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Dynamic changes in host gene expression associated with H5N8 avian influenza virus infection in mice

Su-Jin Park1, Mukesh Kumar2, Hyeok-il Kwon1

  • 1College of Medicine and Medical Research Institute, Chungbuk National University, Cheongju 361-763, Republic of Korea.

Scientific Reports
|November 19, 2015
PubMed

Insights

Highly pathogenic avian influenza (HPAI) H5N8 shows moderate pathogenicity in mice. Early immune gene induction may protect against H5N8, unlike H5N1, offering insights into avian influenza virus virulence mechanisms.

Area of Science:

  • Virology
  • Immunology
  • Transcriptomics

Background:

  • Global outbreaks of highly pathogenic avian influenza (HPAI) A(H5N8) are emerging.
  • H5N8 exhibits moderate pathogenicity in mice compared to H5N1.
  • Mechanisms underlying avian influenza pathogenicity remain unclear.

Purpose of the Study:

  • To investigate the differential pathogenicity mechanisms of HPAI H5N8 and H5N1 viruses in mice.
  • To compare host and pathogen transcriptomes in response to H5N8 and H5N1 infection.

Main Methods:

  • High-throughput RNA sequencing (RNA-seq) was employed to analyze host and viral transcriptomes.
  • Mice were infected with H5N8 (A/MD/Korea/W452/2014) and H5N1 (A/EM/Korea/W149/2006) viruses.
  • Ingenuity pathway analysis was used to identify key signaling pathways.

Main Results:

  • At 1 day post-infection (dpi), H5N8-infected mice showed higher viral transcripts and immune gene expression than H5N1-infected mice.
  • At 3 and 7 dpi, H5N1 infection led to more viral gene sequencing, higher viral titers, and increased virulence.
  • H5N1 infection significantly upregulated death receptor signaling compared to H5N8 infection at later time points.

Conclusions:

  • Early immune gene induction in H5N8-infected mice correlates with moderate pathogenicity.
  • Differential host-pathogen interactions and signaling pathway activation contribute to the distinct virulence of H5N8 and H5N1 viruses.
  • This study provides novel insights into the molecular mechanisms driving avian influenza pathogenicity.

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