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Insight into Influenza: A Virus Cap-Snatching.

Corey De Vlugt1, Dorota Sikora2, Martin Pelchat3

  • 1Department of Biochemistry, Microbiology and Immunology, Faculty of Medicine, University of Ottawa, Ottawa, ON K1H 8M5, Canada. cdevlugt@outlook.com.

Viruses
|November 21, 2018
PubMed
Summary

Influenza A virus (IAV) mRNA transcription relies on cap-snatching, where viral polymerase steals cellular transcripts. This review highlights the crucial role of RNA polymerase II (RNAPII) promoter-proximal pausing in efficient IAV replication.

Keywords:
cap-snatchinginfluenza A virusprime-and-realignpromoter-proximal pausing

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Area of Science:

  • Virology
  • Molecular Biology
  • Gene Expression

Background:

  • The influenza A virus (IAV) genome comprises eight single-stranded RNA segments.
  • Viral RNA segments associate with RNA-dependent RNA polymerase (RdRp) and nucleoprotein, forming ribonucleoprotein complexes.
  • IAV transcription involves hijacking host cell machinery.

Purpose of the Study:

  • To review current knowledge on IAV cap-snatching.
  • To propose a model for IAV mRNA transcription.
  • To emphasize the role of RNAPII in IAV replication.

Main Methods:

  • Literature review of IAV transcription mechanisms.
  • Analysis of host-pathogen interactions during viral gene expression.
  • Hypothesis generation based on existing data.

Main Results:

  • IAV utilizes a cap-snatching mechanism to initiate viral mRNA synthesis.
  • Short, 5'-capped transcripts from host DNA dependent RNA polymerase II (RNAPII) are essential primers.
  • The review suggests RNAPII promoter-proximal pausing is critical for efficient IAV mRNA transcription.

Conclusions:

  • Cap-snatching is a vital process for influenza A virus replication.
  • RNAPII promoter-proximal pausing is likely a prerequisite for efficient IAV cap-snatching.
  • Understanding this mechanism can inform antiviral strategies.