Identification of Keratin 23 as a Hepatitis C Virus-Induced Host Factor in the Human Liver.
Cast your vote
You can rate an item by clicking the amount of stars they wish to award to this item.
When enough users have cast their vote on this item, the average rating will also be shown.
Your vote was cast
Thank you for your feedback
Thank you for your feedback
Leber, Stefan L
Brown, Richard J P
Vondran, Florian W R
MetadataShow full item record
AbstractKeratin proteins form intermediate filaments, which provide structural support for many tissues. Multiple keratin family members are reported to be associated with the progression of liver disease of multiple etiologies. For example, keratin 23 (KRT23) was reported as a stress-inducible protein, whose expression levels correlate with the severity of liver disease. Hepatitis C virus (HCV) is a human pathogen that causes chronic liver diseases including fibrosis, cirrhosis, and hepatocellular carcinoma. However, a link between KRT23 and hepatitis C virus (HCV) infection has not been reported previously. In this study, we investigated KRT23 mRNA levels in datasets from liver biopsies of chronic hepatitis C (CHC) patients and in primary human hepatocytes experimentally infected with HCV, in addition to hepatoma cells. Interestingly, in each of these specimens, we observed an HCV-dependent increase of mRNA levels. Importantly, the KRT23 protein levels in patient plasma decreased upon viral clearance. Ectopic expression of KRT23 enhanced HCV infection; however, CRIPSPR/Cas9-mediated knockout did not show altered replication efficiency. Taken together, our study identifies KRT23 as a novel, virus-induced host-factor for hepatitis C virus.
CitationCells. 2019 Jun 18;8(6). pii: cells8060610. doi: 10.3390/cells8060610.
AffiliationTWINCORE, Zentrum für experimentelle und klinische Infektionsforschung GmbH,Feodor-Lynen Str. 7, 30625 Hannover, Germany.
The following license files are associated with this item:
Except where otherwise noted, this item's license is described as Attribution-NonCommercial-ShareAlike 4.0 International
- New Mechanism of Hepatic Fibrogenesis: Hepatitis C Virus Infection Induces Transforming Growth Factor β1 Production through Glucose-Regulated Protein 94.
- Authors: Jee MH, Hong KY, Park JH, Lee JS, Kim HS, Lee SH, Jang SK
- Issue date: 2015 Dec 30
- N-Myc Downstream-Regulated Gene 1 Restricts Hepatitis C Virus Propagation by Regulating Lipid Droplet Biogenesis and Viral Assembly.
- Authors: Schweitzer CJ, Zhang F, Boyer A, Valdez K, Cam M, Liang TJ
- Issue date: 2018 Jan 15
- Nonstructural 3 Protein of Hepatitis C Virus Modulates the Tribbles Homolog 3/Akt Signaling Pathway for Persistent Viral Infection.
- Authors: Tran SC, Pham TM, Nguyen LN, Park EM, Lim YS, Hwang SB
- Issue date: 2016 Aug 15
- Autotaxin-lysophosphatidic acid receptor signalling regulates hepatitis C virus replication.
- Authors: Farquhar MJ, Humphreys IS, Rudge SA, Wilson GK, Bhattacharya B, Ciaccia M, Hu K, Zhang Q, Mailly L, Reynolds GM, Ashcroft M, Balfe P, Baumert TF, Roessler S, Wakelam MJO, McKeating JA
- Issue date: 2017 May
- Transcriptional suppression of miR-181c by hepatitis C virus enhances homeobox A1 expression.
- Authors: Mukherjee A, Shrivastava S, Bhanja Chowdhury J, Ray R, Ray RB
- Issue date: 2014 Jul