Archives of Virology

, Volume 157, Issue 4, pp 661–668

Avian reovirus triggers autophagy in primary chicken fibroblast cells and Vero cells to promote virus production

Authors

    • Ministry of Education Key Lab for Avian Preventive MedicineCollege of Veterinary Medicine, Yangzhou University
    • College of Bioscience and BiotechnologyYangzhou University
  • Ke Jiang
    • Ministry of Education Key Lab for Avian Preventive MedicineCollege of Veterinary Medicine, Yangzhou University
  • Xiaorong Zhang
    • Ministry of Education Key Lab for Avian Preventive MedicineCollege of Veterinary Medicine, Yangzhou University
  • Miao Zhang
    • College of Bioscience and BiotechnologyYangzhou University
  • Zhizhi Zhou
    • College of Bioscience and BiotechnologyYangzhou University
  • Maozhi Hu
    • College of Bioscience and BiotechnologyYangzhou University
  • Rui Yang
    • Ministry of Education Key Lab for Avian Preventive MedicineCollege of Veterinary Medicine, Yangzhou University
  • Chenli Sun
    • Ministry of Education Key Lab for Avian Preventive MedicineCollege of Veterinary Medicine, Yangzhou University
    • Ministry of Education Key Lab for Avian Preventive MedicineCollege of Veterinary Medicine, Yangzhou University
Original Article

DOI: 10.1007/s00705-012-1226-x

Cite this article as:
Meng, S., Jiang, K., Zhang, X. et al. Arch Virol (2012) 157: 661. doi:10.1007/s00705-012-1226-x

Abstract

Avian reovirus (ARV) is an important cause of disease in poultry. Although ARV is known to induce apoptosis in infected cells, the interaction between ARV and its target cells requires further elucidation. In this report, we show that the ARV isolate strain GX/2010/1 induces autophagy in both Vero and primary chicken embryonic fibroblast (CEF) cells based on the appearance of an increased number of double-membrane vesicles, the presence of GFP-microtubule-associated protein 1 light chain 3 (GFP-LC3) dot formation, and the elevated production of LC3II. We further demonstrate that the class I phosphoinositide 3-kinase (PI3K)/Akt/mTOR pathway contributes to autophagic induction by ARV infection. Moreover, treatment of ARV-infected cells with the autophagy inducer rapamycin increased viral yields, while inhibition of the autophagosomal pathway using chloroquine led to a decrease in virus production. Altogether, our studies strongly suggest that autophagy may play a critical role in determining viral yield during ARV infection.

Copyright information

© Springer-Verlag 2012