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- W3048297715 endingPage "e1008346" @default.
- W3048297715 startingPage "e1008346" @default.
- W3048297715 abstract "Viruses subvert macromolecular pathways in infected host cells to aid in viral gene amplification or to counteract innate immune responses. Roles for host-encoded, noncoding RNAs, including microRNAs, have been found to provide pro- and anti-viral functions. Recently, circular RNAs (circRNAs), that are generated by a nuclear back-splicing mechanism of pre-mRNAs, have been implicated to have roles in DNA virus-infected cells. This study examines the circular RNA landscape in uninfected and hepatitis C virus (HCV)-infected liver cells. Results showed that the abundances of distinct classes of circRNAs were up-regulated or down-regulated in infected cells. Identified circRNAs displayed pro-viral effects. One particular up-regulated circRNA, circPSD3, displayed a very pronounced effect on viral RNA abundances in both hepatitis C virus- and Dengue virus-infected cells. Though circPSD3 has been shown to bind factor eIF4A3 that modulates the cellular nonsense-mediated decay (NMD) pathway, circPSD3 regulates RNA amplification in a pro-viral manner at a post-translational step, while eIF4A3 exhibits the anti-viral property of the NMD pathway. Findings from the global analyses of the circular RNA landscape argue that pro-, and likely, anti-viral functions are executed by circRNAs that modulate viral gene expression as well as host pathways. Because of their long half-lives, circRNAs likely play hitherto unknown, important roles in viral pathogenesis." @default.
- W3048297715 created "2020-08-13" @default.
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- W3048297715 date "2020-08-07" @default.
- W3048297715 modified "2023-10-15" @default.
- W3048297715 title "Host-derived circular RNAs display proviral activities in Hepatitis C virus-infected cells" @default.
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- W3048297715 doi "https://doi.org/10.1371/journal.ppat.1008346" @default.
- W3048297715 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/7437927" @default.
- W3048297715 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/32764824" @default.
- W3048297715 hasPublicationYear "2020" @default.
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