Tumor Cell Development: A Role for Viruses and Telomerase Activity?

Abstract

Telomere biology is an important aspect of human cancer, because the telomere dysfunction and telomerase activity are associated with genomic instability and cellular immortalization. In this article, we review the regulation of telomere dynamics and telomerase activity in virus-related cancers. Viruses may exploit these events to favor its replication and, therefore, may differ from non-viral cancers in this regard. Focusing on Epstein–Barr virus (EBV), human papillomavirus (HPV), hepatitis B virus (HBV), and hepatitis C virus (HCV), which concentrate the majority of the evidence regarding telomere biology and viral cancers), although other viruses are more briefly mentioned, it is noticeable that regulatory mechanisms of telomere dynamics and telomerase activity are virus specific. Such mechanisms include accelerated telomere shortening because of higher rates of cellular proliferation, telomerase activity regulation, and activation of alternative lengthening of telomeres (ALT). Additionally, there is also some evidence supporting a role of viral non-coding RNAs (ncRNAs) and virus-induced alterations in host ncRNAs in telomerase activity. Clarification of the roles of telomere biology in mediating viral cancers would have implications only for developing telomere-targeting anti-cancer approaches and, possibly, to accelerate advances in other telomere-related diseases, such as non-viral cancers and other aging traits.