Your browser doesn't support javascript.
Antiviral immunity triggered by infection-induced host transposable elements.
Hale, Benjamin G.
  • Hale BG; Institute of Medical Virology, University of Zurich, Winterthurerstrasse 190, Zurich, 8057, Switzerland. Electronic address: hale.ben@virology.uzh.ch.
Curr Opin Virol ; 52: 211-216, 2022 02.
Article in English | MEDLINE | ID: covidwho-1588013
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.
Subject(s)

Full text: Available Collection: International databases Database: MEDLINE Main subject: Viruses / DNA Transposable Elements Language: English Journal: Curr Opin Virol Year: 2022 Document Type: Article

Similar

MEDLINE

...
LILACS

LIS


Full text: Available Collection: International databases Database: MEDLINE Main subject: Viruses / DNA Transposable Elements Language: English Journal: Curr Opin Virol Year: 2022 Document Type: Article