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    Rights statement: © 2015 The Authors. Liver International Published by John Wiley & Sons Ltd This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

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Viral genotype correlates with distinct liver gene transcription signatures in chronic hepatitis C virus infection

Research output: Contribution to Journal/MagazineJournal articlepeer-review

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Viral genotype correlates with distinct liver gene transcription signatures in chronic hepatitis C virus infection. / Robinson, Mark W.; Aranday-Cortes, Elihu; Gatherer, Derek; Swann, Rachael; Liefhebber, Jolanda M. P.; Filipe, Ana Da Silva; Sigruener, Alex; Barclay, Stephen T.; Mills, Peter R.; Patel, Arvind H.; McLauchlan, John.

In: Liver International, Vol. 35, No. 10, 10.2015, p. 2256-2264.

Research output: Contribution to Journal/MagazineJournal articlepeer-review

Harvard

Robinson, MW, Aranday-Cortes, E, Gatherer, D, Swann, R, Liefhebber, JMP, Filipe, ADS, Sigruener, A, Barclay, ST, Mills, PR, Patel, AH & McLauchlan, J 2015, 'Viral genotype correlates with distinct liver gene transcription signatures in chronic hepatitis C virus infection', Liver International, vol. 35, no. 10, pp. 2256-2264. https://doi.org/10.1111/liv.12830

APA

Robinson, M. W., Aranday-Cortes, E., Gatherer, D., Swann, R., Liefhebber, J. M. P., Filipe, A. D. S., Sigruener, A., Barclay, S. T., Mills, P. R., Patel, A. H., & McLauchlan, J. (2015). Viral genotype correlates with distinct liver gene transcription signatures in chronic hepatitis C virus infection. Liver International, 35(10), 2256-2264. https://doi.org/10.1111/liv.12830

Vancouver

Robinson MW, Aranday-Cortes E, Gatherer D, Swann R, Liefhebber JMP, Filipe ADS et al. Viral genotype correlates with distinct liver gene transcription signatures in chronic hepatitis C virus infection. Liver International. 2015 Oct;35(10):2256-2264. https://doi.org/10.1111/liv.12830

Author

Robinson, Mark W. ; Aranday-Cortes, Elihu ; Gatherer, Derek ; Swann, Rachael ; Liefhebber, Jolanda M. P. ; Filipe, Ana Da Silva ; Sigruener, Alex ; Barclay, Stephen T. ; Mills, Peter R. ; Patel, Arvind H. ; McLauchlan, John. / Viral genotype correlates with distinct liver gene transcription signatures in chronic hepatitis C virus infection. In: Liver International. 2015 ; Vol. 35, No. 10. pp. 2256-2264.

Bibtex

@article{fcff1115328e4007a08c0f0ce73a6c15,
title = "Viral genotype correlates with distinct liver gene transcription signatures in chronic hepatitis C virus infection",
abstract = "BACKGROUND: Chronic hepatitis C virus (HCV) infection of the liver with either genotype 1 or genotype 3 gives rise to distinct pathologies, and the two viral genotypes respond differently to antiviral therapy.METHODS: To understand these clinical differences, we compared gene transcription profiles in liver biopsies from patients infected with either gt1 or gt3, and uninfected controls.RESULTS: Gt1-infected biopsies displayed elevated levels of transcripts regulated by type I and type III interferons (IFN), including genes that predict response to IFN-α therapy. In contrast, genes controlled by IFN-γ were induced in gt3-infected biopsies. Moreover, IFN-γ levels were higher in gt3-infected biopsies. Analysis of hepatocyte-derived cell lines confirmed that the genes upregulated in gt3 infection were preferentially induced by IFN-γ. The transcriptional profile of gt3 infection was unaffected by IFNL4 polymorphisms, providing a rationale for the reduced predictive power of IFNL genotyping in gt3-infected patients.CONCLUSIONS: The interactions between HCV genotypes 1 and 3 and hepatocytes are distinct. These unique interactions provide avenues to explore the biological mechanisms that drive viral genotype-specific differences in disease progression and treatment response. A greater understanding of the distinct host-pathogen interactions of the different HCV genotypes is required to facilitate optimal management of HCV infection.",
keywords = "genotype, HCV, interferon, ISGs, transcriptomics",
author = "Robinson, {Mark W.} and Elihu Aranday-Cortes and Derek Gatherer and Rachael Swann and Liefhebber, {Jolanda M. P.} and Filipe, {Ana Da Silva} and Alex Sigruener and Barclay, {Stephen T.} and Mills, {Peter R.} and Patel, {Arvind H.} and John McLauchlan",
note = "{\textcopyright} 2015 The Authors. Liver International Published by John Wiley & Sons Ltd This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. ",
year = "2015",
month = oct,
doi = "10.1111/liv.12830",
language = "English",
volume = "35",
pages = "2256--2264",
journal = "Liver International",
issn = "1478-3223",
publisher = "Wiley-Blackwell",
number = "10",

