Amino acidic substitutions in the polymerase N-terminal region of a reassortant betanodavirus strain causing poor adaptation to temperature increase

Abstract Nervous necrosis virus (NNV), Genus Betanodavirus, is the causative agent of viral encephalopathy and retinopathy (VER), a neuropathological disease that causes fish mortalities worldwide. The NNV genome is composed of two single-stranded RNA molecules, RNA1 and RNA2, encoding the RNA polym...

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Main Authors: Sandra Souto, Lucía Vázquez-Salgado, José G. Olveira, Isabel Bandín
Format: Article
Language:English
Published: BMC 2019-06-01
Series:Veterinary Research
Online Access:http://link.springer.com/article/10.1186/s13567-019-0669-4
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spelling doaj-acd77d3d440e4e77a175ba7ae6a62b4c2020-11-25T03:45:51ZengBMCVeterinary Research1297-97162019-06-0150111110.1186/s13567-019-0669-4Amino acidic substitutions in the polymerase N-terminal region of a reassortant betanodavirus strain causing poor adaptation to temperature increaseSandra Souto0Lucía Vázquez-Salgado1José G. Olveira2Isabel Bandín3Instituto de Acuicultura, Departamento de Microbiología y Parasitología-Universidade de Santiago de CompostelaInstituto de Acuicultura, Departamento de Microbiología y Parasitología-Universidade de Santiago de CompostelaInstituto de Acuicultura, Departamento de Microbiología y Parasitología-Universidade de Santiago de CompostelaInstituto de Acuicultura, Departamento de Microbiología y Parasitología-Universidade de Santiago de CompostelaAbstract Nervous necrosis virus (NNV), Genus Betanodavirus, is the causative agent of viral encephalopathy and retinopathy (VER), a neuropathological disease that causes fish mortalities worldwide. The NNV genome is composed of two single-stranded RNA molecules, RNA1 and RNA2, encoding the RNA polymerase and the coat protein, respectively. Betanodaviruses are classified into four genotypes: red-spotted grouper nervous necrosis virus (RGNNV), striped jack nervous necrosis virus (SJNNV), barfin flounder nervous necrosis virus (BFNNV) and tiger puffer nervous necrosis virus (TPNNV). In Southern Europe the presence of RGNNV, SJNNV and their natural reassortants (in both RNA1/RNA2 forms: RGNNV/SJNNV and SJNNV/RGNNV) has been reported. Pathology caused by these genotypes is closely linked to water temperature and the RNA1 segment encoding amino acids 1–445 has been postulated to regulate viral adaptation to temperature. Reassortants isolated from sole (RGNNV/SJNNV) show 6 substitutions in this region when compared with the RGNNV genotype (positions 41, 48, 218, 223, 238 and 289). We have demonstrated that change of these positions to those present in the RGNNV genotype cause low and delayed replication in vitro when compared with that of the wild type strain at 25 and 30 °C. The experimental infections confirmed the impact of the mutations on viral replication because at 25 °C the viral load and the mortality were significantly lower in fish infected with the mutant than in those challenged with the non-mutated virus. It was not possible to challenge fish at 30 °C because of the scarce tolerance of sole to this temperature.http://link.springer.com/article/10.1186/s13567-019-0669-4
collection DOAJ
language English
format Article
sources DOAJ
author Sandra Souto
Lucía Vázquez-Salgado
José G. Olveira
Isabel Bandín
spellingShingle Sandra Souto
Lucía Vázquez-Salgado
José G. Olveira
Isabel Bandín
Amino acidic substitutions in the polymerase N-terminal region of a reassortant betanodavirus strain causing poor adaptation to temperature increase
Veterinary Research
author_facet Sandra Souto
Lucía Vázquez-Salgado
José G. Olveira
Isabel Bandín
author_sort Sandra Souto
title Amino acidic substitutions in the polymerase N-terminal region of a reassortant betanodavirus strain causing poor adaptation to temperature increase
title_short Amino acidic substitutions in the polymerase N-terminal region of a reassortant betanodavirus strain causing poor adaptation to temperature increase
title_full Amino acidic substitutions in the polymerase N-terminal region of a reassortant betanodavirus strain causing poor adaptation to temperature increase
title_fullStr Amino acidic substitutions in the polymerase N-terminal region of a reassortant betanodavirus strain causing poor adaptation to temperature increase
title_full_unstemmed Amino acidic substitutions in the polymerase N-terminal region of a reassortant betanodavirus strain causing poor adaptation to temperature increase
title_sort amino acidic substitutions in the polymerase n-terminal region of a reassortant betanodavirus strain causing poor adaptation to temperature increase
publisher BMC
series Veterinary Research
issn 1297-9716
publishDate 2019-06-01
description Abstract Nervous necrosis virus (NNV), Genus Betanodavirus, is the causative agent of viral encephalopathy and retinopathy (VER), a neuropathological disease that causes fish mortalities worldwide. The NNV genome is composed of two single-stranded RNA molecules, RNA1 and RNA2, encoding the RNA polymerase and the coat protein, respectively. Betanodaviruses are classified into four genotypes: red-spotted grouper nervous necrosis virus (RGNNV), striped jack nervous necrosis virus (SJNNV), barfin flounder nervous necrosis virus (BFNNV) and tiger puffer nervous necrosis virus (TPNNV). In Southern Europe the presence of RGNNV, SJNNV and their natural reassortants (in both RNA1/RNA2 forms: RGNNV/SJNNV and SJNNV/RGNNV) has been reported. Pathology caused by these genotypes is closely linked to water temperature and the RNA1 segment encoding amino acids 1–445 has been postulated to regulate viral adaptation to temperature. Reassortants isolated from sole (RGNNV/SJNNV) show 6 substitutions in this region when compared with the RGNNV genotype (positions 41, 48, 218, 223, 238 and 289). We have demonstrated that change of these positions to those present in the RGNNV genotype cause low and delayed replication in vitro when compared with that of the wild type strain at 25 and 30 °C. The experimental infections confirmed the impact of the mutations on viral replication because at 25 °C the viral load and the mortality were significantly lower in fish infected with the mutant than in those challenged with the non-mutated virus. It was not possible to challenge fish at 30 °C because of the scarce tolerance of sole to this temperature.
url http://link.springer.com/article/10.1186/s13567-019-0669-4
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