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Subgroup J avian leukosis virus infection inhibits autophagy in DF-1 cells

Haixia Liu1, Weisheng Cao, Yuhao Li

  • 1College of Veterinary Medicine, South China Agricultural University, Guangzhou, People's Republic of China.

Virology Journal
|June 19, 2013
PubMed
Abstract

Insights

Subgroup J avian leukosis virus (ALV-J) infection suppresses autophagy in chicken DF-1 cells. Promoting autophagy reduced viral replication, while blocking autophagy enhanced it, revealing a novel host-pathogen interaction.

Area of Science:

  • Virology
  • Cell Biology
  • Immunology

Background:

  • Subgroup J avian leukosis virus (ALV-J) causes tumors in chickens.
  • ALV-J infection alters AKT activity and phosphorylation in DF-1 cells.
  • Host cell responses to ALV-J remain incompletely understood.

Purpose of the Study:

  • To investigate the impact of ALV-J infection on autophagy in chicken DF-1 cells.
  • To elucidate the role of autophagy in ALV-J replication.

Main Methods:

  • Monitoring of microtubule-associated protein 1 light chain 3-II (LC3-II) levels.
  • Fluorescence and transmission electron microscopy to assess autophagy.
  • Manipulation of autophagy using rapamycin and ATG5 knockout.

Main Results:

  • ALV-J infection led to significant autophagy inhibition in DF-1 cells.
  • Autophagy inhibition was confirmed by microscopy.
  • Promoting autophagy decreased ALV-J titers, while ATG5 knockout enhanced viral replication.

Conclusions:

  • ALV-J infection down-regulates autophagy during viral replication in DF-1 cells.
  • This study establishes a link between ALV-J and autophagy modulation.
  • Autophagy plays a role in controlling ALV-J replication.

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