The interplay between infectious pancreatic necrosis virus (IPNV) and the IFN system: IFN signaling is inhibited by IPNV infection

Skjesol, Astrid; Aamo, Toril; Hegseth, Marit Nøst; Robertsen, Børre; Jørgensen, Jorunn B.

doi:10.1016/j.virusres.2009.03.004

Cited by 63 publications

(47 citation statements)

References 35 publications

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“…Although in our study Mx-1 after day 7 was not able to exploit the biological function reported in CHSE-214 cells (Larsen, Rokenes, & Robertsen, 2004) and in vivo studies (Saint-Jean, & Pérez-Prieto, 2007). Skjesol et al (2009) have referred and pointed to VP4 and VP5 proteins like IPNV virulence factors, however is unknown until now. Although, Dobos (1995) found that IPNV replicates in the cytoplasm, and virus and proteins never enter the cell nucleus, we believe that this issue needs to get the focus.…”

Section: Discussioncontrasting

confidence: 56%

Efecto de la temperatura sobre la expresión de genes IFN-1(α), STAT-1 y Mx-1 en alevines de trucha arcoíris Oncorhynchus mykiss (Salmoniformes: Salmonidae) expuestos al el virus de la necrosis pancreática infecciosa (IPNV)

Cortés¹,

Zuñiga

Sais

et al. 2015

RBT

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Abstract:The infectious pancreatic necrosis (IPNV) is the causative agent of an acute illness well characterized in salmonids worldwide. Clinical signs and mortality rates are dependent on several factors such as the viral dose, the age of the fish, the water temperature, among others. An experimental study was conducted to measure the effect of temperature on the gene expression profile of IFN-1(α), STAT-1 and Mx-1 in rainbow trout fry, exposed to IPNV. Fry (n=198) were exposed at 8, 12 and 16°C, and samples were taken for 21 days to determine the virus titer and gene expression. In the first 11 days the greatest viral titer was recorded at 8°C compared with the values obtained at 12 and 16°C. At 8°C, there was a significant increase on day 4 of mRNA Mx-1 (t-test, p<0.05), time in which the viral titer began to decrease. Furthermore, as the viral titer increased, STAT-1 and Mx-1 (r=0.91) and (r=0.96) increased, respectively. The animals were able to recover from day 4 from some of the symptoms of IPN. Clinical disease was developed only in fish exposed to 12°C and all died between days 6 and 14, despite the highly significant increase shown in the average expression level of Mx-1, compared with the values recorded at 8°C and 16°C (Tukey, p<0.0001). Additionally, the expression profiles of IFN-1(α) and STAT-1 decreased completely (~0.016) and (~0.020 times) on day 7. The highest expression level of IFN-1(α), occurred at 16°C (Tukey, p<0.0005). Fry exposed at 16°C were normal during the experiment. IFN-1(α) possibly generated a protector effect from day 2 when they showed a significant expression increase compared with the results at 8°C and 12°C (t-student, p<0.0001); however, STAT-1 was not significantly affected by temperature, although the highest average expression value was recorded at 16°C. Our research supports the expression of relevant anti-viral response genes as IFN-1(α), STAT-1 and Mx-1 are physiologically modulated by the water temperature, directly influencing the development of the IPN disease in rainbow trout. Rev. Biol. Trop. 63 (2): 559-569. Epub 2015 June 01.

