Abstract
Global cancer incidence and mortality are on the rise. Although cancer is fundamentally a non-communicable disease, a large number of cancers are known to have a viral aetiology. A high burden of infectious agents (Human immunodeficiency virus (HIV), human papillomavirus (HPV), hepatitis B virus (HBV)) in certain Sub-Saharan African countries drives the rates of certain cancers. About one-third of all cancers in Africa are attributed to infection. Seven viruses have been identified with carcinogenic characteristics, namely the HPV, HBV, Hepatitis C virus (HCV), Epstein–Barr virus (EBV), Human T cell leukaemia virus 1 (HTLV-1), Kaposi’s Sarcoma Herpesvirus (KSHV), and HIV-1. The cellular splicing machinery is compromised upon infection, and the virus generates splicing variants that promote cell proliferation, suppress signalling pathways, inhibition of tumour suppressors, alter gene expression through epigenetic modification, and mechanisms to evade an immune response, promoting carcinogenesis. A number of these splice variants are specific to virally-induced cancers. Elucidating mechanisms underlying how the virus utilises these splice variants to maintain its latent and lytic phase will provide insights into novel targets for drug discovery. This review will focus on the splicing genomics, epigenetic modifications induced by and current therapeutic strategies against HPV, HBV, HCV, EBV, HTLV-1, KSHV and HIV-1.
Highlights
Cancer is a global burden and is the second leading cause of mortality [1]
This review will focus on the splicing genomics and epigenetic modifications induced by 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 HIV-1
Evidence supports that HPV E4 protein binds to SRPK1 and inhibits the activation of SR protein which is crucial in pre-mRNA processing, thereby regulating alternative splicing [24,42,43]
Summary
Cancer is a global burden and is the second leading cause of mortality [1]. 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. Recent estimates reflect that cancers attributed to HPV infection in Africa are 12.1% and 15.4% in SSA. The estimate for virally-induced cancer in Africa is attributable to EBV infections which is accountable for 2% of all cancer incidences in the continent. Cancers with HIV-1 and HTLV-1 aetiology are estimated to be below 1% in Africa [13] These incidence estimates are based on current registries, and the numbers may not be an accurate reflection of virally-induced cancers. These alterations facilitate the development of tumourigenesis They encode oncoproteins that facilitate viral replication and disrupt significant cellular mechanisms that induce aberrant cell proliferation leading to carcinogenesis [15]. This review will focus on the splicing genomics and epigenetic modifications induced by HPV, HBV, HCV, EBV, HTLV-1, KSHV and HIV-1.
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
