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Porcine sapovirus replication is restricted by the type I interferon response in cell culture

Porcine sapovirus (PSaV) of the family Caliciviridae, is the only member of the genus Sapovirus with cell culture and reverse genetics systems. When combined with the piglet model, these approaches provide a system to understand the molecular basis of sapovirus pathogenesis. The replication of PSaV...

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Autores principales: Hosmillo, Myra, Sorgeloos, Frédéric, Hiraide, Rintaro, Lu, Jia, Goodfellow, Ian, Cho, Kyoung-Oh
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Society for General Microbiology 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4268822/
https://www.ncbi.nlm.nih.gov/pubmed/25304652
http://dx.doi.org/10.1099/vir.0.071365-0
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author Hosmillo, Myra
Sorgeloos, Frédéric
Hiraide, Rintaro
Lu, Jia
Goodfellow, Ian
Cho, Kyoung-Oh
author_facet Hosmillo, Myra
Sorgeloos, Frédéric
Hiraide, Rintaro
Lu, Jia
Goodfellow, Ian
Cho, Kyoung-Oh
author_sort Hosmillo, Myra
collection PubMed
description Porcine sapovirus (PSaV) of the family Caliciviridae, is the only member of the genus Sapovirus with cell culture and reverse genetics systems. When combined with the piglet model, these approaches provide a system to understand the molecular basis of sapovirus pathogenesis. The replication of PSaV in cell culture is, however, restricted, displaying an absolute requirement for bile acids and producing lower levels of infectious virus than other caliciviruses. The effect of bile acids has previously been linked to a reduction in the signal transducer and activator of transcription (STAT1)-mediated signalling pathway. In the current study, we observed that even in the presence of bile acids, PSaV replication in cell culture was restricted by soluble factors produced from infected cells. This effect was at least partially due to secreted IFN because treatment of cells with recombinant porcine IFN-β resulted in significantly reduced viral replication. Moreover, IFN-mediated signalling pathways (IFN, STAT1 and the 2′,5′-oligoadenylate synthetase) were activated during PSaV infection. Characterization of PSaV growth in cell lines deficient in their ability to induce or respond to IFN showed a 100–150-fold increase in infectious virus production, indicating that the primary role of bile acids was not the inactivation of the innate immune response. Furthermore, the use of IFN-deficient cell lines enabled more efficient recovery of PSaV from cDNA constructs. Overall, the highly efficient cell culture and reverse genetics system established here for PSaV highlighted the key role of the innate immune response in the restriction of PSaV infection and should greatly facilitate further molecular studies on sapovirus host–cell interactions.
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spelling pubmed-42688222015-01-01 Porcine sapovirus replication is restricted by the type I interferon response in cell culture Hosmillo, Myra Sorgeloos, Frédéric Hiraide, Rintaro Lu, Jia Goodfellow, Ian Cho, Kyoung-Oh J Gen Virol Animal Porcine sapovirus (PSaV) of the family Caliciviridae, is the only member of the genus Sapovirus with cell culture and reverse genetics systems. When combined with the piglet model, these approaches provide a system to understand the molecular basis of sapovirus pathogenesis. The replication of PSaV in cell culture is, however, restricted, displaying an absolute requirement for bile acids and producing lower levels of infectious virus than other caliciviruses. The effect of bile acids has previously been linked to a reduction in the signal transducer and activator of transcription (STAT1)-mediated signalling pathway. In the current study, we observed that even in the presence of bile acids, PSaV replication in cell culture was restricted by soluble factors produced from infected cells. This effect was at least partially due to secreted IFN because treatment of cells with recombinant porcine IFN-β resulted in significantly reduced viral replication. Moreover, IFN-mediated signalling pathways (IFN, STAT1 and the 2′,5′-oligoadenylate synthetase) were activated during PSaV infection. Characterization of PSaV growth in cell lines deficient in their ability to induce or respond to IFN showed a 100–150-fold increase in infectious virus production, indicating that the primary role of bile acids was not the inactivation of the innate immune response. Furthermore, the use of IFN-deficient cell lines enabled more efficient recovery of PSaV from cDNA constructs. Overall, the highly efficient cell culture and reverse genetics system established here for PSaV highlighted the key role of the innate immune response in the restriction of PSaV infection and should greatly facilitate further molecular studies on sapovirus host–cell interactions. Society for General Microbiology 2015-01 /pmc/articles/PMC4268822/ /pubmed/25304652 http://dx.doi.org/10.1099/vir.0.071365-0 Text en © 2015 The Authors http://creativecommons.org/licenses/by/2.5/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Animal
Hosmillo, Myra
Sorgeloos, Frédéric
Hiraide, Rintaro
Lu, Jia
Goodfellow, Ian
Cho, Kyoung-Oh
Porcine sapovirus replication is restricted by the type I interferon response in cell culture
title Porcine sapovirus replication is restricted by the type I interferon response in cell culture
title_full Porcine sapovirus replication is restricted by the type I interferon response in cell culture
title_fullStr Porcine sapovirus replication is restricted by the type I interferon response in cell culture
title_full_unstemmed Porcine sapovirus replication is restricted by the type I interferon response in cell culture
title_short Porcine sapovirus replication is restricted by the type I interferon response in cell culture
title_sort porcine sapovirus replication is restricted by the type i interferon response in cell culture
topic Animal
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4268822/
https://www.ncbi.nlm.nih.gov/pubmed/25304652
http://dx.doi.org/10.1099/vir.0.071365-0
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