Abstract
High-risk human papillomavirus (HR-HPV) is etiologically associated with the development and progression of cervical cancer, although other factors are involved. Epstein-Barr virus (EBV) detection in premalignant and malignant tissues from uterine cervix has been widely reported; however, its contribution to cervical cancer development is still unclear. Here, a comprehensive analysis regarding EBV presence and its potential role in cervical cancer, the frequency of EBV/HR-HPV coinfection in uterine cervix and EBV infection in tissue-infiltrating lymphocytes were revised. Overall, reports suggest a potential link of EBV to the development of cervical carcinomas in two possible pathways: (1) Infecting epithelial cells, thus synergizing with HR-HPV (direct pathway), and/or (2) infecting tissue-infiltrating lymphocytes that could generate local immunosuppression (indirect pathway). In situ hybridization (ISH) and/or immunohistochemical methods are mandatory for discriminating the cell type infected by EBV. However, further studies are needed for a better understanding of the EBV/HR-HPV coinfection role in cervical carcinogenesis.
Highlights
Cervical cancer constitutes the fourth most frequently diagnosed malignant tumor in women and the first cause of cancer-related death in females
The most important risk factor for cervical cancer development is infection with human papillomavirus (HPV) [3], with 99.7% of cervical carcinomas worldwide caused by high risk (HR)-HPV
While vaccines exist that protect against oncogenic HPV infection, global disparities still remain due to high costs [6,7]
Summary
Cervical cancer constitutes the fourth most frequently diagnosed malignant tumor in women and the first cause of cancer-related death in females. In 2018, 570,000 new cases and 311,000 deaths were estimated worldwide [1] This is the leading diagnosed malignancy in 28 countries and the most frequent cause of cancer deaths in 42 countries, mainly in low- and middle-income countries [2]. The most important risk factor for cervical cancer development is infection with human papillomavirus (HPV) [3], with 99.7% of cervical carcinomas worldwide caused by high risk (HR)-HPV types, such as HPV16 or HPV18 [4,5]. 3.6% of LSILs progress to high-grade squamous intraepithelial lesion (HSIL) [8], with a report of 50% regression in LSILs associated with HPV16 or HPV18 [9]. We review the current literature regarding EBV presence in SILs and cervical cancer together with its potential contribution to HR-HPV-mediated cervical carcinogenesis and tumor progression. We propose an HR-HPV/EBV co-carcinogenesis model, in which HR-HPV/EBV oncoproteins play a key role in both oncogenesis and immune evasion
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