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Updated: Mar 31, 2026

Affinity Purification of Influenza Virus Ribonucleoprotein Complexes from the Chromatin of Infected Cells
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Proton Channel Activity of Influenza A Virus Matrix Protein 2 Contributes to Autophagy Arrest

Yizhong Ren1, Chufang Li2, Liqiang Feng3

  • 1School of Life Sciences, University of Science and Technology of China, Hefei, Anhui, China State Key Laboratory of Respiratory Disease Guangzhou Institutes of Biomedicine and Health, Guangzhou, Guangdong, China.

Journal of Virology
|October 16, 2015
PubMed

Insights

Influenza A virus halts autophagy by accumulating autophagosomes. Amantadine, an antiviral, inhibits this process by targeting the M2 protein

Area of Science:

  • Virology
  • Cell Biology
  • Autophagy Research

Background:

  • Influenza A virus infection is known to disrupt cellular processes.
  • Autophagy, a cellular degradation pathway, is often arrested during viral infections, leading to autophagosome accumulation.

Purpose of the Study:

  • To investigate the mechanism by which influenza A virus arrests autophagy.
  • To determine the role of the M2 protein in autophagy arrest.

Main Methods:

  • Studying autophagosome accumulation in influenza A virus-infected cells.
  • Utilizing amantadine, a proton channel inhibitor, to observe its effect on autophagosome accumulation.
  • Examining cells infected with amantadine-sensitive influenza A virus or expressing the M2 protein.

Main Results:

  • Influenza A virus infection leads to the accumulation of autophagosomes.
  • Amantadine treatment inhibited autophagosome accumulation in infected cells.
  • This inhibition was observed in cells infected with amantadine-sensitive viruses or expressing the M2 protein.

Conclusions:

  • The M2 protein's proton channel activity is implicated in blocking autophagosome-lysosome fusion.
  • This blockage is a potential key mechanism for influenza A virus-induced autophagy arrest.

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