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Updated: Jul 4, 2025

Affinity Purification of Influenza Virus Ribonucleoprotein Complexes from the Chromatin of Infected Cells
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The host RNA polymerase II C-terminal domain is the anchor for replication of the influenza virus genome

Tim Krischuns1, Benoît Arragain2, Catherine Isel3

  • 1Institut Pasteur, Université Paris Cité, CNRS UMR 3569, RNA Biology of Influenza Virus, Paris, France. tim.krischuns@pasteur.fr.

Nature Communications
|February 5, 2024
PubMed

Insights

The influenza virus polymerase (FluPol) uses host RNA polymerase II (RNAP II) not only for transcription but also for replication. RNAP II

Area of Science:

  • Virology
  • Molecular Biology
  • Biochemistry

Background:

  • The influenza virus polymerase (FluPol) is essential for viral genome replication and transcription.
  • Current models suggest FluPol interacts with host factors like RNA polymerase II (RNAP II) and acidic nuclear phosphoprotein 32 (ANP32) to regulate its activity.
  • RNAP II binding is primarily known for its role in cap-snatching during transcription initiation.

Purpose of the Study:

  • To investigate the role of the FluPol-RNAP II binding interface in viral genome replication.
  • To elucidate the mechanisms by which RNAP II influences FluPol's conformational changes and activity.
  • To propose a unified model for the spatial coupling of viral transcription and replication.

Main Methods:

  • Utilized a combination of cell-based assays.
  • Employed in vitro biochemical approaches.
  • Analyzed conformational changes in FluPol.

Main Results:

  • The RNAP II C-terminal domain, along with ANP32, significantly enhances FluPol replication activity.
  • Observed sequential conformational transitions of FluPol from a transcriptase to a replicase state upon binding to the RNAP II C-terminal domain.
  • Demonstrated that the FluPol-RNAP II binding interface plays a critical role in viral genome replication, extending beyond its known function in transcription.

Conclusions:

  • Host RNAP II acts as a central anchor for both influenza virus transcription and replication.
  • The interaction with RNAP II induces conformational changes necessary for switching between transcription and replication.
  • These findings provide new insights into the coordinated regulation of viral transcription and replication and their spatial organization.

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