Capsid amino acids at positions 247 and 270 are involved in the virulence of betanodaviruses to European sea bass

Abstract European sea bass (Dicentrarchus labrax) is severely affected by nervous necrosis disease, caused by nervous necrosis virus (NNV). Two out of the four genotypes of this virus (red-spotted grouper nervous necrosis virus, RGNNV; and striped jack nervous necrosis virus, SJNNV) have been detect...

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Autores principales:	Patricia Moreno, Sandra Souto, Rocio Leiva-Rebollo, Juan J. Borrego, Isabel Bandín, M. Carmen Alonso
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2019
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/d98d9c344c924c87978d799a38e04c0f
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spelling	oai:doaj.org-article:d98d9c344c924c87978d799a38e04c0f2021-12-02T15:09:49ZCapsid amino acids at positions 247 and 270 are involved in the virulence of betanodaviruses to European sea bass10.1038/s41598-019-50622-12045-2322https://doaj.org/article/d98d9c344c924c87978d799a38e04c0f2019-10-01T00:00:00Zhttps://doi.org/10.1038/s41598-019-50622-1https://doaj.org/toc/2045-2322Abstract European sea bass (Dicentrarchus labrax) is severely affected by nervous necrosis disease, caused by nervous necrosis virus (NNV). Two out of the four genotypes of this virus (red-spotted grouper nervous necrosis virus, RGNNV; and striped jack nervous necrosis virus, SJNNV) have been detected in sea bass, although showing different levels of virulence to this fish species. Thus, sea bass is highly susceptible to RGNNV, whereas outbreaks caused by SJNNV have not been reported in this fish species. The role of the capsid protein (Cp) amino acids 247 and 270 in the virulence of a RGNNV isolate to sea bass has been evaluated by the generation of recombinant RGNNV viruses harbouring SJNNV-type amino acids in the above mentioned positions (Mut247Dl965, Mut270Dl965 and Mut247 + 270Dl965). Viral in vitro and in vivo replication, virus virulence and fish immune response triggered by these viruses have been analysed. Mutated viruses replicated on E-11 cells, although showing some differences compared to the wild type virus, suggesting that the mutations can affect the viral cell recognition and entry. In vivo, fish mortality caused by mutated viruses was 75% lower, and viral replication in sea bass brain was altered compared to non-mutated virus. Regarding sea bass immune response, mutated viruses triggered a lower induction of IFN I system and inflammatory response-related genes. Furthermore, mutations caused changes in viral serological properties (especially the mutation in amino acid 270), inducing higher seroconversion and changing antigen recognition.Patricia MorenoSandra SoutoRocio Leiva-RebolloJuan J. BorregoIsabel BandínM. Carmen AlonsoNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 9, Iss 1, Pp 1-11 (2019)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Patricia Moreno Sandra Souto Rocio Leiva-Rebollo Juan J. Borrego Isabel Bandín M. Carmen Alonso Capsid amino acids at positions 247 and 270 are involved in the virulence of betanodaviruses to European sea bass
description	Abstract European sea bass (Dicentrarchus labrax) is severely affected by nervous necrosis disease, caused by nervous necrosis virus (NNV). Two out of the four genotypes of this virus (red-spotted grouper nervous necrosis virus, RGNNV; and striped jack nervous necrosis virus, SJNNV) have been detected in sea bass, although showing different levels of virulence to this fish species. Thus, sea bass is highly susceptible to RGNNV, whereas outbreaks caused by SJNNV have not been reported in this fish species. The role of the capsid protein (Cp) amino acids 247 and 270 in the virulence of a RGNNV isolate to sea bass has been evaluated by the generation of recombinant RGNNV viruses harbouring SJNNV-type amino acids in the above mentioned positions (Mut247Dl965, Mut270Dl965 and Mut247 + 270Dl965). Viral in vitro and in vivo replication, virus virulence and fish immune response triggered by these viruses have been analysed. Mutated viruses replicated on E-11 cells, although showing some differences compared to the wild type virus, suggesting that the mutations can affect the viral cell recognition and entry. In vivo, fish mortality caused by mutated viruses was 75% lower, and viral replication in sea bass brain was altered compared to non-mutated virus. Regarding sea bass immune response, mutated viruses triggered a lower induction of IFN I system and inflammatory response-related genes. Furthermore, mutations caused changes in viral serological properties (especially the mutation in amino acid 270), inducing higher seroconversion and changing antigen recognition.
format	article
author	Patricia Moreno Sandra Souto Rocio Leiva-Rebollo Juan J. Borrego Isabel Bandín M. Carmen Alonso
author_facet	Patricia Moreno Sandra Souto Rocio Leiva-Rebollo Juan J. Borrego Isabel Bandín M. Carmen Alonso
author_sort	Patricia Moreno
title	Capsid amino acids at positions 247 and 270 are involved in the virulence of betanodaviruses to European sea bass
title_short	Capsid amino acids at positions 247 and 270 are involved in the virulence of betanodaviruses to European sea bass
title_full	Capsid amino acids at positions 247 and 270 are involved in the virulence of betanodaviruses to European sea bass
title_fullStr	Capsid amino acids at positions 247 and 270 are involved in the virulence of betanodaviruses to European sea bass
title_full_unstemmed	Capsid amino acids at positions 247 and 270 are involved in the virulence of betanodaviruses to European sea bass
title_sort	capsid amino acids at positions 247 and 270 are involved in the virulence of betanodaviruses to european sea bass
publisher	Nature Portfolio
publishDate	2019
url	https://doaj.org/article/d98d9c344c924c87978d799a38e04c0f
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Capsid amino acids at positions 247 and 270 are involved in the virulence of betanodaviruses to European sea bass

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