{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,23]],"date-time":"2026-10-23T12:55:16Z","timestamp":1792760116481,"version":"4.5.0"},"reference-count":31,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2026,6,6]],"date-time":"2026-06-06T00:00:00Z","timestamp":1780704000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2026,6,6]],"date-time":"2026-06-06T00:00:00Z","timestamp":1780704000000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Reviews in Medical Virology"],"published-print":{"date-parts":[[2026,7]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>Oncogenic viruses cause approximately 20% of cancers globally burden, with Epstein\u2013Barr virus and high\u2010risk Human papillomavirus recognized as major contributors to epithelial malignancies. Increasing evidence suggests that EBV\u2013HPV co\u2010infection may enhance tumour progression through overlapping molecular and immunological mechanisms, particularly in cervical, oropharyngeal, and nasopharyngeal cancers. This review critically summarizes current evidence regarding the cooperative role of EBV and HPV in carcinogenesis while distinguishing viral co\u2010presence from biologically active co\u2010infection. EBV latent proteins, including LMP1, LMP2A, and EBNA1, activate oncogenic signalling pathways such as NF\u2010\u03baB, PI3K\/Akt, and JAK\/STAT, whereas HPV oncoproteins E6 and E7 disrupt p53 and retinoblastoma (Rb) tumour suppressor pathways. Together, these alterations may promote genomic instability, chronic inflammation, immune evasion, epigenetic dysregulation, and epithelial\u2013mesenchymal transition (EMT), thereby enhancing invasive and metastatic potential. Epidemiological studies report higher frequencies of EBV\u2013HPV co\u2010detection in advanced lesions and aggressive tumours; however, causal synergy remains insufficiently validated because of methodological heterogeneity and variability in viral detection techniques, including PCR, in situ hybridization, and immunohistochemistry. Emerging technologies such as spatial transcriptomics and single\u2010cell profiling may improve characterization of biologically meaningful co\u2010infection. In addition, circulating viral DNA, viral microRNAs, and HPV genotyping are being explored as biomarkers for disease monitoring and prognosis. Therapeutic strategies targeting viral oncogenes, immune checkpoints, and gene\u2010editing technologies also represent promising investigational approaches. Overall, EBV\u2013HPV co\u2010infection represents a biologically plausible but incompletely understood contributor to tumour aggressiveness, emphasizing the need for standardized diagnostics, longitudinal studies, and functional experimental\u00a0models.<\/jats:p>","DOI":"10.1002\/rmv.70173","type":"journal-article","created":{"date-parts":[[2026,6,6]],"date-time":"2026-06-06T18:34:32Z","timestamp":1780770872000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Synergistic Oncogenesis Cooperative Role of Epstein Barr Virus and Human Papillomavirus in Cancer Progression"],"prefix":"10.1002","volume":"36","author":[{"given":"Neetesh","family":"Jindal","sequence":"first","affiliation":[{"name":"Department of Virology ICMR\u2010Rajendra Memorial Research Institute of Medical Sciences  Patna 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