Abstract
Recent reports have pointed to the link between persistent inflammation, oxidative stress, and carcinogenesis; however most of the studies concerning the role of viruses in head and neck cancer (HNC) are focused mainly on one type of virus. Our present study aimed to study the relationship between Epstein–Barr virus/human papilloma virus (EBV/HPV) coinfection and glutathione peroxidase (GPx) and superoxide dismutase (SOD) level in oropharyngeal cancer. Fresh-frozen tumor tissue samples were collected from 128 patients with oropharyngeal cancer infected with EBV or HPV or with EBV/HPV coinfection. After DNA extraction, EBV and HPV DNA was detected using a polymerase chain reaction (PCR) assay. GPx and SOD activity was determined in homogenates of cancer tissue using diagnostic kits produced by Randox Laboratories. Both GPx and SOD activity was statistically lower in patients with EBV/HPV coinfection than in a single EBV or HPV infection. Analysis of GPx and SOD activity in relation to histological grading and tumor, node (TN) classification revealed that in poorly-differentiated tumors, the level of antioxidant enzymes was lower compared with well-differentiated lesions and in cases with greater tumor dimensions and lymph-node involvement, both GPx and SOD activity was decreased. Further studies are necessary to clarify the influence of interplay between EBV, HPV, and oxidative stress on malignant transformation of upper aerodigestive tract epithelial cells.
Highlights
Oncogenic virus-induced cancers are an important global concern nowadays
There was no significant difference in the activity of glutathione peroxidase (GPx) and superoxide dismutase (SOD) in patients infected with only Epstein–Barr virus (EBV) or human papilloma virus (HPV)
We have noted that in poorly-differentiated tumors, GPx and SOD activity was decreased compared with well-differentiated lesions
Summary
Oncogenic virus-induced cancers are an important global concern nowadays. According to various reports, all human cancers are non-communicable diseases, infections may contribute to about13–20 % of global human cancer burden, and it is estimated that about 35 % of all infection-associated malignancies are attributable to human papilloma virus (HPV) and Epstein–Barr virus (EBV) [1,2,3,4].EBV and HPV infections are associated with different cancers, including gastric, cervical, and breastViruses 2020, 12, 1008; doi:10.3390/v12091008 www.mdpi.com/journal/virusesViruses 2020, 12, 1008 carcinoma, as well as head and neck cancer (HNC) [5]. EBV and HPV coinfection plays an important role in the malignant transformation of epithelial cells [6,7]. EBNA1 expressed in all types of EBV latency is the only protein expressed in all EBV-positive tumors and sometimes the only protein expressed. It is responsible for maintaining the EBV genome in latently infected cells, but it can contribute to cell immortalization and malignant transformation via interferences with tumor suppressors, induction of DNA damage, and altering of signaling pathways [10]
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