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Section: Discussioncontrasting

confidence: 56%

Efecto de la temperatura sobre la expresión de genes IFN-1(α), STAT-1 y Mx-1 en alevines de trucha arcoíris Oncorhynchus mykiss (Salmoniformes: Salmonidae) expuestos al el virus de la necrosis pancreática infecciosa (IPNV)

Cortés¹,

Zuñiga

Sais

et al. 2015

RBT

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“…IPNV itself does not induce IFN or Mx in TO or CHSE cells (20,21,42). In fact, proteins encoded by IPNV inhibit both activation of the IFNa1 promoter (unpublished results) and inhibit IFNa1-mediated signaling (49). Anti-IFNa1 also seemed to reduce the antiviral activity of IFN-␥ against SAV3, but here the mechanism is less clear since the virus itself is known to induce IFN.…”

Section: Discussionmentioning

confidence: 89%

Antiviral Activity of Salmonid Gamma Interferon against Infectious Pancreatic Necrosis Virus and Salmonid Alphavirus and Its Dependency on Type I Interferon

Sun

Skjæveland

Svingerud

et al. 2011

J Virol

Self Cite

106

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“…Further, in light of recent publications showing that IPNV has the ability to reduce/block IFNα-induced responses in vitro [24], [25] we examined replication differences between TA and TT strains under IFNα-1 influence. We therefore performed an in vitro study with the purpose to explore the possibility that TA and TT strains differ in their sensitivity to IFN-α1 induced antiviral responses.…”

Section: Resultsmentioning

confidence: 99%

Stress-Induced Reversion to Virulence of Infectious Pancreatic Necrosis Virus in Naïve Fry of Atlantic Salmon (Salmo salar L.)

et al. 2013

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We have studied stress-induced reversion to virulence of infectious pancreatic necrosis virus (IPNV) in persistently infected Atlantic salmon (Salmo salar L.) fry. Naïve fry were persistently infected with a virulent strain (T217A221 of major structural virus protein 2, VP2) or a low virulent (T217T221) variant of IPNV. The fry were infected prior to immunocompetence as documented by lack of recombination activating gene-1, T-cell receptor and B-cell receptor mRNA expression at time of challenge. The fish were followed over 6 months and monitored monthly for presence of virus and viral genome mutations. No mutation was identified in the TA or TT group over the 6 months period post infection. Six months post infection TA and TT infected groups were subject to daily stress for 7 days and then sampled weekly for an additional period of 28 days post stress. Stress-responses were documented by down-regulation of mRNA expression of IFN-α1 and concomitant increase of replication levels of T217T221 infected fish at day 1 post stress. By 28 days post stress a T221A reversion was found in 3 of 6 fish in the T217T221 infected group. Sequencing of reverted isolates showed single nucleotide peaks on chromatograms for residue 221 for all three isolates and no mix of TA and TT strains. Replication fitness of reverted (TA) and non-reverted (TT) variants was studied in vitro under an antiviral state induced by recombinant IFN-α1. The T217A221 reverted variant replicated to levels 23-fold higher than the T217T221 strain in IFN-α1 treated cells. Finally, reverted TA strains were virulent when tested in an in vivo trial in susceptible salmon fry. In conclusion, these results indicate that stress plays a key role in viral replication in vivo and can facilitate conditions that will allow reversion from attenuated virus variants of IPNV.

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The interplay between infectious pancreatic necrosis virus (IPNV) and the IFN system: IFN signaling is inhibited by IPNV infection

Cited by 63 publications

References 35 publications

Efecto de la temperatura sobre la expresión de genes IFN-1(α), STAT-1 y Mx-1 en alevines de trucha arcoíris Oncorhynchus mykiss (Salmoniformes: Salmonidae) expuestos al el virus de la necrosis pancreática infecciosa (IPNV)

Efecto de la temperatura sobre la expresión de genes IFN-1(α), STAT-1 y Mx-1 en alevines de trucha arcoíris Oncorhynchus mykiss (Salmoniformes: Salmonidae) expuestos al el virus de la necrosis pancreática infecciosa (IPNV)

Antiviral Activity of Salmonid Gamma Interferon against Infectious Pancreatic Necrosis Virus and Salmonid Alphavirus and Its Dependency on Type I Interferon

Stress-Induced Reversion to Virulence of Infectious Pancreatic Necrosis Virus in Naïve Fry of Atlantic Salmon (Salmo salar L.)

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