Research Papers:

Inhibition of avian tumor virus replication by CCCH-type zinc finger antiviral protein

Mingjun Zhu, Xiaoqian Ma, Xiyao Cui, Jing Zhou, Chengui Li, Libo Huang, Yingli Shang and Ziqiang Cheng _

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Oncotarget. 2017; 8:58865-58871. https://doi.org/10.18632/oncotarget.19378

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Mingjun Zhu1, Xiaoqian Ma1, Xiyao Cui1, Jing Zhou1, Chengui Li1, Libo Huang1, Yingli Shang1 and Ziqiang Cheng1

1College of Veterinary Medicine, Shandong Agricultural University, Tai’an, 271018, China

Correspondence to:

Ziqiang Cheng, email: [email protected]

Keywords: chicken CCCH type zinc finger antiviral protein, avian leukosis virus subgroup J, overexpression, RNAi

Received: February 18, 2017     Accepted: July 12, 2017     Published: July 19, 2017


CCCH type zinc finger antiviral protein (ZAP) is a host restriction factor that inhibits the replication of a variety of viruses in mammals. However, little is known about its antiviral activity on avian tumor virus. Avian leukosis virus subgroup J (ALV-J), an oncogenic retrovirus, induces myelocytomas and various other tumors in meat and egg type chickens. Here, we identified a chicken ZAP (chZAP) that increased at early stage, and subsequently decreased after infection of ALV-J in DF-1 cells, indicating the inducible feature of the endogenous chZAP. To demonstrate the inhibitory effect on ALV-J replication by chZAP, we expressed exogenous chZAP by lentivirus based vectors in DF-1 cells that infected by ALV-J. The result showed that overexpression of chZAP significantly inhibited ALV-J replication at both mRNA level and protein level. Consequently, knockdown of endogenous chZAP by RNAi facilitated ALV-J replication in DF-1 cells. Further, we demonstrated that chZAP interacts with SU protein (encode by gp85 gene) of ALV-J in cytoplasm. Taken together, our results demonstrated that chZAP inhibits ALV-J by both mRNA and protein pathway and it may shed light on a novel antiviral approach in poultry.

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