Epidermodysplasia Verruciformis: Functional Role of E6 and E7 Oncoproteins as the Link between Viral Infection to Carcinogenesis

Abstract

Background: Cancer is the most dreadful disease since last few decades. Besides all causative reasons, it is observed that one in every five cancers globally is linked with infectious diseases. Among all the infectious oncogenic viruses, 35% of the human cancers have been caused by Human Papilloma Viruses (HPVs). One such type is Epidermodysplasia Verruciformis (EV), a tropical disease also known as the Tree man syndrome. Hypothesis: EV is one of the most potential illustrations linking viral infection with skin carcinogenesis. The HPV virus acts as a cofactor with the UV radiation. The lesions caused by invasion of the HPV in the sun exposed wounded areas of the EV patients clearly links βHPV and cellular proliferation where EVER1 and EVER2 gene mutations are equally cardinal. When the viral infection persists, the somatic mutations over time accumulate, leading to precancerous lesions at first, followed by the malignant transformation. Two out of the eight proteins that the HPV genome codes for namely E6 and E7, account for the high-risk type HPVs that cause cancer. Both work similarly but on different sites. Both E6 and E7 proteins encode the main HPV's oncoprotein which promotes cell progression and viral replication. Results and Conclusion: The role of E6 and/or E7 in tumor progression, metastasis promotion, NOTCH and TGFβ pathway modification, DNA methyltransferase stimulation, histone modification, E-cathedrine modification etc. have been described in this review for the better understanding of the linkage between viral infection and carcinogenesis process.