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PLoS Pathog. 2018 Apr 30;14(4):e1006980. doi: 10.1371/journal.ppat.1006980. eCollection 2018 Apr.

Viral targeting of TFIIB impairs de novo polymerase II recruitment and affects antiviral immunity.

Author information

Innate Immunity Laboratory, Max-Planck Institute of Biochemistry, Martinsried/Munich, Germany.
Institute of Virology, Medical Center-University of Freiburg, Freiburg, Germany.
Faculty of Medicine, University of Freiburg, Freiburg, Germany.
Technical University of Munich, School of Medicine, Institute of Virology, Munich, Germany.
German Center for Infection Research (DZIF), Munich partner site, Munich, Germany.


Viruses have evolved a plethora of mechanisms to target host antiviral responses. Here, we propose a yet uncharacterized mechanism of immune regulation by the orthomyxovirus Thogoto virus (THOV) ML protein through engaging general transcription factor TFIIB. ML generates a TFIIB depleted nuclear environment by re-localizing it into the cytoplasm. Although a broad effect on gene expression would be anticipated, ML expression, delivery of an ML-derived functional domain or experimental depletion of TFIIB only leads to altered expression of a limited number of genes. Our data indicate that TFIIB is critically important for the de novo recruitment of Pol II to promoter start sites and that TFIIB may not be required for regulated gene expression from paused promoters. Since many immune genes require de novo recruitment of Pol II, targeting of TFIIB by THOV represents a neat mechanism to affect immune responses while keeping other cellular transcriptional activities intact. Thus, interference with TFIIB activity may be a favourable site for therapeutic intervention to control undesirable inflammation.

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