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Keratin 8 Mutations Were Associated With Susceptibility to Chronic Hepatitis B and Related Progression.
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- Author(s): Ye, Junzhao; Wu, Yanqin; Li, Minrui; Gong, Xiaorong; Zhong, Bihui
- Source:
Journal of Infectious Diseases; 2/1/2020, Vol. 221 Issue 3, p464-473, 10p- Subject Terms:
KERATIN; GAIN-of-function mutations; CHRONIC hepatitis B; LIVER failure; LOGISTIC regression analysis; DNA; HEPATITIS B virus; PROTEINS; DISEASE progression; RESEARCH; GENETIC mutation; LIVER tumors; RESEARCH methodology; HEPATITIS viruses; CIRRHOSIS of the liver; CASE-control method; EVALUATION research; MEDICAL cooperation; NUCLEOTIDES; COMPARATIVE studies; DISEASE susceptibility; GENES; EPITHELIAL cells; LONGITUDINAL method; DISEASE complications - Source:
- Additional Information
- Abstract:
Background: Keratin 8 and 18 (K8/K18) are the exclusively expressed keratins intermediate filaments pair in hepatocytes that protect against liver injuries and viral infection. We aimed to explore the genetic link between keratin variants and chronic hepatitis B virus (CHB) infection in a large cohort from a high-epidemic area.Methods: Genomic deoxyribonucleic acid was isolated from patients, and Sanger sequencing was applied to analyze variations in exon regions of K8/18. Biochemical and functional analysis of novel mutations was also performed.Results: The 713 participants comprised 173 healthy controls and 540 patients, which covered chronic hepatitis (n = 174), decompensated cirrhosis (n = 192), and primary liver carcinoma (n = 174). The frequency of mutations in K8/18 was significantly higher among patients than among controls (8.15% vs 0.58%, P < .001). Significant differences were found between the chronic hepatitis subgroup and controls in multiple comparisons (6.32% vs 0.58%, P = .006). All 21 missense mutations (3.89%) were detected in the keratin 8 (K8), including 4 novel conserved missense variants (R469C, R469H, A447V, and K483T). Multivariate logistic regression analysis demonstrated a higher risk of acute-on-chronic liver failure (ACLF) and missense variants (odds ratio = 4.38, P = .035). Transfection of these variants caused keratin network disruption in vivo.Conclusions: Novel K8 cytoskeleton-disrupting variants predispose toward ACLF in CHB. [ABSTRACT FROM AUTHOR] - Abstract: Copyright of Journal of Infectious Diseases is the property of Oxford University Press / USA and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
- Abstract:
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