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Na(+)/K (+)-ATPase β1 subunit interacts with M2 proteins of influenza A and B viruses and affects the virus

ShuoFu Mi1, Yan Li, JingHua Yan

  • 1CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences, Beijing 100101, China.

Science China. Life Sciences
|November 25, 2010
PubMed

Insights

Researchers discovered that the host protein ATP1B1 interacts with influenza M2/BM2 proteins. Knocking down ATP1B1 suppressed influenza virus replication, highlighting its crucial role in the virus-host interplay.

Area of Science:

  • Virology
  • Cell Biology
  • Biochemistry

Background:

  • Influenza viruses (A and B) utilize matrix proteins M2/BM2, which function as proton channels essential for viral replication.
  • The host factors interacting with M2/BM2 and the function of their cytoplasmic domains remain largely uncharacterized.

Purpose of the Study:

  • To identify host factors interacting with influenza M2/BM2 proteins.
  • To elucidate the role of these interactions in the virus-host interplay and viral replication.

Main Methods:

  • Yeast two-hybrid screening to identify interacting proteins.
  • Establishment of a stable ATP1B1 knockdown MDCK cell line.
  • Assessment of influenza virus replication in knockdown cells.

Main Results:

  • The β1 subunit of the host Na+/K+-ATPase (ATP1B1) was identified as an interactor of the M2/BM2 cytoplasmic domains.
  • ATP1B1 knockdown significantly suppressed influenza A/WSN/33 virus replication.
  • This suggests a critical role for ATP1B1 in supporting influenza virus replication.

Conclusions:

  • The cytoplasmic domain of influenza M2/BM2 proteins plays a significant role in virus-host interactions.
  • ATP1B1 is a host factor crucial for efficient influenza virus replication, likely through its interaction with M2/BM2.

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