}

RIS

TY - JOUR

T1 - Viral genotype correlates with distinct liver gene transcription signatures in chronic hepatitis C virus infection

AU - Robinson, Mark W.

AU - Aranday-Cortes, Elihu

AU - Gatherer, Derek

AU - Swann, Rachael

AU - Liefhebber, Jolanda M. P.

AU - Filipe, Ana Da Silva

AU - Sigruener, Alex

AU - Barclay, Stephen T.

AU - Mills, Peter R.

AU - Patel, Arvind H.

AU - McLauchlan, John

N1 - © 2015 The Authors. Liver International Published by John Wiley & Sons Ltd This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

PY - 2015/10

Y1 - 2015/10

N2 - BACKGROUND: Chronic hepatitis C virus (HCV) infection of the liver with either genotype 1 or genotype 3 gives rise to distinct pathologies, and the two viral genotypes respond differently to antiviral therapy.METHODS: To understand these clinical differences, we compared gene transcription profiles in liver biopsies from patients infected with either gt1 or gt3, and uninfected controls.RESULTS: Gt1-infected biopsies displayed elevated levels of transcripts regulated by type I and type III interferons (IFN), including genes that predict response to IFN-α therapy. In contrast, genes controlled by IFN-γ were induced in gt3-infected biopsies. Moreover, IFN-γ levels were higher in gt3-infected biopsies. Analysis of hepatocyte-derived cell lines confirmed that the genes upregulated in gt3 infection were preferentially induced by IFN-γ. The transcriptional profile of gt3 infection was unaffected by IFNL4 polymorphisms, providing a rationale for the reduced predictive power of IFNL genotyping in gt3-infected patients.CONCLUSIONS: The interactions between HCV genotypes 1 and 3 and hepatocytes are distinct. These unique interactions provide avenues to explore the biological mechanisms that drive viral genotype-specific differences in disease progression and treatment response. A greater understanding of the distinct host-pathogen interactions of the different HCV genotypes is required to facilitate optimal management of HCV infection.

AB - BACKGROUND: Chronic hepatitis C virus (HCV) infection of the liver with either genotype 1 or genotype 3 gives rise to distinct pathologies, and the two viral genotypes respond differently to antiviral therapy.METHODS: To understand these clinical differences, we compared gene transcription profiles in liver biopsies from patients infected with either gt1 or gt3, and uninfected controls.RESULTS: Gt1-infected biopsies displayed elevated levels of transcripts regulated by type I and type III interferons (IFN), including genes that predict response to IFN-α therapy. In contrast, genes controlled by IFN-γ were induced in gt3-infected biopsies. Moreover, IFN-γ levels were higher in gt3-infected biopsies. Analysis of hepatocyte-derived cell lines confirmed that the genes upregulated in gt3 infection were preferentially induced by IFN-γ. The transcriptional profile of gt3 infection was unaffected by IFNL4 polymorphisms, providing a rationale for the reduced predictive power of IFNL genotyping in gt3-infected patients.CONCLUSIONS: The interactions between HCV genotypes 1 and 3 and hepatocytes are distinct. These unique interactions provide avenues to explore the biological mechanisms that drive viral genotype-specific differences in disease progression and treatment response. A greater understanding of the distinct host-pathogen interactions of the different HCV genotypes is required to facilitate optimal management of HCV infection.

KW - genotype

KW - HCV

KW - interferon

KW - ISGs

KW - transcriptomics

U2 - 10.1111/liv.12830

DO - 10.1111/liv.12830

M3 - Journal article

C2 - 25800823

VL - 35

SP - 2256

EP - 2264

JO - Liver International

JF - Liver International

SN - 1478-3223

IS - 10

ER -