Virus Details


VHFID1502

Host Factor Information

Gene Name ZC3HAV1
HF Protein Name Zinc finger CCCH-type containing, antiviral 1
HF Function Inhibits avian tumor virus replication
Uniprot ID F1NWL9
Protein Sequence View Fasta Sequence
NCBI Gene ID N.A.
Host Factor (HF) Name in Paper ZAP
Gene synonyms N.A.
Ensemble Gene ID ENSGALG00000013911
Ensemble Transcript ENSGALT00000022552
KEGG ID Go to KEGG Database
Gene Ontology ID(s) GO:0003950, GO:0046872,
MINT ID N.A.
STRING Click to see interaction map
GWAS Analysis Click to see gwas analysis
OMIM ID N.A.
PANTHER ID N.A.
PDB ID(s) N.A.,
pfam ID PF00644, PF02825,
Drug Bank ID N.A.,
ChEMBL ID N.A.
Organism Gallus gallus (Chicken)

Pathogen Information

Virus Name Avian leukosis virus
Virus Short Name ALV
Order Unassigned
Virus Family Retroviridae
Virus Subfamily Orthoretrovirinae
Genus Alpharetrovirus
Species Avian leukosis virus
Host Vertebrates
Cell Tropism N.A.
Associated Disease Malignancies
Mode of Transmission N.A.
VIPR DB link N.A.
ICTV DB link https://talk.ictvonline.org/ictv-reports/ictv_9th_report/reverse-transcribing-dna-and-rna-viruses-2011/w/rt_viruses/161/retroviridae
Virus Host DB link http://www.genome.jp/virushostdb/view/?virus_lineage=Retroviridae

Publication Information

Paper Title Inhibition of avian tumor virus replication by CCCH-type zinc nger antiviral protein
Author's Name Mingjun Zhu, Xiaoqian Ma, Xiyao Cui, Jing Zhou, Chengui Li, Libo Huang, Yingli Shang and Ziqiang Cheng
Journal Name Oncotarget
Pubmed ID 28938603
Abstract 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.
Used Model DF-1 and 293T cells
DOI 10.18632/oncotarget.19378