Early viral uptake and host-associated immune response in the tissues of seven-band grouper following a bath challenge with nervous necrosis virus

2020 ◽  
Vol 103 ◽  
pp. 454-463
Author(s):  
Rahul Krishnan ◽  
Jong-Oh Kim ◽  
Syed Shariq Nazir Qadiri ◽  
Jae-Ok Kim ◽  
Myung-Joo Oh
Keyword(s):  
Immune Response ◽  
Nervous Necrosis Virus ◽  
Necrosis Virus ◽  
Bath Challenge

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

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Patricia Moreno ◽  
Sandra Souto ◽  
Rocio Leiva-Rebollo ◽  
Juan J. Borrego ◽  
Isabel Bandín ◽  
...  
Keyword(s):  
Amino Acids ◽  
Immune Response ◽  
Fish Species ◽  
Sea Bass ◽  
Fish Mortality ◽  
Wild Type Virus ◽  
Nervous Necrosis Virus ◽  
Necrosis Virus ◽  
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 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.

Immune response against grouper nervous necrosis virus by vaccination of virus-like particles

Vaccine ◽  
2006 ◽  
Vol 24 (37-39) ◽  
pp. 6282-6287 ◽  
Author(s):  
Wangta Liu ◽  
Chi-Hsin Hsu ◽  
Chiung-Yin Chang ◽  
Hsin-Hong Chen ◽  
Chan-Shing Lin
Keyword(s):  
Immune Response ◽  
Nervous Necrosis Virus ◽  
Necrosis Virus ◽  
Virus Like Particles

scholarly journals Immune Response of Senegalese Sole against Betanodavirus Mutants with Modified Virulence

Pathogens ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 1388
Author(s):  
Juan Gémez-Mata ◽  
Sandra Souto ◽  
Isabel Bandín ◽  
María del Carmen Alonso ◽  
Juan José Borrego ◽  
...  
Keyword(s):  
Immune Response ◽  
Nervous Necrosis Virus ◽  
Senegalese Sole ◽  
Coding Region ◽  
Necrosis Virus ◽  
A Genome ◽  
Positive Sense ◽  
The Complement System ◽  
Reference Strains ◽  
Viral Encephalopathy And Retinopathy

Nervous necrosis virus (NNV), genus Betanodavirus, the etiological agent of the viral encephalopathy and retinopathy (VER), presents a genome with two positive-sense single-stranded RNA segments. Striped jack nervous necrosis virus (SJNNV) and red-spotted grouper nervous necrosis virus (RGNNV), together with reassortants RGNNV/SJNNV, are the betanodaviruses predominantly isolated in Southern Europe. An RGNNV/SJNNV reassortant isolated from Senegalese sole (wt160) causes high mortalities in this fish species. This virus presents differences in the sequence of the 3’ non-coding region (NCR) of both segments compared to RGNNV and SJNNV reference strains. Previously, it has been reported that the reversion of two of these differences (nucleotides 1408 and 1412) in the RNA2 3’NCR to the SJNNV-type (recombinant r1408-1412) resulted in a decrease in sole mortality. In the present study, we have applied an OpenArray® to analyse the involvement of sole immune response in the virulence of several recombinants: the r1408-1412 and two recombinants, developed in the present study, harbouring mutations at positions 3073 and 3093 of RNA1 3’NCR to revert them to RGNNV-type. According to the correlation values and to the number of expressed genes, the infection with the RNA2-mutant provoked the most different immune response compared to the immune response triggered after the infection with the rest of the viruses, and the exclusive and high upregulation of genes related to the complement system. The infection with the RNA1-mutants also provoked a decrease in mortality and their replication was delayed at least 24 h compared to the wt160 replication, which could provoke the lag observed in the immune response. Furthermore, the infection with the RNA1-mutants provoked the exclusive expression of pkr and the downregulation of il17rc.

Sign in / Sign up

Export Citation Format

Share Document