Oncogenes and RNA splicing of human tumor viruses

Abstract

Approximately 10.8% of human cancers are associated with infection by an oncogenic virus. These viruses include human papillomavirus (HPV), Epstein–Barr virus (EBV), Merkel cell polyomavirus (MCV), human T-cell leukemia virus 1 (HTLV-1), Kaposi's sarcoma-associated herpesvirus (KSHV), hepatitis C virus (HCV) and hepatitis B virus (HBV). These oncogenic viruses, with the exception of HCV, require the host RNA splicing machinery in order to exercise their oncogenic activities, a strategy that allows the viruses to efficiently export and stabilize viral RNA and to produce spliced RNA isoforms from a bicistronic or polycistronic RNA transcript for efficient protein translation. Infection with a tumor virus affects the expression of host genes, including host RNA splicing factors, which play a key role in regulating viral RNA splicing of oncogene transcripts. A current prospective focus is to explore how alternative RNA splicing and the expression of viral oncogenes take place in a cell- or tissue-specific manner in virus-induced human carcinogenesis.

• EBV
• HBV
• HCV
• HPV
• HTLV-1
• KSHV
• MCV
• RNA splicing

This research program was supported by the Intramural Research Program of the National Cancer Institute, Center for Cancer Research, National Institutes of Health. Masahiko Ajiro was supported by the Japan Society for the Promotion of Science (JSPS) Research Fellowship for Japanese biomedical and behavioral researchers at the National Institutes of Health.