Antiviral immunity triggered by infection-induced host transposable elements

Abstract

Host silencing of transposable elements (TEs) is critical to prevent genome damage and inappropriate inflammation. However, new evidence suggests that a virus-infected host may re-activate TEs and co-opt them for antiviral defense. RNA-Seq and specialized bioinformatics have revealed the diversity of virus infections that induce TEs. Furthermore, studies with influenza virus have uncovered how infection-triggered changes to the SUMOylation of TRIM28, an epigenetic co-repressor, lead to TE de-repression. Importantly, there is a growing appreciation of how de-repressed TEs stimulate antiviral gene expression, either via cis-acting enhancer functions or via their recognition as viral mimetics by innate immune nucleic acid sensors (e.g. RIG-I, mda-5 and cGAS). Understanding how viruses trigger, and counteract, TE-based antiviral immunity should provide insights into pathogenic mechanisms.