shared pathogenic mechanisms. Differential expression analysis identified 4115 genes modulated by GV infection and 861 by HPV16 persistence, with 74 common differentially expressed genes (DEGs) displaying consistent trends. Enrichment analyses revealed that these DEGs participate in metabolic pathways, immune defense, host\u2013pathogen interactions, and carcinogenesis. Protein\u2013protein interaction networks and Random Forest (RF) feature selection pinpointed radical S\u2010adenosyl methionine domain containing 2 (RSAD2) and Interferon\u2010induced protein with tetratricopeptide repeats 1 (IFIT1) as central hub genes. Upstream transcription analysis identified the homer_AGTTTCAGTTTC_ISRE motif and established a ceRNA network involving hsa\u2010miR\u2010654\u20105p, IFIT1\/RSAD2, and lncRNAs. Mendelian randomization (MR) and colocalization analyses linked RSAD2 downregulation to an increased risk of cervical carcinoma in situ (rs2595163, PPH4\u2009=\u20090.62), while ROC analysis demonstrated strong diagnostic potential for the combined hub gene expression. Notably, single\u2010cell transcriptomics revealed distinct RSAD2 and IFIT1 expression patterns in immune and epithelial cells during the progression from HPV infection to cervical cancer. Collectively, these findings support RSAD2 and IFIT1 as promising biomarkers and therapeutic targets for HPV\u2010related cervical lesions.\n                  <\/jats:p>","DOI":"10.1155\/mi\/2582989","type":"journal-article","created":{"date-parts":[[2025,6,5]],"date-time":"2025-06-05T09:20:19Z","timestamp":1749115219000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Integrative Analysis of Shared Pathogenic Genes and Potential Mechanisms in\n                    <i>Gardnerella vaginalis<\/i>\n                    and Persistent HPV16 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