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It highlights global oral HPV prevalence in healthy individuals versus head and neck cancer, alongside reported persistence rates and the generally unclear natural history. It also addresses differences in p16 expression as an HPV surrogate, links regional India-specific burden and risk factors, and explains why treatment de-escalation remains limited despite improved outcomes in HPV-associated oropharyngeal cancers. ",{"@graph":69,"@context":122},[70,84,105],{"@type":71,"itemListElement":72},"BreadcrumbList",[73,77,79,82],{"item":74,"name":75,"@type":76,"position":8},"https://docshare.wps.com","Home","ListItem",{"item":78,"name":9,"@type":76,"position":14},"https://docshare.wps.com/document/",{"item":80,"name":35,"@type":76,"position":81},"https://docshare.wps.com/document/healthcare/",3,{"item":83,"name":65,"@type":76,"position":19},"https://docshare.wps.com/document/dynamics-of-oral-human-papillomavirus-infection-in-healthy-population-and-head-and-neck-cancer/376874/",{"url":83,"name":65,"@type":85,"image":86,"author":91,"headline":65,"publisher":94,"fileFormat":97,"inLanguage":63,"description":67,"dateModified":98,"datePublished":99,"encodingFormat":97,"isAccessibleForFree":100,"interactionStatistic":101},"DigitalDocument",{"url":87,"@type":88,"width":89,"height":90},"https://docshare.wps.com/thumbnails/dynamics-of-oral-human-papillomavirus-infection-in-healthy-population-and-head-and-neck-cancer/376874.png","ImageObject",300,407,{"name":92,"@type":93},"Ophelia","Person",{"url":74,"name":95,"@type":96},"DocShare","Organization","application/pdf","2026-10-29","2026-09-24",true,{"@type":102,"interactionType":103,"userInteractionCount":52},"InteractionCounter",{"@type":104},"ViewAction",{"@type":106,"mainEntity":107},"FAQPage",[108,114,118],{"name":109,"@type":110,"acceptedAnswer":111},"What is the main focus of this review on oral HPV and head and neck cancer?","Question",{"text":112,"@type":113},"It analyzes existing literature on how oral HPV infection changes over time and how HPV-associated head and neck cancer develops, including gaps that require further research.","Answer",{"name":115,"@type":110,"acceptedAnswer":116},"Why is treatment de-escalation not currently widely implementable for HPV-associated cancers?",{"text":117,"@type":113},"Evidence is limited, and lack of concordance for p16 as a surrogate marker for HPV detection in head and neck cancer complicates clinical decision-making.",{"name":119,"@type":110,"acceptedAnswer":120},"How do HR-HPV infections contribute to oncogenesis in head and neck tissues?",{"text":121,"@type":113},"HR-HPV E6/E7 proteins can drive carcinogenesis through immune evasion and disruption of cytokine signaling and antigen presentation, and malignant transformation can follow deregulated viral gene expression.","https://schema.org",{"og:url":83,"og:type":124,"og:title":65,"og:site_name":95,"og:description":67},"article",{"robots":126,"canonical":83},"index,follow",{"doc_id":128,"site_id":62},376874,1790462207,{"code":4,"msg":5,"data":131},{"doc_id":128,"user_id":132,"nickname":92,"user_avatar":133,"doc_module":4,"category_id":34,"category_name":35,"doc_title":65,"doc_description":67,"doc_content":134,"file_id":135,"file_url":136,"file_type":137,"file_size":138,"view_count":52,"is_deleted":4,"is_public":8,"is_downloadable":8,"audit_status":8,"page_count":139,"language":140,"language_code":63,"site_id":62,"html_lang":63,"table_of_contents":141,"faqs":142,"seo_title":143,"seo_description":67,"update_tm":144,"read_time":145},7971461741311,"https://ap-avatar.wpscdn.com/avatar/74000253aff267980c6?x-image-process=image/resize,m_fixed,w_180,h_180&k=1779345379180704826","DOI: 10. 1002/cam4 .5686  \nREVIEW  \nDynamics of oral human papillomavirus infection in healthy population and head and neck cancer  \nN. V. Vani1 | R. Madhanagopal1 | R. Swaminathan1 | T. S. Ganesan2   \n1Epidemiology, Biostatistics, and Tumour Registry, Cancer Institute (WIA), Chennai, India  \n2Medical Oncology, Cancer Institute (WIA), Chennai, India  \nCorrespondence  \nT. S. Ganesan, Department of Medical Oncology & Clinical Research, Laboratory for Cancer Biology, Cancer Institute (WIA), 38 Sardar Patel Road, Chennai, Tamil Nadu 600036, India.  \nEmail: [tsganesan@gmail.com](tsganesan@gmail.com)  \nPresent address  \nT. S. Ganesan, Department of Medical Oncology, Sri Ramachandra Institute of Higher Education and Research, Chennai, India  \nFunding information  \nThe Wellcome Trust DBT India Alliance, Grant/Award Number: IA/ CPHE/18/1/503946  \n1 | INTRODUCTION  \nAbstract  \nThe recent increase in high-risk human papillomavirus (HR-HPV)-associated oral and oropharyngeal cancers has gained considerable importance due to their distinct clinical and molecular characteristics. However, the natural history of oral HPV from acquisition to persistence and malignant transformation is still unclear. The global prevalence of oral HPV infection in healthy individuals ranges from 0.67% to 35%, while 31%–38.5% in head and neck cancer (HNC). The persistence rate of oral HR-HPV infection is 5.5% –12.8% globally. India has the highest HNC burden due to apparent differences in predisposing factors compared with the West. The prevalence of oral HPV in healthy individuals and its contribution to HNC is less evident in Indian studies. HR-HPV-associated HNC in this region accounts for 26%, with an active infection in 8%–15% of these tumors. There is a lack of concordance in the expression of p16 as a surrogate marker for HPV detection in HNC because of differences in behavioral risk factors. Due toa lack of evidence, treatment de-escalation cannot be implemented despite the improved outcome of HPV-associated oropharyngeal cancers. This review critically analyzes the existing literature on the dynamics of oral HPV infection and HPV-associated HNC, identifying potential avenues for future research. A better understanding of the oncogenic role of HR-HPV in HNC will help to formulate novel therapeutic approaches and is expected to have a significant public health impact as preventive strategies can be implemented.  \nKEYWORDS  \ndynamics, head and neck cancer, human papillomavirus, oral infection, prevention  \n(6.1 per 100,000 women and 20.9 per 100,000 men) in the Indian subcontinent, accounting for one-third of the  \nThe global incidence of head and neck cancer (HNC) isabout 660,000 cases, with a mortality of 325,000 patients annually.1 Tobacco consumption (smoking and smokeless) has contributed to an increased incidence of HNC  \nglobal burden.2 The recent increase in HNC in nonsmoking, nonalcoholic young individuals is primarily attributed to mucosal high-risk human papillomavirus (HR-HPV) infection.3 Though Zur Hausen reported the oncogenic  \nThis is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.  \n© 2023 The Authors. Cancer Medicine published by John Wiley & Sons Ltd.  \nrole of HPV in cervical cancer in 1974, its role in HNC was identified later by Syrjanen.4 Extensive research has proven that HR-HPV-associated HNC is a distinct clinical entity that differs substantially from those caused by traditional risk factors, for example, smoking, in all aspects—genetic, molecular, epidemiological, and clinical. This review critically analyzes the existing literature on the dynamics of oral HPV infection and HPV-associated HNC, identifying potential avenues for future research. It also traces the pathogenesis and the epidemiology of HR-HPVassociated HNC globally and in India, which has a higher disease burden and exhibit","cbCaisw5QuEAxT41","https://ap.wps.com/l/cbCaisw5QuEAxT41","pdf",390244,15,"English","# Introduction\n# Pathophysiology of HR-HPV-associated HNC","[{\"question\":\"What is the main focus of this review on oral HPV and head and neck cancer?\",\"answer\":\"It analyzes existing literature on how oral HPV infection changes over time and how HPV-associated head and neck cancer develops, including gaps that require further research.\"},{\"question\":\"Why is treatment de-escalation not currently widely implementable for HPV-associated cancers?\",\"answer\":\"Evidence is limited, and lack of concordance for p16 as a surrogate marker for HPV detection in head and neck cancer complicates clinical decision-making.\"},{\"question\":\"How do HR-HPV infections contribute to oncogenesis in head and neck tissues?\",\"answer\":\"HR-HPV E6/E7 proteins can drive carcinogenesis through immune evasion and disruption of cytokine signaling and antigen presentation, and malignant transformation can follow deregulated viral gene expression.\"}]","Dynamics of oral human papillomavirus infection in healthy population and head and neck cancer | PDF",1790221888,38]