Infectious Pancreatic Necrosis Virus VP5 Is Dispensable for Virulence and Persistence

Santi, Nina; Song, Haichen; Vakharia, Vikram N.; Evensen, Øystein

doi:10.1128/jvi.79.14.9206-9216.2005

Cited by 71 publications

(72 citation statements)

References 50 publications

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“…In case of IPNV, Hong et al (19) reported that VP5, a nonstructural protein, inhibits the apoptosis of virus-infected cells. However, Santi et al (37) reported that VP5 is dispensable for the growth of IPNV, which suggests the possibility that VP5 is not the only factor for the inhibition of apoptosis in IPNV-infected cells. In this study, we showed that IPNV infection increased the expression of a cellular protein, salmon annexin 1 and that the increased expression of salmon annexin 1 inhibits the apoptosis of IPNV-infected cells and supports the growth of IPNV in cells.…”

Section: Discussionmentioning

confidence: 99%

Identification and Functional Analysis of Salmon Annexin 1 Induced by a Virus Infection in a Fish Cell Line

Hwang

Moon

Kim

et al. 2007

J Virol

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In this study, we investigated changes in protein expression of fish cells induced by infection of infectious pancreatic necrosis virus (IPNV) using two-dimensional electrophoresis and matrix-assisted laser desorptiontime of flight proton motive force analysis and identified a novel type of salmon annexin 1 that is induced in fish cells by infection with IPNV. Northern blotting showed that this annexin is overexpressed in IPNV-infected cells compared to control cells, and further analysis revealed that it has a 1,509-bp full-length cDNA sequence with an open reading frame encoding 339 amino acids (GenBank accession no. AY944135). Amino acid sequence analysis revealed that this protein belongs to the annexin 1 subfamily. By applying RNA interference, the mRNA levels of salmon annexin 1 were suppressed and, under these conditions, apoptosis of IPNV-infected cells was significantly increased. While small interfering RNA (siRNA) treatment did not affect the levels of the viral proteins significantly until 10 h postinfection, it reduced the titer of extracellular virus to 25% of that of a scrambled siRNA-treated control. These data provide evidence of an antiapoptotic function for salmon annexin 1 that is important for IPNV growth in cultured cells.

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Section: Discussionmentioning

confidence: 99%

Identification and Functional Analysis of Salmon Annexin 1 Induced by a Virus Infection in a Fish Cell Line

Hwang

Moon

Kim

et al. 2007

J Virol

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“…Recently, to study the role of VP5 protein in virulence of IPNV, we recovered three viruses: one encoding a truncated 12-kDa VP5 (rNVI15), another encoding a full-length 15-kDa VP5 (rNVI15-15K), and one lacking the expression of VP5 (rNVI15-⌬VP5). All three viruses are virulent and cause Ͼ80% mortality in Atlantic salmon smolts, suggesting that VP5 is not directly involved in the virulence of IPNV (32).…”

mentioning

confidence: 99%

“…This protein has been detected in infected cells; however, it is not essential for virus replication in vitro (22,36). Recently, it has been shown that this protein is dispensable for viral replication in vivo, and it is not involved in persistent infection or virulence of the virus (32). Segment B encodes a 94-kDa protein, VP1, which functions as the virion associated RNA-dependent RNA polymerase (7,9).…”

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confidence: 99%

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

Song

Santi

Evensen

et al. 2005

J Virol

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133

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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.

