Detection of Viruses with Oncogenic and Oncomodulatory Potential in Head and Neck Tumors-External Auricle

It is estimated that approximately 90% of all head and neck cancers are squamous cell carcinomas with a complex and multifactorial etiology. Molecular and epidemiological studies provide evidence for the role of oncogenic viruses in the initiation and/or oncomodulation of head and neck squamous cell carcinoma. Objectives: The present study aimed to detect the presence of high- and low-risk HPV, BKPyV, EBV, HCMV, HSVs in biopsy samples of squamous cell carcinoma of the external auricle in patients in Bulgaria. Materials and Methods: The study included 41 biopsy specimens from etiologically undiagnosed cases of squamous cell carcinoma of the external auricle. Molecular biological methods were used to detect the viruses-conventional and nested PCR, and sequence analysis. Results: The results obtained showed that none of the samples were found to have a high-risk HPV genotype. The highest percentage of samples showed genotype 6/11, and the lowest number of samples showed low-risk genotype 44. Of all herpesviruses, EBV was found in the largest proportion of samples, being present in the sample as a co-infection with HPV and always together with genotype 6/11. The frequency distribution, as a percentage and number of samples, of the possibilities for co-infection of EBV with each of the HPV genotypes was established. Of the remaining herpesviruses, the presence of HSV 2 was not confirmed in any of the samples. HSV 1 was present in only three of the samples, as a co-infection with genotypes 6/11, 42 and 43. When examining the samples for the presence of HCMV, only one positive sample was found, with both HPV 6/11 and 42 additionally present in the sample. Conclusions: For the first time, HPV, BKPyV, EBV, HCMV and HSVs were investigated and their possible involvement alone or as co-infection in the carcinogenesis of squamous cell carcinoma of the external auricle in patients in Bulgaria. The presence of the mentioned viruses, as well as the non-random distribution of EBV + HPV 6/11 and EBV + HPV 44, proven by us, does not necessarily make them etiological agents, but they could, through different and known mechanisms, influence the initiation and/or modulation of carcinogenesis.