Interferon-λ4 (IFNL4) transcript expression in human liver tissue samples

Eradication of hepatitis C virus (HCV) infection, both spontaneous and treatment-induced, is marked by the wildtype allele C of a single nucleotide polymorphism upstream of the IL28B gene, rs12979860. This favorable allele was recently described to be in linkage disequilibrium with the wildtype alle...

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Bibliographic Details
Published in:PloS one 2013-12, Vol.8 (12), p.e84026-e84026
Main Authors: Amanzada, Ahmad, Kopp, Waltraut, Spengler, Ulrich, Ramadori, Giuliano, Mihm, Sabine
Format: Article
Language:English
Subjects:
Adult
Age
Alleles
Biopsy
Blood & organ donations
Cohort Studies
Cytokines
Deoxyribonucleic acid
DNA
DNA methylation
Endocrinology
Etiology
Female
Gastroenterology
Gene expression
Gene Expression Regulation
Gene polymorphism
Genotypes
Hepacivirus - physiology
Hepatitis
Hepatitis B
Hepatitis B, Chronic - genetics
Hepatitis B, Chronic - pathology
Hepatitis C
Hepatitis C, Chronic - genetics
Hepatitis C, Chronic - pathology
Hepatocytes
Hepatology
Humans
In vivo methods and tests
Infections
Interferon
Interleukins - genetics
Linkage disequilibrium
Liver
Liver - metabolism
Liver - pathology
Liver - virology
Liver diseases
Male
Middle Aged
Patients
Poly (I:C)
Polymorphism
Ribonucleic acid
RNA
RNA, Messenger - genetics
RNA, Messenger - metabolism
Single-nucleotide polymorphism
Substance abuse treatment
Transcription activation
Viral infections
Viral Load
Viruses
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Summary:Eradication of hepatitis C virus (HCV) infection, both spontaneous and treatment-induced, is marked by the wildtype allele C of a single nucleotide polymorphism upstream of the IL28B gene, rs12979860. This favorable allele was recently described to be in linkage disequilibrium with the wildtype allele TT of a dinucleotide polymorphism, ss469415590, located within a new protein-coding gene. While the TT allele introduces a frame-shift and disrupts the open reading frame, only the variant allele, ΔG, creates a novel type III interferon (IFN) protein, IFN-λ4/IFNL4. Absence of IFNL4 is thus supposed to favor resolution of HCV infection. As to date IFNL4 mRNA transcription has only been investigated in polyI:C-stimulated primary human hepatocytes and not yet in HCV infection in vivo, this study analyzed IFNL4 mRNA expression in human liver biopsy specimens. Samples were obtained from patients with a broad panel of disorders including no liver disease, liver diseases of non-viral etiology, chronic hepatitis B and chronic hepatitis C. Hepatic IFNL4 transcripts were detectable exclusively in a subgroup of chronic hepatitis C patients (24/45). Their amounts were positively related to liver HCV RNA copy numbers (p = 0.0023, r = 0.56) suggesting that the hepatic viral load influences IFNL4 transcription irrespective of IFNL4 governing genotype. Both, the IFNL4 creating allele ΔG (p
ISSN:1932-6203
1932-6203
DOI:10.1371/journal.pone.0084026