Abstract
With between 10% and 15% of human cancers attributable to viral infection, there is great interest, from both a scientific and clinical viewpoint, as to how these pathogens modulate host cell functions. Seven human tumour viruses have been identified as being involved in the development of specific malignancies. It has long been known that the introduction of chromosomal aberrations is a common feature of viral infections. Intensive research over the past two decades has subsequently revealed that viruses specifically interact with cellular mechanisms responsible for the recognition and repair of DNA lesions, collectively known as the DNA damage response (DDR). These interactions can involve activation and deactivation of individual DDR pathways as well as the recruitment of specific proteins to sites of viral replication. Since the DDR has evolved to protect the genome from the accumulation of deleterious mutations, deregulation is inevitably associated with an increased risk of tumour formation. This review summarises the current literature regarding the complex relationship between known human tumour viruses and the DDR and aims to shed light on how these interactions can contribute to genomic instability and ultimately the development of human cancers.
Highlights
Over the past two decades interest in the relationship between viruses and the DNA damage response (DDR) has increased exponentially
Double-strand breaks in DNA can be repaired by non-homologous end joining (NHEJ) that operates throughout the cell cycle (Figure 4)
It is clear from the literature summarised here that the interaction between human tumour viruses and the DDR can contribute to an increase in genomic instability during viral infection
Summary
Over the past two decades interest in the relationship between viruses and the DNA damage response (DDR) has increased exponentially. Over the past few years a number of excellent reviews of the virus/DDR relationship have been published [1,9,10,11]. Some of these have focused on particular aspects of the DDR whereas others have concentrated on particular viral species. We have tried to draw together the relevant published literature specific to viruses associated with human tumours in vivo, including relevant RNA viruses as well as those with a DNA genome. By adopting this approach it is hoped that an appreciation can be gained of how the interaction between a virus and the DDR may contribute to its oncogenic potential and, to cancer development
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