scholarly journals Molecular Determinants of Infectious Pancreatic Necrosis Virus Virulence and Cell Culture Adaptation

2005 ◽  
Vol 79 (16) ◽  
pp. 10289-10299 ◽  
Author(s):  
Haichen Song ◽  
Nina Santi ◽  
Øystein Evensen ◽  
Vikram N. Vakharia
Keyword(s):  
Cell Culture ◽  
Amino Acid ◽  
Atlantic Salmon ◽  
Pancreatic Necrosis ◽  
Virulent Strain ◽  
Single Amino Acid ◽  
Wild Type Virus ◽  
Salmon Fry ◽  
Molecular Determinants ◽  
Infectious Pancreatic Necrosis

ABSTRACT Infectious pancreatic necrosis viruses (IPNVs) exhibit a wide range of virulence in salmonid species. In previous studies, we have shown that the amino acid residues at positions 217 and 221 in VP2 are implicated in virulence. To pinpoint the molecular determinants of virulence in IPNV, we generated recombinant IPNV strains using the cRNA-based reverse-genetics system. In two virulent strains, residues at positions 217 and 247 were replaced by the corresponding amino acids of a low-virulence strain. The growth characteristics of the recovered chimeric strains in cell culture were similar to the low-virulence strains, and these viruses induced significantly lower mortality in Atlantic salmon fry than the parent strains did in in vivo challenge studies. Furthermore, the virulent strain was serially passaged in CHSE-214 cells 10 times and was completely characterized by nucleotide sequencing. Deduced amino acid sequence analyses revealed a single amino acid substitution of Ala to Thr at position 221 in VP2 of this virus, which became highly attenuated and induced 15% cumulative mortality in Atlantic salmon fry, compared to 68% mortality induced by the virulent parent strain. The attenuated strain grows to higher titers in CHSE cells and can be distinguished antigenically from the wild-type virus by use of a monoclonal antibody. However, the virulent strain passaged 10 times in RTG-2 cells was stable, and it retained its antigenicity and virulence. Our results indicate that residues Thr at position 217 (Thr217) and Ala221 of VP2 are the major determinants of virulence in IPNV of the Sp serotype. Highly virulent isolates possess residues Thr217 and Ala221; moderate- to low-virulence strains have Pro217 and Ala221; and strains containing Thr221 are almost avirulent, irrespective of the residue at position 217.

scholarly journals The susceptibility of Atlantic salmon fry to freshwater infectious pancreatic necrosis is largely explained by a major QTL

Heredity ◽  
2009 ◽  
Vol 105 (3) ◽  
pp. 318-327 ◽  
Author(s):  
R D Houston ◽  
C S Haley ◽  
A Hamilton ◽  
D R Guy ◽  
J C Mota-Velasco ◽  
...  
Keyword(s):  
Atlantic Salmon ◽  
Pancreatic Necrosis ◽  
Salmon Fry ◽  
Infectious Pancreatic Necrosis ◽  
Major Qtl

scholarly journals Identification of a New Infectious Pancreatic Necrosis Virus (IPNV) Variant in Atlantic Salmon (Salmo salar L.) that can Cause High Mortality Even in Genetically Resistant Fish

2021 ◽  
Vol 12 ◽  
Author(s):  
Borghild Hillestad ◽  
Stein Johannessen ◽  
Geir Olav Melingen ◽  
Hooman K. Moghadam
Keyword(s):  
Amino Acid ◽  
Atlantic Salmon ◽  
Pancreatic Necrosis ◽  
Single Gene ◽  
Head Kidney ◽  
Comparative Sequence Analysis ◽  
Infectious Pancreatic Necrosis Virus ◽  
Life Cycles ◽  
New Variant ◽  
Infectious Pancreatic Necrosis

Infectious pancreatic necrosis (IPN) is an important viral disease of salmonids that can affect fish during various life cycles. In Atlantic salmon, selecting for genetically resistant fish against IPN has been one of the most highly praised success stories in the history of fish breeding. During the late 2000s, the findings that resistance against this disease has a significant genetic component, which is mainly controlled by variations in a single gene, have helped to reduce the IPN outbreaks to a great extent. In this paper, we present the identification of a new variant of the IPN virus from a field outbreak in Western Norway that had caused mortality, even in genetically resistant salmon. We recovered and assembled the full-length genome of this virus, following the deep-sequencing of the head-kidney transcriptome. The comparative sequence analysis revealed that for the critical amino acid motifs, previously found to be associated with the degree of virulence, the newly identified variant is similar to the virus’s avirulent form. However, we detected a set of deduced amino acid residues, particularly in the hypervariable domain of the VP2, that collectively are unique to this variant compared to all other reference sequences assessed in this study. We suggest that these mutations have likely equipped the virus with the capacity to escape the host defence mechanism more efficiently, even in the genetically deemed IPN resistant fish.

