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Updated: Jun 6, 2026

Production of High-Titer Infectious Influenza Pseudotyped Particles with Envelope Glycoproteins from Highly Pathogenic H5N1 and Avian H7N9 Viruses
08:10

Production of High-Titer Infectious Influenza Pseudotyped Particles with Envelope Glycoproteins from Highly Pathogenic H5N1 and Avian H7N9 Viruses

Published on: January 15, 2020

The mouse-lethal H5N1 influenza virus carrying the PB2-384L/443R/460M characteristics acquired in avian hosts can

Weipeng Lin1, Guohua Deng1, Xin Xing1

  • 1State Key Laboratory of Animal Disease Control and Prevention, Harbin Veterinary Research Institute, CAAS, Harbin, People's Republic of China.

Emerging Microbes & Infections
|June 5, 2026
PubMed

Insights

H5N1 avian influenza viruses can infect humans without common adaptive mutations. Specific PB2 protein changes (PB2-384L/443R/460M) enhance interaction with human ANP32A/B, increasing H5N1 virus lethality and zoonotic risk.

Area of Science:

  • Virology
  • Molecular Biology
  • Public Health

Background:

  • Acidic nuclear phosphoprotein 32 kDa members (ANP32A/B) restrict avian influenza virus polymerase in mammals.
  • Avian influenza viruses often acquire PB2 mutations (e.g., E627K, D701N) for human adaptation.
  • Some H5N1 viruses infect humans without these canonical mutations, necessitating further investigation.

Purpose of the Study:

  • To elucidate the molecular mechanisms behind H5N1 avian influenza virus adaptation to human hosts.
  • To identify specific viral factors enabling H5N1 replication in humans independent of known adaptive mutations.
  • To assess the zoonotic potential and public health implications of H5N1 evolution.

Main Methods:

  • Comparative analysis of H5N1 virus strains (A/chicken/LN/SD035/2018 and A/duck/JL/S1261/2019) in mice.
  • Construction and evaluation of single-gene reassortant viruses and mutants.
  • Assessment of viral polymerase activity and interaction with human ANP32A/B proteins.

Main Results:

  • The PB2 protein signature (384L/443R/460M) was critical for the high lethality of the LN35 H5N1 strain in mice.
  • This PB2 signature enables efficient utilization of human ANP32A/B by the H5N1 virus polymerase.
  • The PB2-384L/443R/460M signature enhances H5N1 virus-RNA ribonucleoprotein (vRNP) interaction with human ANP32A/B and promotes vRNP assembly.

Conclusions:

  • Key amino acid substitutions in the H5N1 virus PB2 gene can emerge in avian hosts, enhancing its ability to interact with human ANP32A/B.
  • These adaptations increase the virus's replication efficiency and pathogenic potential in humans.
  • The findings highlight the significant zoonotic and public health risks posed by the continued circulation and evolution of H5N1 in avian populations.
Keywords:
ANP32A/BAvian influenza virusH5N1adaptationvRNP assembly

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