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Updated: May 4, 2026

Multi-target Parallel Processing Approach for Gene-to-structure Determination of the Influenza Polymerase PB2 Subunit
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Multi-target Parallel Processing Approach for Gene-to-structure Determination of the Influenza Polymerase PB2 Subunit

Published on: June 28, 2013

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The PB2 E627K mutation contributes to the high polymerase activity and enhanced replication of H7N9 influenza virus

Hong Zhang1, Xuyong Li2, Jing Guo2

  • 1Key Laboratory of Molecular Virology & Immunology, Institut Pasteur of Shanghai, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, PR China.

The Journal of General Virology
|January 8, 2014
PubMed

Insights

The PB2 E627K mutation enhances H7N9 influenza virus replication and virulence in mice. This finding is crucial for understanding the pathogenicity of the H7N9 influenza outbreak.

Area of Science:

  • Virology
  • Molecular Biology
  • Public Health

Background:

  • Human infection with avian H7N9 influenza virus was first identified in China in March 2013.
  • The H7N9 outbreak reported 135 cases and 44 fatalities by August 2013.
  • Genetic analyses revealed mutations in H7N9 viruses associated with human adaptation and pandemic potential.

Purpose of the Study:

  • To investigate the role of specific polymerase gene mutations in H7N9 virus emergence and pathogenicity.
  • To determine the functional impact of the PB2 E627K mutation on H7N9 virus replication and virulence.

Main Methods:

  • Isolation and genetic analysis of H7N9 viruses from patients.
  • Assessing the effect of the PB2 E627K mutation on viral replication and PB2 polymerase activity.
  • Evaluating H7N9 virus virulence in a mouse model.

Main Results:

  • The PB2 E627K mutation was present in over 70% of H7N9 patient isolates.
  • This mutation significantly enhanced H7N9 virus replication by increasing PB2 polymerase activity.
  • The PB2 E627K mutation was found to enhance H7N9 virus virulence in mice.

Conclusions:

  • The PB2 E627K mutation plays a significant role in the pathogenicity of H7N9 influenza viruses.
  • This mutation likely contributed to the emergence and severity of the 2013 H7N9 outbreak.
  • Understanding mutation-driven pathogenicity is key for pandemic preparedness.

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