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

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...

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Bibliographic Details
Published in:Veterinary Research
Main Authors: Vazquez-Salgado, Lucia, Olveira, Jose G., Bandin, Isabel
Other Authors: Souto, Sandra
Format: Article in Journal/Newspaper
Language:English
Published: 2019
Subjects:
atlantic halibut nodavirus
viral encephalopathy ;capsprotein
in-vitro
infection
replication ;turbot ;localization
virulence
signals
Turbot
Online Access:http://prodinra.inra.fr/ft/27E67981-0867-45AB-9534-817093B3CDDB
http://prodinra.inra.fr/record/485212
https://doi.org/10.1186/s13567-019-0669-4
Description
Summary: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 degrees C. The experimental infections confirmed the impact of the mutations on viral replication because at 25 degrees 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 degrees C because of the scarce tolerance of sole to this temperature.

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