| Gene Name | CTHRC1 |
| HF Protein Name | Collagen triple helix repeat-containing protein 1 |
| HF Function | Facilitates HBV replication |
| Uniprot ID | Q96CG8 |
| Protein Sequence | View Fasta Sequence |
| NCBI Gene ID | 115908 |
| Host Factor (HF) Name in Paper | CTHRC1 |
| Gene synonyms | N.A. |
| Ensemble Gene ID | ENSG00000164932 |
| Ensemble Transcript | ENST00000330295 [Q96CG8-1];ENST00000520337 [Q96CG8-3] |
| KEGG ID | Go to KEGG Database |
| Gene Ontology ID(s) | GO:0005109, GO:0005576, GO:0005578, GO:0005581, GO:0005615, GO:0005737, GO:0016477, GO:0017147, GO:0032092, GO:0033690, GO:0043932, GO:0045669, GO:0060071, GO:0060122, GO:0090090, GO:0090103, GO:0090177, |
| MINT ID | N.A. |
| STRING | Click to see interaction map |
| GWAS Analysis | Click to see gwas analysis |
| OMIM ID | 610635 |
| PANTHER ID | N.A. |
| PDB ID(s) | N.A., |
| pfam ID | N.A., |
| Drug Bank ID | N.A., |
| ChEMBL ID | N.A. |
| Organism | Homo sapiens (Human) |
| Virus Name | Hepatitis B virus |
| Virus Short Name | HBV |
| Order | Unassigned |
| Virus Family | Hepadnaviridae |
| Virus Subfamily | N.A. |
| Genus | Orthohepadnavirus |
| Species | Hepatitis B virus |
| Host | Human, mammals |
| Cell Tropism | Hepatocytes |
| Associated Disease | Hepatitis, hepatocellular carcinoma(chronic infections), cirrhosis |
| Mode of Transmission | Sexual contact, blood, maternal-neonatal |
| 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/155/hepadnaviridae |
| Virus Host DB link | N.A. |
| Paper Title | Hepatitis B virus hijacks CTHRC1 to evade host immunity and maintain replication |
| Author's Name | Lan Bai, Wei Zhang, Li Tan, Hongchuan Yang, Maolin Ge, Chengliang Zhu, Rui Zhang, Yanhua Cao, Junbo Chen, Zhen Luo Wenzhe Ho, Fang Liu, Kailang Wu, Jianguo Wu |
| Journal Name | Journal Of Molecular Cell Biology |
| Pubmed ID | 26180054 |
| Abstract | Hepatitis B virus (HBV) infection causes acute and chronic liver diseases, but is not directly cytopathic. Liver injury results from repeated attempts of the cellular immune response system to control the viral infection. Here, we investigate the roles of cellular factors and signaling pathways involved in the regulation of HBV replication to reveal the mechanism underlying HBV infection and pathogenesis. We show that collagen triple helix repeat containing 1 (CTHRC1) expression is elevated in HBV-infected patients and in HBV-transfected cells through epigenetic modification and transcriptional regulation. CTHRC1 facilitates HBV replication in cultured cells and BALB/c mice by activating the PKCalpha/ERK/JNK/c-Jun cascade to repress the IFN/JAK/STAT pathway. HBV-activated CTHRC1 downregulates the activity of type I interferon (IFN), the production of IFN-stimulated genes (ISGs), and the phosphorylation of signal transducer and activator of transcription 1/2 (STAT1/2), whereas it upregulates the phosphorylation and ubiquitination of type I IFN receptors (IFNARalpha/beta). Thus, our results show that HBV uses a novel mechanism to hijack cellular factors and signal cascades in order to evade host antiviral immunity and maintain persistent infection. We also demonstrate that CTHRC1 has a novel role in viral infection. |
| Used Model | HepG2, HepG2.2.15 and L02 cells |
| DOI | 10.1093/jmcb/mjv048 |
