Research Papers:

Newcastle disease virus-induced autophagy mediates antiapoptotic signaling responses in vitro and in vivo

Yinfeng Kang _, Runyu Yuan, Bin Xiang, Xiaqiong Zhao, Pei Gao, Xu Dai, Ming Liao and Tao Ren

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Oncotarget. 2017; 8:73981-73993. https://doi.org/10.18632/oncotarget.18169

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Yinfeng Kang1,2,3,*, Runyu Yuan1,3,4,*, Bin Xiang1,3, Xiaqiong Zhao1,3, Pei Gao1,3, Xu Dai1,3, Ming Liao1,3 and Tao Ren1,3

1College of Veterinary Medicine, Key Laboratory of Zoonosis Prevention and Control of Guangdong Province, South China Agricultural University, Guangzhou, 510642, China

2State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Department of Experimental Research, Sun Yat-sen University Cancer Center, Guangzhou, 510060, China

3Key Laboratory of Animal Vaccine Development, Ministry of Agriculture, Guangzhou, 510642, China

4Key Laboratory for Repository and Application of Pathogenic Microbiology, Research Center for Pathogens Detection Technology of Emerging Infectious Diseases, Guangdong Provincial Center for Disease Control and Prevention, Guangzhou, 511430, China

*These authors contributed equally to this work

Correspondence to:

Yinfeng Kang, email: [email protected]

Tao Ren, email: [email protected]

Keywords: Newcastle disease virus, autophagy, apoptosis, relationship, replication

Received: February 09, 2017     Accepted: May 12, 2017     Published: May 25, 2017


In this study, we investigated the role of autophagy and apoptosis in Newcastle disease virus (NDV)-infected chicken cells and tissues. NDV-infected and starvation-induced chick embryo fibroblasts (CEF) cells showed higher autophagosome formation than mock-infected CEF cells on transmission electron microscopy. The NDV-infected CEF cells showed enhanced conversion of microtubule-associated protein 1 light chain 3-I (LC3-I) to LC3-II and degradation of p62/SQSTM1. The diminished conversion of LC3-I to LC3-II and cleaved caspase 3 and poly (ADP-ribose) polymerase (PARP) in ultraviolet-inactivated NDV-infected cells suggested that autophagosome formation was necessary for NDV replication. Inhibition of autophagy by chloroquine (CQ) enhanced apoptosis resulting in increased cleavage of caspase 3 and PARP and AnnexinV/propidium iodide staining. Autophagy induction by rapamycin resulted in upregulation of all autophagy-related genes except Beclin 1, anti-apoptosis factors, and proinflammatory cytokines in the NDV-infected spleen and lung tissues. Subsequently, decreased apoptosis was observed in NDV-infected spleens and lungs than mock-infected organs. The pan-caspase inhibitor ZVAD-FMK promoted conversion of LC3-I to LC3-II, the degradation of p62/SQSTM1, NDV replication and cell viability by inhibiting apoptosis. Our study demonstrates that apoptosis inhibition enhances autophagy and promoted cell survival and NDV replication.

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