Journal
MICROORGANISMS
Volume 10, Issue 9, Pages -Publisher
MDPI
DOI: 10.3390/microorganisms10091754
Keywords
herpesvirus; latency; RNA modifications; DNA modifications; m6A; 5mC; m5C; pseudouridinilation; 2 '-O-me; histone modifications
Categories
Funding
- ANID-Millennium Science Initiative Program [ICN09_016]
- Millennium Institute on Immunology and Immunotherapy [ICN09_016/ICN 2021_045, P09/016-F]
- FONDECYT grant from ANID [1190864, 1190156]
- Regional Government of Antofagasta through the Innovation Fund for Competitiveness [FIC-R 2017, 30488811-0]
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Herpesviruses are highly prevalent double-stranded DNA viruses that can cause a wide range of clinical manifestations and diseases. Chemical modifications of viral RNA and DNA play critical roles in modulating the life cycle of herpesviruses during the lytic and latent phases of infection.
Herpesviruses are double-stranded DNA viruses occurring at a high prevalence in the human population and are responsible for a wide array of clinical manifestations and diseases, from mild to severe. These viruses are classified in three subfamilies (Alpha-, Beta- and Gammaherpesvirinae), with eight members currently known to infect humans. Importantly, all herpesviruses can establish lifelong latent infections with symptomatic or asymptomatic lytic reactivations. Accumulating evidence suggest that chemical modifications of viral RNA and DNA during the lytic and latent phases of the infections caused by these viruses, are likely to play relevant roles in key aspects of the life cycle of these viruses by modulating and regulating their replication, establishment of latency and evasion of the host antiviral response. Here, we review and discuss current evidence regarding epitranscriptomic and epigenetic modifications of herpesviruses and how these can influence their life cycles. While epitranscriptomic modifications such as m(6)A are the most studied to date and relate to positive effects over the replication of herpesviruses, epigenetic modifications of the viral genome are generally associated with defense mechanisms of the host cells to suppress viral gene transcription. However, herpesviruses can modulate these modifications to their own benefit to persist in the host, undergo latency and sporadically reactivate.
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