Aberrant splicing events and epigenetics in viral oncogenomics : current therapeutic strategies

Abstract

Cancer is a global burden and is the second leading cause of mortality. It is largely a non-communicable disease attributable to the accumulation of damaged DNA and deleterious mutations in vital genes caused by exposure to carcinogens. Besides, viruses with oncogenic potential are also known to cause cancer through infections. Approximately, 12–20% of all cancers have a viral aetiology. Oncovirus infections are potentially modifiable risk factors, and targeting infections can be useful in prevention measures. In 2018, the global cancer cases attributable to infections were estimated to be 2.2 million. The International Agency for Research on Cancer (IARC) has identified seven different cancer-causing viruses namely the Human papillomaviruses (HPV), Hepatitis B virus (HBV), Hepatitis C virus (HCV), Epstein–Barr virus (EBV), Human T cell leukaemia virus 1 (HTLV-1), Kaposi’s Sarcoma Herpesvirus (KSHV) and Human immunodeficiency virus 1 (HIV-1). HIV-1 contributes to cancer development through immunosuppression by permitting the co-infection of other oncogenic viruses. With the exception of KSHV, the IARC classified these viruses as group one human carcinogens and further categorised these based on the viral genome as DNA viruses or RNA viruses. HPV, HBV and HCV are major contributors to cancers associated with viral infections, and the number of cases varies based on geographic locations. In 2018, Eastern Asia had the highest number of infection-related cancer, with 37.9 cases per 100,000 person-years, closely followed by Sub-Saharan Africa (SSA) with 33.1 cases per 100,000 person-years. A number of these infection-related cancers can be prevented with effective infection control through available vaccines, awareness and understanding of the risk factors.