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Activation of the DNA Damage Response by RNA Viruses

School of Cancer Sciences, College of Medicine and Dentistry, University of Birmingham, Birmingham B15 2TT, UK
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Academic Editor: Wolf-Dietrich Heyer
Biomolecules 2016, 6(1), 2; https://doi.org/10.3390/biom6010002
Received: 28 September 2015 / Revised: 17 November 2015 / Accepted: 24 November 2015 / Published: 6 January 2016
(This article belongs to the Special Issue DNA Damage Response)
RNA viruses are a genetically diverse group of pathogens that are responsible for some of the most prevalent and lethal human diseases. Numerous viruses introduce DNA damage and genetic instability in host cells during their lifecycles and some species also manipulate components of the DNA damage response (DDR), a complex and sophisticated series of cellular pathways that have evolved to detect and repair DNA lesions. Activation and manipulation of the DDR by DNA viruses has been extensively studied. It is apparent, however, that many RNA viruses can also induce significant DNA damage, even in cases where viral replication takes place exclusively in the cytoplasm. DNA damage can contribute to the pathogenesis of RNA viruses through the triggering of apoptosis, stimulation of inflammatory immune responses and the introduction of deleterious mutations that can increase the risk of tumorigenesis. In addition, activation of DDR pathways can contribute positively to replication of viral RNA genomes. Elucidation of the interactions between RNA viruses and the DDR has provided important insights into modulation of host cell functions by these pathogens. This review summarises the current literature regarding activation and manipulation of the DDR by several medically important RNA viruses. View Full-Text
Keywords: RNA viruses; retroviruses; DNA damage response; HIV-1; HTLV-1; HCV; Influenza A; IBV RNA viruses; retroviruses; DNA damage response; HIV-1; HTLV-1; HCV; Influenza A; IBV
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Ryan, E.L.; Hollingworth, R.; Grand, R.J. Activation of the DNA Damage Response by RNA Viruses. Biomolecules 2016, 6, 2.

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