Literature DB >> 25040496

Association between human papilloma virus/Epstein-Barr virus coinfection and oral carcinogenesis.

Ru Jiang1, Oleksandr Ekshyyan, Tara Moore-Medlin, Xiaohua Rong, Sean Nathan, Xin Gu, Fleurette Abreo, Eben L Rosenthal, Mingxia Shi, Joseph T Guidry, Rona S Scott, Lindsey M Hutt-Fletcher, Cherie-Ann O Nathan.   

Abstract

BACKGROUND: The recent epidemic of head and neck squamous cell carcinomas associated with human papilloma virus (HPV) has not addressed its association with lymphoid tissue in the oropharynx or the potential role of Epstein-Barr virus (EBV)/HPV coinfection.
METHODS: The prevalence of HPV and EBV infection/coinfection and CD21 mRNA expression were determined in normal and cancerous tissues from the oropharynx using in situ hybridization (ISH), p16, and quantitative reverse transcriptase PCR (qRT-PCR). The effects of coinfection on tumorigenicity were evaluated using proliferation and invasion assays.
RESULTS: Normal oropharynx, tonsil, non-cancer base of tongue (BOT), and BOT from sleep apnea patients demonstrated EBV positivity ranging from 7% to 36% depending on the site and methods of detection used (qRT-PCR or ISH). Among non-malignant BOT samples, HPV positivity was noted only in 20%. The percent of tonsil and BOT cancers positive for HPV (up to 63% and 80%, respectively) or coinfected with HPV/EBV (up to 25% and 70%, respectively) were both significantly associated with cancer status. Notably, HPV/EBV coinfection was observed only in malignant tissue originating in lymphoid-rich oropharynx sites (tonsil, BOT). CD21 mRNA (the major EBV attachment receptor) was detected in tonsil and BOT epithelium, but not in soft-palate epithelium. Coinfected cell lines showed a significant increase in invasiveness (P < 0.01).
CONCLUSIONS: There is a high prevalence of HPV/EBV infection and coinfection in BOT and tonsil cancers, possibly reflecting their origins in lymphoid-rich tissue. In vitro, cells modeling coinfection have an increased invasive potential.
© 2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.

Entities:  

Keywords:  Epstein-Barr virus; coinfection; human papilloma virus; oral carcinogenesis; squamous cell carcinoma; tumorigenesis

Mesh:

Substances:

Year:  2014        PMID: 25040496      PMCID: PMC4286485          DOI: 10.1111/jop.12221

Source DB:  PubMed          Journal:  J Oral Pathol Med        ISSN: 0904-2512            Impact factor:   4.253


  30 in total

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2.  Immunofluorescence in cells derived from Burkitt's lymphoma.

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3.  Combined Epstein-Barr virus and human papillomavirus infection in nasopharyngeal carcinoma.

Authors:  C H Rassekh; P L Rady; I Arany; S K Tyring; S Knudsen; K H Calhoun; H Seikaly; B J Bailey
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4.  Oral dysplasia and squamous cell carcinoma: correlation between increased expression of CD21, Epstein-Barr virus and CK19.

Authors:  Ru Jiang; Xin Gu; Tara N Moore-Medlin; Cherie-Ann Nathan; Lindsey M Hutt-Fletcher
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Review 5.  Human papillomavirus related head and neck cancer survival: a systematic review and meta-analysis.

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8.  EBV and not HPV sensitizes tobacco-associated head and neck cancer cell line FaDu to radiotherapy.

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9.  Inhibition of Epstein-Barr Virus Replication in Human Papillomavirus-Immortalized Keratinocytes.

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Review 10.  Emerging and re-emerging infectious disease in otorhinolaryngology.

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