Abstract
Epstein–Barr virus (EBV) belongs to the group of gamma-herpes viruses and was the first recognized human oncovirus. EBV is responsible for infectious mononucleosis and multiple lymphoid and epithelial malignancies including B-cell lymphomas (Burkitt lymphoma, Hodgkin lymphoma, and post-transplant lymphoproliferative disorder), various T-cell/NK lymphoproliferative disorders, nasopharyngeal carcinoma, and gastric carcinoma, respectively. In addition, the presence of EBV has been documented in other cancers including breast, prostate, oral, and salivary gland carcinomas. The presence and role of EBV in cervical cancer and its precursor lesions (CIN) have also been described, but the results from the literature are inconsistent, and the causal role of EBV in cervical cancer pathogenesis has not been established yet. In the present review, we briefly surveyed and critically appraised the current literature on EBV in cervical cancer and its variants (lymphoepithelioma-like carcinoma) as well as its precursor lesions (CIN). In addition, we discussed the possible interactions between EBV and human papilloma virus as well as between EBV and immune checkpoint regulators (PD-L1). Though further studies are needed, the available data suggest a possible causal relationship between EBV and cervical cancer pathogenesis.
Highlights
Infectious agents contribute to approximately 18% of all cancers worldwide [1]
We have proposed that viruses alone or in collaboration may induce oncogene activation and promote the epithelial–mesenchymal transition, one of the key steps in cancer progression and meta stasis (Figure 1) [66]
Recent breakthrough advances in cancer treatment are mainly due to the therapeutic effects of immune checkpoint inhibitors [such as anti-programmed cell death-1 (PD-1)/PD-L1] that have revolutionized management of several cancers including non-small-cell lung carcinoma, renal cell carcinoma, advanced urothelial carcinoma, Merkel cell carcinoma, microsatellite instable (MSI-H) colorectal carcinoma, malignant melanoma, and classical Hodgkin lymphoma (HL) [82,83,84]
Summary
Infectious agents contribute to approximately 18% of all cancers worldwide [1]. These agents include bacteria (e.g., Helicobacter pylori), viruses [human papilloma virus (HPV), hepatitis B virus, hepatitis C virus, Epstein–Barr virus (EBV), human herpes virus-8, human T-cell lymphotropic virus-1 (HTLV-1), and Merkel cell polyomavirus], and parasites (e.g., Schistosoma and liver flukes) [1,2,3,4,5,6,7]. The cancers associated with the abovementioned infections include several hematologic {lymphomas/lymphoproliferative disorders [Hodgkin lymphoma (HL), Burkitt lymphoma, posttransplant lymphoproliferative disorder, various T-cell/NK lymphoproliferative disorders]} and solid malignancies (carcinomas: nasopharyngeal, hepatocellular, gastric, cervical, Merkel cell, and bladder carcinoma). Viral infections within the cancer cells are not mutually exclusive, and synergistic oncogenic effects can and likely occur (see the paragraph on EBV in cervical cancer) [8, 11]
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