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- W3200424348 abstract "Defective interfering (DI) RNAs arise during influenza virus replication, can be packaged into particles (DIPs) and suppress spread of wildtype (WT) virus. However, the molecular signatures of DI RNAs and the mechanism underlying antiviral activity are incompletely understood. Here, we show that any central deletion is sufficient to convert a viral RNA into a DI RNA and that antiviral activity of DIPs is inversely correlated with DI RNA length when induction of the interferon (IFN) system is disfavored. When induction of the IFN system was allowed, it was found to be the major contributor to DIP antiviral activity. Finally, while both DIPs and influenza virus triggered expression of IFN-stimulated genes (ISG) only virus stimulated robust expression of IFN. These results suggest a key role of innate immune activation in DIP antiviral activity and point towards previously unappreciated differences in DIP- and influenza virus-mediated activation of the effector functions of the IFN system." @default.
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- W3200424348 date "2021-09-23" @default.
- W3200424348 modified "2023-10-16" @default.
- W3200424348 title "Interferon induction and not replication interference mainly determines anti-influenza virus activity of defective interfering particles" @default.
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- W3200424348 doi "https://doi.org/10.1101/2021.09.20.461172" @default.
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