Virus Details


VHFID3191

Host Factor Information

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

Pathogen Information

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.

Publication Information

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