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Updated: Sep 17, 2025

Affinity Purification of Influenza Virus Ribonucleoprotein Complexes from the Chromatin of Infected Cells
11:20

Affinity Purification of Influenza Virus Ribonucleoprotein Complexes from the Chromatin of Infected Cells

Published on: June 3, 2012

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Host cellular protein RAB33B facilitates influenza viral replication and modulates M2 trafficking by enhancing

Shaotang Ye1,2,3, Zhen Wang1, Gang Lu1

  • 1College of Veterinary Medicine, South China Agricultural University, Guangzhou, China.

Veterinary Research
|July 2, 2025
PubMed

Insights

Influenza A virus M2 protein hijacks host autophagy via RAB33B to enhance viral replication. This study reveals RAB33B

Area of Science:

  • Virology
  • Cell Biology
  • Molecular Biology

Background:

  • Influenza A virus (IAV) poses a significant global health risk.
  • The IAV M2 protein is vital for multiple stages of the viral life cycle.
  • IAV is known to disrupt host autophagy to promote its replication, but the exact mechanisms are unclear.

Purpose of the Study:

  • To elucidate the mechanisms by which IAV M2 manipulates host autophagy.
  • To identify host factors involved in IAV M2-mediated autophagy regulation.
  • To understand the role of these factors in viral replication.

Main Methods:

  • Analysis of cellular transcriptional responses to IAV M2 overexpression.
  • Identification and characterization of key host proteins involved in the process.
  • Investigating protein interactions and cellular trafficking pathways.

Main Results:

  • RAB GTPase protein RAB33B was identified as a key factor, significantly upregulated by IAV M2.
  • RAB33B enhances IAV replication by promoting autophagy.
  • Autophagy mediates the interaction between IAV M2, RAB33B, and LC3, facilitating M2 trafficking via autophagic vesicles.
  • ATG16L1 and TBC1D25 also contribute to IAV M2-induced autophagy and viral replication.

Conclusions:

  • RAB33B is essential for IAV M2 trafficking to the plasma membrane.
  • IAV M2 utilizes RAB33B-mediated autophagy to facilitate viral replication.
  • This reveals a novel mechanism of IAV M2 transport and highlights potential antiviral targets.
Keywords:
IAVM2 proteinRAB33Bautophagyhost–pathogen interactionmembrane trafficking

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