Gene Name | CXCL16 |
HF Protein Name | C-X-C motif chemokine ligand 16 |
HF Function | Entry Receptor for virus |
Uniprot ID | F7CTX0 |
Protein Sequence | View Fasta Sequence |
NCBI Gene ID | 100061442 |
Host Factor (HF) Name in Paper | CXCL16 |
Gene synonyms | NA. |
Ensemble Gene ID | ENSECAG00000018406 |
Ensemble Transcript | ENSECAT00000019475; ENSECAP00000015940; ENSECAG00000018406 |
KEGG ID | Go to KEGG Database |
Gene Ontology ID(s) | N.A., |
MINT ID | N.A. |
STRING | Click to see interaction map |
GWAS Analysis | Click to see gwas analysis |
OMIM ID | N.A. |
PANTHER ID | PTHR14385 |
PDB ID(s) | N.A., |
pfam ID | N.A., |
Drug Bank ID | N.A., |
ChEMBL ID | N.A. |
Organism | Equus caballus |
Virus Name | Equine Arteritis Virus |
Virus Short Name | EAV |
Order | Nidovirales |
Virus Family | Arteriviridae |
Virus Subfamily | N.A. |
Genus | Equartevirus |
Species | Equine Arteritis Virus |
Host | Vertebrates |
Cell Tropism | Primarily lung macrophages and later in lymph nodes |
Associated Disease | Vascular lesions, fever, edema, abortion |
Mode of Transmission | Genital and respiratory tract secretions. |
VIPR DB link | N.A. |
ICTV DB link | https://talk.ictvonline.org/ictv-reports/ictv_9th_report/positive-sense-rna-viruses-2011/w/posrna_viruses/220/arteriviridae |
Virus Host DB link | N.A. |
Paper Title | Equine Arteritis Virus Uses Equine CXCL16 as an Entry Receptor |
Author's Name | Sanjay Sarkar, Lakshman Chelvarajan, Yun Young Go, Frank Cook, Sergey Artiushin, Shankar Mondal, Kelsi Anderson, John Eberth, Peter J. Timoney, Theodore S. Kalbfleisch, Ernest Bailey, Udeni B. R. Balasuriya |
Journal Name | Journal Of Virology |
Pubmed ID | 26764004 |
Abstract | Previous studies in our laboratory have identified equine CXCL16 (EqCXCL16) to be a candidate molecule and possible cell entry receptor for equine arteritis virus (EAV). In horses, the CXCL16 gene is located on equine chromosome 11 (ECA11) and encodes a glycosylated, type I transmembrane protein with 247 amino acids. Stable transfection of HEK-293T cells with plasmid DNA carrying EqCXCL16 (HEK-EqCXCL16 cells) increased the proportion of the cell population permissive to EAV infection from <3% to almost 100%. The increase in permissiveness was blocked either by transfection of HEK-EqCXCL16 cells with small interfering RNAs (siRNAs) directed against EqCXCL16 or by pretreatment with guinea pig polyclonal antibody against EqCXCL16 protein (Gp anti-EqCXCL16 pAb). Furthermore, using a virus overlay protein-binding assay (VOPBA) in combination with far-Western blotting, gradient-purified EAV particles were shown to bind directly to the EqCXCL16 protein in vitro. The binding of biotinylated virulent EAV strain Bucyrus at 4°C was significantly higher in HEK-EqCXCL16 cells than nontransfected HEK-293T cells. Finally, the results demonstrated that EAV preferentially infects subpopulations of horse CD14(+) monocytes expressing EqCXCL16 and that infection of these cells is significantly reduced by pretreatment with Gp anti-EqCXCL16 pAb. The collective data from this study provide confirmatory evidence that the transmembrane form of EqCXCL16 likely plays a major role in EAV host cell entry processes, possibly acting as a primary receptor molecule for this virus. |
Used Model | EECs cells |
DOI | 10.1128/JVI.02455-15 |