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

Virol J. 2013 Jun 17:10:196. doi: 10.1186/1743-422X-10-196.

Abstract

Background: Subgroup J avian leukosis virus (ALV-J) infection can induce tumor-related diseases in chickens. Previous studies by our laboratory demonstrated that ALV-J infection of DF-1 cells resulted in altered activity and phosphorylation of AKT. However, little is known about the subsequent activation of host DF-1 cells.

Results: In the current study, autophagy inhibition was observed for ALV-J infected DF-1 cells. Our data showed that the autophagosome protein, microtubule-associated protein 1 light chain 3-II (LC3-II), was reduced considerably in DF-1 cells infected with active ALV-J, while no change was observed for cells infected with inactivated ALV-J. Autophagy inhibition was also confirmed by fluorescence microscopy and transmission electron microscopy. Interestingly, when autophagy was promoted by rapamycin, the titers of ALV-J replication were decreased, and the replication level of ALV-J was significantly enhanced when atg5 (autophagy-related gene 5) was knocked out.

Conclusions: These results suggested that ALV-J infection could down-regulate autophagy in DF-1 cells during viral replication. This study is the first to report on the relationship between ALV-J infection and autophagy in DF-1 cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Autophagy*
  • Avian Leukosis Virus / pathogenicity*
  • Avian Leukosis Virus / physiology*
  • Cell Line
  • Chickens
  • Host-Pathogen Interactions*
  • Microscopy, Electron, Transmission
  • Microscopy, Fluorescence
  • Microtubule-Associated Proteins / antagonists & inhibitors

Substances

  • Microtubule-Associated Proteins