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

Jiang, Ru; Ekshyyan, Oleksandr; Moore-Medlin, Tara; Rong, Xiaohua; Nathan, Sean; Gu, Xia; Abreo, Fleurette; Rosenthal, Eben L.; Shi, Mingxia; Guidry, Jessie; Scott, Rona S.; Hutt-Fletcher, Lindsey; Nathan, Cherie‐Ann O.

doi:10.1111/jop.12221

Cited by 79 publications

(96 citation statements)

References 28 publications

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“…Some studies have detected the presence of both viral genomes in oral squamous cell carcinomas [19, 20] and nasopharyngeal carcinomas [21], and Jiang et al found a significant association of the presence of EBV and HPV together in oropharyngeal cancers of the tonsil and base of tongue [20]. In addition, Shimabuku et al [22] found that co-expression of EBV latent membrane protein-1 and HPV 16 E6 in primary mouse fibroblasts induced anchorage-independent growth and caused tumor formation in nude mice.…”

Section: Discussionmentioning

confidence: 99%

Human papillomavirus promotes Epstein-Barr virus maintenance and lytic reactivation in immortalized oral keratinocytes

et al. 2016

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Epstein-Barr virus and human papillomaviruses are human tumor viruses that infect and replicate in upper aerodigestive tract epithelia and cause head and neck cancers. The productive phases of both viruses are tied to stratified epithelia highlighting the possibility that these viruses may affect each other’s life cycles. Our lab has established an in vitro model system to test the effects of EBV and HPV co-infection in stratified squamous oral epithelial cells. Our results indicate that HPV increases maintenance of the EBV genome in the co-infected cells and promotes lytic reactivation of EBV in upper layers of stratified epithelium. Expression of the HPV oncogenes E6 and E7 were found to be necessary and sufficient to account for HPV-mediated lytic reactivation of EBV. Our findings indicate that HPV increases the capacity of epithelial cells to support the EBV life cycle, which could in turn increase EBV-mediated pathogenesis in the oral cavity.

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Section: Discussionmentioning

confidence: 99%

Human papillomavirus promotes Epstein-Barr virus maintenance and lytic reactivation in immortalized oral keratinocytes

et al. 2016

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“…EBV-HPV co-infection was observed in half of the samples, which supports the hypothesis of Kumar et al, 5 which proposes that infection by multiple oncogenic viral agents acts as an important risk factor in oral carcinoma. Similarly, Jiang et al 29 suggest that co-infection may have a bigger effect on invasion than on proliferation.…”

Section: 23mentioning

confidence: 99%

Prevalence of HPV and EBV infection and their relationship with the p53 and PCNA expression in oral carcinoma patients.

Veitía¹,

Liuzzi

Ávila

et al. 2017

J Oral Res

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Introduction: Infection caused by potentially oncogenic viruses, such as HPV and EBV, favors the role of certain oncoproteins that can induce dysplasias and malignant lesions. Objective: To evaluate the prevalence of HPV and EBV and their relation with the expression of p53 and PCNA in patients with oral carcinoma. Methodology: Twenty-seven oral squamous cell carcinomas (OSCC) were evaluated; DNA extraction was conducted using the QIAamp DNA mini kit; viral detection was obtained using the IN-NO-LiPA kit for HPV, and nested PCR was used for EBV. The evaluation of molecular markers was performed through immunohistochemical staining. Results: The mean age of the patients was 60.55±13.94 years, and 52% of these were female. Of the patients, 59% were tobacco users and 63% were alcohol consumers. HPV was detected in 70% of the patients with the predominance of genotype 16 (60%). As for EBV infection, it was observed in 59% of cases. p53 and PCNA immunopositivity corresponded to 44% and 59%, respectively. The tongue was the anatomical location with highest positivity for both viruses as well as for the expression of molecular markers. The 48% of the cases presented infection by both viruses. Conclusion: HPV and EBV infection together with the expression of p53 and PCNA were more frequently observed in advanced stages of the disease, suggesting a more relevant role in the progression than in tumor genesis.

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“…Next, we examined the EBV latent gene expression program of the EBV-positive FaDu cell lines. The FADu-EBV and FaDu-HE were previously shown to express equal levels of LMP2 mRNA [4]. Both FaDu-EBV and FaDu-HE were positive for LMP1 mRNA, but levels differed between the two EBV-positive cell lines (Figure 1).…”

Section: Resultsmentioning

confidence: 87%

“…Co-infection of HPV and EBV has been reported in nasopharyngeal, hypopharyngeal and oral cancers. Recently, we have shown that co-infection of these viruses in lymphoid rich sites (tonsil and BOT) of the head and neck is significantly associated with cancer status [4]. Head and neck tobacco associated cancers are recalcitrant to treatment because of multiple mutations that limit the identification of specific molecular targets.…”

Section: Discussionmentioning

confidence: 99%

“…Over the last few years strong association between EBV and HPV has been reported and it is presumed that EBV and high risk HPV co-infection may have a significant role in the neoplastic transformation of oral epithelial cells. Accordingly co-infection of these viruses have been reported in nasopharyngeal carcinomas (15–52.9%), other head and neck tumors (11%), oral cancers (13%) and SCC of the tonsil (25%) and base of tongue (70%) [4]. …”

Section: Introductionmentioning

confidence: 99%

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

Anandharaj¹,

Ekshyyan²,

Jia³

et al. 2015

Acta Oto-Laryngologica

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Conclusion EBV radiosensitized the p53 mutant tobacco associated head and neck cell line, FaDu. Objectives In the head and neck, HPV is a major risk factor associated with tonsil and base of tongue cancers, while a majority of undifferentiated nasopharyngeal cancers are positive for EBV. Clinically, head and neck tumors positive for HPV or EBV are more radiosensitive than tumors associated with tobacco and alcohol. We aimed to evaluate whether viral infections can sensitize tobacco-associated head and neck squamous cell carcinoma cell line that harbors multiple mutations, especially TP53, to radiotherapy. Method Four FaDu cell lines (vector control - FaDu-DN; FaDu expressing HPV16 E6/E7 – FaDu-HPV; FaDu infected with EBV – FaDu-EBV; and FaDu-HPV infected with EBV – FaDu-HE) were evaluated for their radiation sensitivity using clonogenic assay. Cell cycle, protein expression, apoptosis and cellular senescence were analyzed. Results FaDu-EBV and FaDu-HE exhibited significantly increased radiosensitivity in comparison with the control cell line. Radiation-induced cell cycle arrest was altered in all cell lines expressing viral genes. The observed distribution of cells at G1 and S phases was associated with a significant increase in expression of p21 protein along with decreased levels of pAKT/AKT and pERK/ERK ratio (p<0.05) and increased cellular senescence (p<0.05).

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

Cited by 79 publications

References 28 publications

Human papillomavirus promotes Epstein-Barr virus maintenance and lytic reactivation in immortalized oral keratinocytes

Human papillomavirus promotes Epstein-Barr virus maintenance and lytic reactivation in immortalized oral keratinocytes

Prevalence of HPV and EBV infection and their relationship with the p53 and PCNA expression in oral carcinoma patients.

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

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