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Cyclophilin A restricts influenza A virus replication through degradation of the M1 protein

Xiaoling Liu1, Zhendong Zhao, Chongfeng Xu

  • 1Center for Molecular Virology, CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences, Beijing, China.

Plos One
|February 21, 2012
PubMed

Insights

Cyclophilin A (CypA) restricts influenza virus replication by promoting the degradation of the M1 protein. Depleting CypA increases influenza virus infectivity and viral protein levels.

Area of Science:

  • Virology
  • Molecular Biology
  • Cell Biology

Background:

  • Cyclophilin A (CypA) is a peptidyl-prolyl isomerase implicated in the replication of various viruses.
  • CypA interacts with the influenza virus M1 protein, potentially hindering early viral replication stages.

Purpose of the Study:

  • To elucidate the molecular mechanism by which CypA influences influenza virus replication.
  • To investigate the role of CypA in the early stages of influenza virus infection.

Main Methods:

  • Established a 293T cell line with depleted endogenous CypA.
  • Assessed influenza virus replication, infectivity, and protein levels.
  • Investigated the effect of CypA on viral genome replication, transcription, and mRNA nuclear export.
  • Examined the impact of CypA on M1 protein degradation via the ubiquitin/proteasome pathway.

Main Results:

  • CypA was found to inhibit the initiation of influenza virus replication.
  • Influenza virus infectivity was significantly higher in cells lacking CypA.
  • CypA did not affect viral genome replication, transcription, or mRNA nuclear export.
  • CypA reduced viral protein levels by enhancing M1 protein degradation through the ubiquitin/proteasome pathway.

Conclusions:

  • CypA acts as a restriction factor for influenza virus replication.
  • The mechanism involves CypA-mediated acceleration of M1 protein degradation.
  • Targeting the CypA-M1 interaction could be a strategy for antiviral therapies.

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