Characterization of HCV interactions with Toll-like receptors and RIG-I in liver cells.
The aim of this study was to examine the mechanisms of IFN induction and viral escape. In order to accomplish the goal we compared our new hepatoma cell line LH86, which has intact TLR3 and RIG-I expression and responds to HCV by inducing IFN, with Huh7.5 cells which lack those features.The initial...
| Main Authors: | , , , , , , |
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| Format: | Article |
| Language: | English |
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Public Library of Science (PLoS)
2011-01-01
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| Series: | PLoS ONE |
| Online Access: | http://europepmc.org/articles/PMC3117876?pdf=render |
| _version_ | 1819198414002323456 |
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| author | Erika A Eksioglu Haizhen Zhu Lilly Bayouth Jennifer Bess Hong-Yan Liu David R Nelson Chen Liu |
| author_facet | Erika A Eksioglu Haizhen Zhu Lilly Bayouth Jennifer Bess Hong-Yan Liu David R Nelson Chen Liu |
| author_sort | Erika A Eksioglu |
| collection | DOAJ |
| description | The aim of this study was to examine the mechanisms of IFN induction and viral escape. In order to accomplish the goal we compared our new hepatoma cell line LH86, which has intact TLR3 and RIG-I expression and responds to HCV by inducing IFN, with Huh7.5 cells which lack those features.The initial interaction of LH86 cells, Huh7.5 cells or their transfected counter parts (LH86 siRIG-I, siTLR3 or siTLR7 and Huh7.5 RIG-I, TLR3 or TLR7) after infection with HCV (strain JFH-1) was studied by measuring the expression levels of IFNβ, TRAIL, DR4, DR5 and their correlation to viral replication.HCV replicating RNA induces IFN in LH86 cells. The IFN induction system is functional in LH86, and the expression of the RIG-I and TLR3 in LH86 is comparable to the primary hepatocytes. Both proteins appear to play important roles in suppression of viral replication. We found that innate immunity against HCV is associated with the induction of apoptosis by RIG-I through the TRAIL pathway and the establishment of an antiviral state by TLR3. HCV envelope proteins interfere with the expression of TLR3 and RIG-I.These findings correlate with the lower expression level of PRRs in HCV chronic patients and highlight the importance of the PRRs in the initial interaction of the virus and its host cells. This work represents a novel mechanism of viral pathogenesis for HCV and demonstrates the role of PRRs in viral infection. |
| first_indexed | 2024-12-23T03:00:03Z |
| format | Article |
| id | doaj.art-6e86694c68e44d069f2feb0ca56b2973 |
| institution | Directory Open Access Journal |
| issn | 1932-6203 |
| language | English |
| last_indexed | 2024-12-23T03:00:03Z |
| publishDate | 2011-01-01 |
| publisher | Public Library of Science (PLoS) |
| record_format | Article |
| series | PLoS ONE |
| spelling | doaj.art-6e86694c68e44d069f2feb0ca56b29732022-12-21T18:02:27ZengPublic Library of Science (PLoS)PLoS ONE1932-62032011-01-0166e2118610.1371/journal.pone.0021186Characterization of HCV interactions with Toll-like receptors and RIG-I in liver cells.Erika A EksiogluHaizhen ZhuLilly BayouthJennifer BessHong-Yan LiuDavid R NelsonChen LiuThe aim of this study was to examine the mechanisms of IFN induction and viral escape. In order to accomplish the goal we compared our new hepatoma cell line LH86, which has intact TLR3 and RIG-I expression and responds to HCV by inducing IFN, with Huh7.5 cells which lack those features.The initial interaction of LH86 cells, Huh7.5 cells or their transfected counter parts (LH86 siRIG-I, siTLR3 or siTLR7 and Huh7.5 RIG-I, TLR3 or TLR7) after infection with HCV (strain JFH-1) was studied by measuring the expression levels of IFNβ, TRAIL, DR4, DR5 and their correlation to viral replication.HCV replicating RNA induces IFN in LH86 cells. The IFN induction system is functional in LH86, and the expression of the RIG-I and TLR3 in LH86 is comparable to the primary hepatocytes. Both proteins appear to play important roles in suppression of viral replication. We found that innate immunity against HCV is associated with the induction of apoptosis by RIG-I through the TRAIL pathway and the establishment of an antiviral state by TLR3. HCV envelope proteins interfere with the expression of TLR3 and RIG-I.These findings correlate with the lower expression level of PRRs in HCV chronic patients and highlight the importance of the PRRs in the initial interaction of the virus and its host cells. This work represents a novel mechanism of viral pathogenesis for HCV and demonstrates the role of PRRs in viral infection.http://europepmc.org/articles/PMC3117876?pdf=render |
| spellingShingle | Erika A Eksioglu Haizhen Zhu Lilly Bayouth Jennifer Bess Hong-Yan Liu David R Nelson Chen Liu Characterization of HCV interactions with Toll-like receptors and RIG-I in liver cells. PLoS ONE |
| title | Characterization of HCV interactions with Toll-like receptors and RIG-I in liver cells. |
| title_full | Characterization of HCV interactions with Toll-like receptors and RIG-I in liver cells. |
| title_fullStr | Characterization of HCV interactions with Toll-like receptors and RIG-I in liver cells. |
| title_full_unstemmed | Characterization of HCV interactions with Toll-like receptors and RIG-I in liver cells. |
| title_short | Characterization of HCV interactions with Toll-like receptors and RIG-I in liver cells. |
| title_sort | characterization of hcv interactions with toll like receptors and rig i in liver cells |
| url | http://europepmc.org/articles/PMC3117876?pdf=render |
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