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Mouse-adapted H9N2 influenza A virus PB2 protein M147L and E627K mutations are critical for high virulence

Jingjing Wang1, Yipeng Sun, Qi Xu

  • 1Key Laboratory of Animal Epidemiology and Zoonosis, Ministry of Agriculture, College of Veterinary Medicine, China Agricultural University, Beijing, China.

Plos One
|July 19, 2012
PubMed

Insights

H9N2 influenza virus adapted to mice showed increased virulence. Specific mutations in the PB2 gene, particularly the combination of M147L and E627K, were critical for enhanced pathogenicity in mammals.

Area of Science:

  • Virology
  • Pathogen Adaptation
  • Influenza Virus Research

Background:

  • H9N2 influenza viruses are widespread in avian species and pose a zoonotic risk.
  • Human infections with H9N2 can cause typical disease, raising concerns about potential adaptation and increased virulence.

Purpose of the Study:

  • To investigate the genetic underpinnings of H9N2 influenza virus host range and pathogenicity in mammals.
  • To generate and characterize a mouse-adapted H9N2 virus with enhanced virulence.

Main Methods:

  • Generation of a mouse-adapted H9N2 virus (SD16-MA) through sequential lung passages in mice.
  • Genomic analysis to identify amino acid substitutions in SD16-MA compared to the wild-type (SD16).
  • Assessment of viral replication and virulence in mice, focusing on specific gene segments (PB2, HA, M1).

Main Results:

  • SD16-MA exhibited significantly higher virulence than SD16 after 8 passages.
  • Five key amino acid substitutions were identified: PB2 (M147L, V250G, E627K), HA (L226Q), and M1 (R210K).
  • While all identified mutations enhanced replication, only PB2 significantly increased virulence. The combination of PB2 M147L and E627K was crucial for increased pathogenicity.

Conclusions:

  • The PB2 gene plays a critical role in the adaptation and increased pathogenicity of H9N2 influenza virus in mammalian hosts.
  • Specific amino acid substitutions at positions 147 (M147L) and 627 (E627K) within the PB2 protein are essential for enhanced virulence.
  • Understanding these genetic determinants is vital for assessing the pandemic potential of H9N2 influenza viruses.

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