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Peer-reviewedCC BY 4.0Viruses

Influenza A Virus RNA Polymerase Is Enriched on the Chromatin of Innate Immune Response Genes

  • Jia Yi1,2,3
  • Jessica Morel4,5
  • Mickaël Costallat1,2
  • Nathalie Lejal4
  • Bernard Delmas4
  • Christian Muchardt1,2
  • Eric Batsché1,2
5 affiliations
  1. 1Computational, Quantitative, and Synthetic Biology (CQSB), Centre National de la Recherche Scientifique (CNRS), Sorbonne Université, 75005 Paris, France.
  2. 2UMR 7238 CNRS, Institut de Biologie Paris-Seine (IBPS), Sorbonne Université, 75005 Paris, France.
  3. 3Doctoral School Life Science Complexity (ED515), Sorbonne Université, 75005 Paris, France.
  4. 4Unité de Virologie et Immunologie Moléculaires (VIM), UMR 0892, UVSQ, University Paris-Saclay, INRAE Centre de Recherche Île-de-France-Jouy-en-Josas-Antony, 78352 Jouy-en-Josas, France.
  5. 5Doctoral School Structure and Dynamics of Living Systems (ED577), University Paris-Saclay, 78352 Jouy-en-Josas, France.
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Abstract

The influenza A virus hijacks host cell machinery by “snatching” molecular caps from cellular RNAs to prime its own transcription. While this process is typically associated with the beginning of genes, this study reveals that the viral RNA polymerase exerts a far-reaching influence on host gene expression. Using genome-wide mapping and comparative pathway analyses, we show that viral polymerase (FluPol) recruitment is decoupled from general host transcriptional activity; instead, FluPol is markedly enriched at a distinct subset of promoters and enhancers associated with defense-related pathways. Beyond the initiation site, FluPol remains associated with host transcripts throughout elongation, extending into downstream-of-gene (DoG) regions. It further accumulates at gene ends, potentially contributing to widespread defects in transcription termination. By remaining linked to host transcripts across the entire gene body, FluPol could extend its opportunity for cap-snatching and impair the recycling of cellular transcription machinery. Together, these findings demonstrate how FluPol accumulation across key cellular defense loci spans from initiation through to termination, driving host transcriptional attenuation.

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Cite

BibTeXRIS
BibTeX
@article{yi2026influenza,
  title = {{Influenza A Virus RNA Polymerase Is Enriched on the Chromatin of Innate Immune Response Genes}},
  author = {Jia Yi and Jessica Morel and Mickaël Costallat and Nathalie Lejal and Bernard Delmas and Christian Muchardt and Eric Batsché},
  journal = {Viruses},
  year = {2026},
  month = sep,
  doi = {10.3390/v18101063},
  url = {https://hal.science/hal-05768045v1},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Influenza A Virus RNA Polymerase Is Enriched on the Chromatin of Innate Immune Response Genes
AU  - Jia Yi
AU  - Jessica Morel
AU  - Mickaël Costallat
AU  - Nathalie Lejal
AU  - Bernard Delmas
AU  - Christian Muchardt
AU  - Eric Batsché
PY  - 2026
DA  - 2026/09/24
JO  - Viruses
DO  - 10.3390/v18101063
UR  - https://hal.science/hal-05768045v1
AB  - The influenza A virus hijacks host cell machinery by “snatching” molecular caps from cellular RNAs to prime its own transcription. While this process is typically associated with the beginning of genes, this study reveals that the viral RNA polymerase exerts a far-reaching influence on host gene expression. Using genome-wide mapping and comparative pathway analyses, we show that viral polymerase (FluPol) recruitment is decoupled from general host transcriptional activity; instead, FluPol is markedly enriched at a distinct subset of promoters and enhancers associated with defense-related pathways. Beyond the initiation site, FluPol remains associated with host transcripts throughout elongation, extending into downstream-of-gene (DoG) regions. It further accumulates at gene ends, potentially contributing to widespread defects in transcription termination. By remaining linked to host transcripts across the entire gene body, FluPol could extend its opportunity for cap-snatching and impair the recycling of cellular transcription machinery. Together, these findings demonstrate how FluPol accumulation across key cellular defense loci spans from initiation through to termination, driving host transcriptional attenuation.
SN  - 1999-4915
ER  -