Mapping of human papilloma virus, p16, and epstein‐barr virus in non‐malignant tonsillar disease

Abstract

Objectives Due to their location in the entrance of the aero‐digestive tract, tonsils are steadily exposed to viruses. Human papilloma virus (HPV) and Epstein‐Barr virus (EBV) are two potentially oncogenic viruses that tonsils encounter. The incidence of HPV positive tonsillar cancer is on the rise and it is unknown when infection with HPV occurs. Aim To investigate if tonsils are infected with HPV and EBV, to study the co‐expression of HPV and its surrogate marker p16, and to evaluate the number of EBV positive cells in benign tonsillar disease. Materials and Methods Tonsils from 40 patients in a university hospital were removed due to hypertrophy, chronic or recurrent infection. These were analyzed for presence of HPV, its surrogate marker p16, and EBV. HPV was studied using PapilloCheck (a PCR method), while p16 was identified in epithelial and lymphoid tissue with immunohistochemistry and EBV using EBER‐ISH (Epstein‐Barr encoding region–in situ hybridization). Results HPV was not detected, and p16 was present at low numbers in all epithelial samples as well as in 92.5% of the lymphoid tonsillar samples. At least one EBER‐positive cell was seen in 65% of cases. Larger numbers of EBER‐expressing cells were only seen in two cases. Conclusion These findings demonstrate that EBV and HPV infect tonsils independently, but further studies are warranted to confirm their infectious relationship. Level of Evidence Cross‐sectional study

PCR Detection of Epstein-Barr Virus (EBV) DNA in Patients with Head and Neck Squamous Cell Carcinoma, in Patients with Chronic Tonsillitis, and in Healthy Individuals

“…In a study of patients with nonmalignant tonsils, of the above viruses, only DNA-EBV was detected in more than half of the samples. The authors concluded that HPV and EBV infected independently of each other [ 60 ]. Interestingly, in vitro studies suggest that in the case of coinfection in oral squamous epithelial cells, the presence of HPV may increase the pathogenesis of EBV [ 44 ].…”