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Completion of the Entire Hepatitis C Virus Life Cycle in Vero Cells Derived from Monkey Kidney
A hepatitis C virus (HCV) cell culture system incorporating the JFH-1 strain and the human hepatoma cell line HuH-7 enabled the production of infectious HCV particles. Several host factors were identified as essential for HCV replication. Supplementation of these factors in nonhepatic human cell lin...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
American Society for Microbiology
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4916372/ https://www.ncbi.nlm.nih.gov/pubmed/27302754 http://dx.doi.org/10.1128/mBio.00273-16 |
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author | Murayama, Asako Sugiyama, Nao Wakita, Takaji Kato, Takanobu |
author_facet | Murayama, Asako Sugiyama, Nao Wakita, Takaji Kato, Takanobu |
author_sort | Murayama, Asako |
collection | PubMed |
description | A hepatitis C virus (HCV) cell culture system incorporating the JFH-1 strain and the human hepatoma cell line HuH-7 enabled the production of infectious HCV particles. Several host factors were identified as essential for HCV replication. Supplementation of these factors in nonhepatic human cell lines enabled HCV replication and particle production. Vero cells established from monkey kidney are commonly used for the production of vaccines against a variety of viruses. In this study, we aimed to establish a novel Vero cell line to reconstruct the HCV life cycle. Unmodified Vero cells did not allow HCV infection or replication. The expression of microRNA 122 (miR-122), an essential factor for HCV replication, is notably low in Vero cells. Therefore, we supplemented Vero cells with miR-122 and found that HCV replication was enhanced. However, Vero cells that expressed miR-122 still did not allow HCV infection. We supplemented HCV receptor molecules and found that scavenger receptor class B type I (SRBI) was essential for HCV infection in Vero cells. The supplementation of apolipoprotein E (ApoE), a host factor important for virus production, enabled the production of infectious virus in Vero cells. Finally, we created a Vero cell line that expressed the essential factors miR-122, SRBI, and ApoE; the entire HCV life cycle, including infection, replication, and infectious virus production, was completed in these cells. In conclusion, we demonstrated that miR-122, SRBI, and ApoE were necessary and sufficient for the completion of the entire HCV life cycle in nonhuman, nonhepatic Vero cells. |
format | Online Article Text |
id | pubmed-4916372 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | American Society for Microbiology |
record_format | MEDLINE/PubMed |
spelling | pubmed-49163722016-06-23 Completion of the Entire Hepatitis C Virus Life Cycle in Vero Cells Derived from Monkey Kidney Murayama, Asako Sugiyama, Nao Wakita, Takaji Kato, Takanobu mBio Research Article A hepatitis C virus (HCV) cell culture system incorporating the JFH-1 strain and the human hepatoma cell line HuH-7 enabled the production of infectious HCV particles. Several host factors were identified as essential for HCV replication. Supplementation of these factors in nonhepatic human cell lines enabled HCV replication and particle production. Vero cells established from monkey kidney are commonly used for the production of vaccines against a variety of viruses. In this study, we aimed to establish a novel Vero cell line to reconstruct the HCV life cycle. Unmodified Vero cells did not allow HCV infection or replication. The expression of microRNA 122 (miR-122), an essential factor for HCV replication, is notably low in Vero cells. Therefore, we supplemented Vero cells with miR-122 and found that HCV replication was enhanced. However, Vero cells that expressed miR-122 still did not allow HCV infection. We supplemented HCV receptor molecules and found that scavenger receptor class B type I (SRBI) was essential for HCV infection in Vero cells. The supplementation of apolipoprotein E (ApoE), a host factor important for virus production, enabled the production of infectious virus in Vero cells. Finally, we created a Vero cell line that expressed the essential factors miR-122, SRBI, and ApoE; the entire HCV life cycle, including infection, replication, and infectious virus production, was completed in these cells. In conclusion, we demonstrated that miR-122, SRBI, and ApoE were necessary and sufficient for the completion of the entire HCV life cycle in nonhuman, nonhepatic Vero cells. American Society for Microbiology 2016-06-14 /pmc/articles/PMC4916372/ /pubmed/27302754 http://dx.doi.org/10.1128/mBio.00273-16 Text en Copyright © 2016 Murayama et al. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution 4.0 International license (http://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Research Article Murayama, Asako Sugiyama, Nao Wakita, Takaji Kato, Takanobu Completion of the Entire Hepatitis C Virus Life Cycle in Vero Cells Derived from Monkey Kidney |
title | Completion of the Entire Hepatitis C Virus Life Cycle in Vero Cells Derived from Monkey Kidney |
title_full | Completion of the Entire Hepatitis C Virus Life Cycle in Vero Cells Derived from Monkey Kidney |
title_fullStr | Completion of the Entire Hepatitis C Virus Life Cycle in Vero Cells Derived from Monkey Kidney |
title_full_unstemmed | Completion of the Entire Hepatitis C Virus Life Cycle in Vero Cells Derived from Monkey Kidney |
title_short | Completion of the Entire Hepatitis C Virus Life Cycle in Vero Cells Derived from Monkey Kidney |
title_sort | completion of the entire hepatitis c virus life cycle in vero cells derived from monkey kidney |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4916372/ https://www.ncbi.nlm.nih.gov/pubmed/27302754 http://dx.doi.org/10.1128/mBio.00273-16 |
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