Pathogenesis of Infectious Pancreatic Necrosis in Atlantic Salmon (Salmo salar)

1979 ◽  
Vol 36 (5) ◽  
pp. 587-591 ◽  
Author(s):  
Robert N. Swanson ◽  
James H. Gillespie
Keyword(s):  
Atlantic Salmon ◽  
Salmo Salar ◽  
Pancreatic Necrosis ◽  
Virus Concentration ◽  
Live Virus ◽  
Atlantic Salmon Salmo Salar ◽  
Salmon Fry ◽  
Infectious Pancreatic Necrosis ◽  
Low Levels ◽  
Acinar Tissue

Atlantic salmon (Salmo salar) fry and yearling were found to undergo an active but subclinical infection following exposure to infectious pancreatic necrosis (IPN) virus. Eight-week-old Atlantic salmon fry were fed live virus and the mortality and virus concentration in these fry were recorded over a period of 78 d following exposure. Yearling Atlantic salmon were inoculated intraperitoneally with IPN virus and the concentration of virus in the pancreas–intestine, kidneys, spleen, liver, and gonads of inoculated fish was determined over a period of 74 d following inoculation. Virus first appeared in the fry 3 d postinoculation (DPI) and virus titers reached a peak by 8 DPI. Low levels of virus persisted in fry sampled 78 DPI. Virus first appeared in the pancreas–intestine of Atlantic salmon 12 h postinoculation (HPI) and was detected in the kidneys, liver, and spleen by 72 HPI. Peak virus titers were reached in the pancreas–intestine by 72 HPI. Both the pancreas–intestine and kidneys continued to support viral growth frequently and appeared to be important reservoirs of virus. At no time was virus isolated from the gonads of inoculated yearling. Histological examination of yearlings revealed degenerative changes in the pancreatic acinar tissue and in some cases focal necrosis in the liver. No histological abnormalities were found in IPN-infected fry. Key words: infectious pancreatic necrosis, Atlantic salmon, virus, histology

scholarly journals Relationship between apoptosis and the BH2 domain sequence of the VP5 peptide of infectious pancreatic necrosis virus

2014 ◽  
pp. 3990-4002 ◽  
Author(s):  
Cesar Ortega S ◽  
Sylvia Rodríguez S ◽  
Juan Carlos Espinoza ◽  
Juan Kuznar ◽  
Alex Romero ◽  
...  
Keyword(s):  
Amino Acid ◽  
Pancreatic Necrosis ◽  
Virulent Strain ◽  
Critical Factor ◽  
Infectious Pancreatic Necrosis Virus ◽  
Viral Titer ◽  
Necrosis Virus ◽  
Infected Cells ◽  
Infectious Pancreatic Necrosis ◽  
Pancreatic Necrosis Virus

ABSTRACTObjective. To determine whether the level of apoptosis induced by infectious pancreatic necrosis virus (IPNV) is related to the amino acid sequence of the BH2 domain of the VP5 protein and the level of infectivity. Materials and methods. Three IPNV strains were used, the VP2 protein gene was amplified for genotyping and the VP5 sequence was also obtained. The infectivity of the strains was calculated using the viral titer obtained at 12, 24, 36 and 45 hpi in CHSE-214 cells. The percentage of apoptosis in infected cells was visualized by TUNEL assay and immunohistochemistry (caspase 3 detection). Results. The V70/06 and V33/98 strains corresponded to genotype Sp, while V112/06 to VR-299; the amino acid analysis of the V70/06 strain allows its classification as middle virulent strain and V33/98 and V112/06 strains as low virulent ones; infection with the V112/06 strain produced a lower viral titer (p<0.05). The VP5 gene of the 3 strains showed four homologous domains to Bcl-2, however, the BH2 domain was truncated in V70/06 and V33/98 (12 kDa), being complete (15kDa) in V112/06, which also showed the Trp155 residue, equivalent to Trp188 considered as a critical factor for the function of Bcl-2. The average apoptosis was below 12%, showing no differences between strains (p>0.05). Conclusions. The results showed that the differences in the BH2 sequence of the VP5 protein, infectivity and the VP2 sequence are not associated with the modulation of apoptosis.

scholarly journals Identification of a new Infectious Pancreatic Necrosis Virus (IPNV) isolate in Atlantic salmon (Salmo salar L.) that causes mortality in resistant fish

2021 ◽  
Author(s):  
Borghild Hillestad ◽  
Stein Johannessen ◽  
Geir Olav Melingen ◽  
Hooman K Moghadam
Keyword(s):  
Amino Acid ◽  
Atlantic Salmon ◽  
Pancreatic Necrosis ◽  
Single Gene ◽  
Hypervariable Region ◽  
Viral Disease ◽  
Comparative Sequence Analysis ◽  
Infectious Pancreatic Necrosis Virus ◽  
Life Cycles ◽  
Infectious Pancreatic Necrosis

Infectious pancreatic necrosis (IPN) is an important viral disease of salmonids that can affect fish during various life cycles. In Atlantic salmon, selecting for genetically resistant animals against IPN has been one of the most highly praised success stories in the history of fish breeding. The findings that resistance against this disease has a significant genetic component, which is mainly controlled by variations in a single gene, has helped to reduce the IPN outbreaks over the past decade to a great extent. In this paper, we present the identification of a new isolate of the IPN virus, from a field outbreak, that had caused mortality, even in the genetically resistant animals. We recovered and assembled the full-length genome of this virus, following deep-sequencing of an infected tissue. The comparative sequence analysis revealed that for the critical amino acid motifs, previously found to be associated with the degree of virulence, the newly identified isolate is similar to the virus's avirulent form. However, we detected a set of deduced amino acid residues, particularly in the hypervariable region of the polyprotein, that collectively are unique to this strain compared to all other reference sequences assessed in this study. We suggest that these mutations have likely equipped the virus with the capacity to escape the host defence mechanism more efficiently, even in the genetically deemed IPN resistant animals.

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