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“…Özellikle yavru ve genç salmonid balıklarda yüksek mortalite ile seyreder. Etken, RNA grubundan Aquabirnavirüs ailesinde IPN virüsü (IPNV)'dür (4,9,18,20).…”

Section: Introductionunclassified

Gökkuşağı alabalıklarında (Oncorhynchus mykiss Walbaum, 1792) enfeksiyöz pankreatik nekrozun patogenezisinde apoptozisin rolü

Nihat;ALBAYRAK¹

2010

Ankara Üniversitesi Veteriner Fakültesi Dergisi

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Özet: Çalışmada, bir balık işletmesinde iştahsızlık ve yüzme bozuklukları gösteren, ortalama 5 g ağırlığında, 12 adet gökkuşağı alabalığı incelendi. Histopatolojik incelemede, pankreasta ekzokrin bezlerin ve Langerhans adacıklarının fokal ya da diffuz nekrozları görüldü. İmmunohistokimyasal incelemede; infeksiyöz pankreatik nekroz (IPN) viral antijenleri, yoğun olarak pankreas, karaciğer, kalp ve iskelet kasları daha az olarak da, böbrek, dalak, mide, bağırsaklar ve solungaçlarda ortaya konuldu. Ters transkriptaz polimeraz zincir reaksiyonu (RT-PCR) sonucunda; IPN virüsünü işaret eden yaklaşık 206 bp aralığında görüntü elde edildi. Apoptozis göstergelerinden TUNEL (Terminal Transferase dUTP Nick End Labeling), kaspaz-3, -8 ve -9 pozitiflikleri; apoptozisin iskelet ve kalp kasında içsel ve dışsal uyarımlarla, karaciğer, dalak, böbrekler, sekonder lameller, mide, pilorik keseler ve bağırsaklarda içsel yol ile indüklendiğini göstermektedir. Buna karşın, IPN virüsü için primer hedef organ olan pankreasta apoptotik hücre ölümü, hastalığın patogenezisinde çok etkin değildi. Sonuçta; çalışma bulguları IPN'un patogenezisinde apoptotik hücre ölüm mekanizmasının virüsün lehine olduğunu göstermektedir.Anahtar sözcükler: Apoptozis, gökkuşağı alabalığı (Oncorhynchus mykiss), IPN, immunohistokimya, RT-PCR. Role of apoptosis in pathogenesis of infectious pancreatic necrosis in rainbow trout (Oncorhynchus mykiss Walbaum, 1792)Summary: In this study, total of 12 rainbow trout (average weight 5 g) from a fish farm were examined. Clinically, the fish showed inappetite and irregular swimming. In histopathological examination, focal to diffuse acinar cell degeneration and necrosis were observed in pancreas. Immunohistochemically, IPN viral antigens appeared especially in the pancreas, liver, cardiac and skeletal muscles, and occasionally in the kidneys, spleen, stomach, intestines and gills. In Reverse transcriptase-polymerase chain reaction (RT-PCR) examination, appropriately sized product (206 bp) were amplified from tissue samples and specific signals for IPN virus were observed. Apoptosis signals TUNEL (Terminal Transferase dUTP Nick End Labeling), caspases-3, -8 and -9 positivities) indicated that apoptosis was induced both by intrinsic and extrinsic pathways in the skeleton and cardiac muscles, whereas by only intrinsic pathway in the liver, spleen, kidneys, gills, stomach and intestines. However, signals of apoptotic cell death were not clearly detected in pathogenesis of IPN in the pancreas as the main target organ. In conclusion, our results suggest that apoptosis, a cell death mechanism, could be appeared in favor of IPN virus in pathogenesis of the disease in field conditions.

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Infectious Pancreatic Necrosis Virus VP5 Is Dispensable for Virulence and Persistence

Abstract: Infectious pancreatic necrosis virus (IPNV) is the causative agent of infectious pancreatic necrosis (IPN)disease

Cited by 71 publications

References 50 publications

Identification and Functional Analysis of Salmon Annexin 1 Induced by a Virus Infection in a Fish Cell Line

Identification and Functional Analysis of Salmon Annexin 1 Induced by a Virus Infection in a Fish Cell Line

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

Gökkuşağı alabalıklarında (Oncorhynchus mykiss Walbaum, 1792) enfeksiyöz pankreatik nekrozun patogenezisinde apoptozisin rolü

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