CXCL10 is produced in hepatitis A virus-infected cells in an IRF3-dependent but IFN-independent manner

Abstract Acute hepatitis A caused by hepatitis A virus (HAV) infection is accompanied by severe liver injury in adult patients, and the liver injury is associated with the production of chemokines. Herein, we investigated the mechanism of how HAV infection induces the production of CXCR3 and CCR5 ch...

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Autores principales:	Pil Soo Sung, Seon-Hui Hong, Jeewon Lee, Su-Hyung Park, Seung Kew Yoon, Woo Jin Chung, Eui-Cheol Shin
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/1bb8a9aa06fb436e8c8b0745ea72679e
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spelling	oai:doaj.org-article:1bb8a9aa06fb436e8c8b0745ea72679e2021-12-02T16:06:40ZCXCL10 is produced in hepatitis A virus-infected cells in an IRF3-dependent but IFN-independent manner10.1038/s41598-017-06784-x2045-2322https://doaj.org/article/1bb8a9aa06fb436e8c8b0745ea72679e2017-07-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-06784-xhttps://doaj.org/toc/2045-2322Abstract Acute hepatitis A caused by hepatitis A virus (HAV) infection is accompanied by severe liver injury in adult patients, and the liver injury is associated with the production of chemokines. Herein, we investigated the mechanism of how HAV infection induces the production of CXCR3 and CCR5 chemokines, such as CXCL10, CCL4 and CCL5. The production of CXCL10, CCL4 and CCL5 was markedly increased by HAV (HM-175/18f) infection in the culture of primary human hepatocytes and HepG2 cells. In particular, CXCL10 was produced in HAV-infected cells, not in neighboring uninfected cells. Moreover, these chemokines were significantly increased in the sera of acute hepatitis A patients. The production of IFN-λs was also robustly induced by HAV infection, and the blocking of secreted IFN-λs partially abrogated the production of CCL4 and CCL5 in HAV-infected cells. However, CXCL10 production was not decreased by the blocking of IFN-λs. Instead, CXCL10 production was reduced by silencing the expression of RIG-I-like receptor (RLR) signal molecules, such as mitochondrial antiviral signaling protein and interferon regulatory factor 3, in HAV-infected cells. In conclusion, HAV infection strongly induces the production of helper 1 T cell-associated chemokines, particularly CXCL10 via RLR signaling, even without secreted IFNs.Pil Soo SungSeon-Hui HongJeewon LeeSu-Hyung ParkSeung Kew YoonWoo Jin ChungEui-Cheol ShinNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-12 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Pil Soo Sung Seon-Hui Hong Jeewon Lee Su-Hyung Park Seung Kew Yoon Woo Jin Chung Eui-Cheol Shin CXCL10 is produced in hepatitis A virus-infected cells in an IRF3-dependent but IFN-independent manner
description	Abstract Acute hepatitis A caused by hepatitis A virus (HAV) infection is accompanied by severe liver injury in adult patients, and the liver injury is associated with the production of chemokines. Herein, we investigated the mechanism of how HAV infection induces the production of CXCR3 and CCR5 chemokines, such as CXCL10, CCL4 and CCL5. The production of CXCL10, CCL4 and CCL5 was markedly increased by HAV (HM-175/18f) infection in the culture of primary human hepatocytes and HepG2 cells. In particular, CXCL10 was produced in HAV-infected cells, not in neighboring uninfected cells. Moreover, these chemokines were significantly increased in the sera of acute hepatitis A patients. The production of IFN-λs was also robustly induced by HAV infection, and the blocking of secreted IFN-λs partially abrogated the production of CCL4 and CCL5 in HAV-infected cells. However, CXCL10 production was not decreased by the blocking of IFN-λs. Instead, CXCL10 production was reduced by silencing the expression of RIG-I-like receptor (RLR) signal molecules, such as mitochondrial antiviral signaling protein and interferon regulatory factor 3, in HAV-infected cells. In conclusion, HAV infection strongly induces the production of helper 1 T cell-associated chemokines, particularly CXCL10 via RLR signaling, even without secreted IFNs.
format	article
author	Pil Soo Sung Seon-Hui Hong Jeewon Lee Su-Hyung Park Seung Kew Yoon Woo Jin Chung Eui-Cheol Shin
author_facet	Pil Soo Sung Seon-Hui Hong Jeewon Lee Su-Hyung Park Seung Kew Yoon Woo Jin Chung Eui-Cheol Shin
author_sort	Pil Soo Sung
title	CXCL10 is produced in hepatitis A virus-infected cells in an IRF3-dependent but IFN-independent manner
title_short	CXCL10 is produced in hepatitis A virus-infected cells in an IRF3-dependent but IFN-independent manner
title_full	CXCL10 is produced in hepatitis A virus-infected cells in an IRF3-dependent but IFN-independent manner
title_fullStr	CXCL10 is produced in hepatitis A virus-infected cells in an IRF3-dependent but IFN-independent manner
title_full_unstemmed	CXCL10 is produced in hepatitis A virus-infected cells in an IRF3-dependent but IFN-independent manner
title_sort	cxcl10 is produced in hepatitis a virus-infected cells in an irf3-dependent but ifn-independent manner
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/1bb8a9aa06fb436e8c8b0745ea72679e
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CXCL10 is produced in hepatitis A virus-infected cells in an IRF3-dependent but IFN-independent manner

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