SJNNV down-regulates RGNNV replication in European sea bass by the induction of the type I interferon system

Abstract European sea bass is highly susceptible to the betanodavirus RGNNV genotype, although the SJNNV genotype has also been detected in this fish species. The coexistence of both genotypes may affect the replication of both viruses by viral interaction or by stimulation of the host antiviral def...
Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Carballo, Carlos [verfasserIn] Garcia-Rosado, Esther [verfasserIn] Borrego, Juan J. [verfasserIn] Alonso, M. Carmen [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2016

Schlagwörter:	Head Kidney Infectious Hematopoietic Necrosis Virus Nervous Necrosis Virus Striped Jack Nervous Necrosis Virus Viral Nervous Necrosis Virus

Übergeordnetes Werk:	Enthalten in: Veterinary research - London : BioMed Central, 1993, 47(2016), 1 vom: 08. Jan.
Übergeordnetes Werk:	volume:47 ; year:2016 ; number:1 ; day:08 ; month:01

Links:	Volltext

DOI / URN:	10.1186/s13567-015-0304-y

Katalog-ID:	SPR031820530

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520			\|a Abstract European sea bass is highly susceptible to the betanodavirus RGNNV genotype, although the SJNNV genotype has also been detected in this fish species. The coexistence of both genotypes may affect the replication of both viruses by viral interaction or by stimulation of the host antiviral defense system in which the IFN I system plays a key role. IFN I triggers the transcription of interferon-stimulated genes, including Mx genes, whose expression has been used as a reporter of IFN I activity. The present study evaluated the effect of a primary exposure to an SJNNV isolate on a subsequent RGNNV infection and analyzed the role of the IFN I system in controlling VNNV infections in sea bass using different in vivo approaches. VNNV infection and Mx transcription were comparatively evaluated after single infections, superinfection (SJ+RG) and co-infection (poly I:C+RG). The single RGNNV infection resulted in a 24% survival rate, whereas the previous SJNNV or poly I:C inoculation increased the survival rate up to 96 and 100%, respectively. RGNNV replication in superinfection was reduced compared with RGNNV replication after a single inoculation. Mx transcription analysis shows differential induction of the IFN I system by both isolates. SJNNV was a potent Mx inducer, whereas RGNNV induced lower Mx transcription and did not interfere with the IFN I system triggered by SJNNV or poly I:C. This study demonstrates that an antiviral state exists after SJNNV and poly I:C injection, suggesting that the IFN I system plays an important role against VNNV infections in sea bass.
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allfields	10.1186/s13567-015-0304-y doi (DE-627)SPR031820530 (SPR)s13567-015-0304-y-e DE-627 ger DE-627 rakwb eng 630 640 ASE 46.00 bkl Carballo, Carlos verfasserin aut SJNNV down-regulates RGNNV replication in European sea bass by the induction of the type I interferon system 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract European sea bass is highly susceptible to the betanodavirus RGNNV genotype, although the SJNNV genotype has also been detected in this fish species. The coexistence of both genotypes may affect the replication of both viruses by viral interaction or by stimulation of the host antiviral defense system in which the IFN I system plays a key role. IFN I triggers the transcription of interferon-stimulated genes, including Mx genes, whose expression has been used as a reporter of IFN I activity. The present study evaluated the effect of a primary exposure to an SJNNV isolate on a subsequent RGNNV infection and analyzed the role of the IFN I system in controlling VNNV infections in sea bass using different in vivo approaches. VNNV infection and Mx transcription were comparatively evaluated after single infections, superinfection (SJ+RG) and co-infection (poly I:C+RG). The single RGNNV infection resulted in a 24% survival rate, whereas the previous SJNNV or poly I:C inoculation increased the survival rate up to 96 and 100%, respectively. RGNNV replication in superinfection was reduced compared with RGNNV replication after a single inoculation. Mx transcription analysis shows differential induction of the IFN I system by both isolates. SJNNV was a potent Mx inducer, whereas RGNNV induced lower Mx transcription and did not interfere with the IFN I system triggered by SJNNV or poly I:C. This study demonstrates that an antiviral state exists after SJNNV and poly I:C injection, suggesting that the IFN I system plays an important role against VNNV infections in sea bass. Head Kidney (dpeaa)DE-He213 Infectious Hematopoietic Necrosis Virus (dpeaa)DE-He213 Nervous Necrosis Virus (dpeaa)DE-He213 Striped Jack Nervous Necrosis Virus (dpeaa)DE-He213 Viral Nervous Necrosis Virus (dpeaa)DE-He213 Garcia-Rosado, Esther verfasserin aut Borrego, Juan J. verfasserin aut Alonso, M. Carmen verfasserin aut Enthalten in Veterinary research London : BioMed Central, 1993 47(2016), 1 vom: 08. Jan. (DE-627)312853653 (DE-600)2012391-7 1297-9716 nnns volume:47 year:2016 number:1 day:08 month:01 https://dx.doi.org/10.1186/s13567-015-0304-y kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_213 GBV_ILN_230 GBV_ILN_252 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 46.00 ASE AR 47 2016 1 08 01
spelling	10.1186/s13567-015-0304-y doi (DE-627)SPR031820530 (SPR)s13567-015-0304-y-e DE-627 ger DE-627 rakwb eng 630 640 ASE 46.00 bkl Carballo, Carlos verfasserin aut SJNNV down-regulates RGNNV replication in European sea bass by the induction of the type I interferon system 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract European sea bass is highly susceptible to the betanodavirus RGNNV genotype, although the SJNNV genotype has also been detected in this fish species. The coexistence of both genotypes may affect the replication of both viruses by viral interaction or by stimulation of the host antiviral defense system in which the IFN I system plays a key role. IFN I triggers the transcription of interferon-stimulated genes, including Mx genes, whose expression has been used as a reporter of IFN I activity. The present study evaluated the effect of a primary exposure to an SJNNV isolate on a subsequent RGNNV infection and analyzed the role of the IFN I system in controlling VNNV infections in sea bass using different in vivo approaches. VNNV infection and Mx transcription were comparatively evaluated after single infections, superinfection (SJ+RG) and co-infection (poly I:C+RG). The single RGNNV infection resulted in a 24% survival rate, whereas the previous SJNNV or poly I:C inoculation increased the survival rate up to 96 and 100%, respectively. RGNNV replication in superinfection was reduced compared with RGNNV replication after a single inoculation. Mx transcription analysis shows differential induction of the IFN I system by both isolates. SJNNV was a potent Mx inducer, whereas RGNNV induced lower Mx transcription and did not interfere with the IFN I system triggered by SJNNV or poly I:C. This study demonstrates that an antiviral state exists after SJNNV and poly I:C injection, suggesting that the IFN I system plays an important role against VNNV infections in sea bass. Head Kidney (dpeaa)DE-He213 Infectious Hematopoietic Necrosis Virus (dpeaa)DE-He213 Nervous Necrosis Virus (dpeaa)DE-He213 Striped Jack Nervous Necrosis Virus (dpeaa)DE-He213 Viral Nervous Necrosis Virus (dpeaa)DE-He213 Garcia-Rosado, Esther verfasserin aut Borrego, Juan J. verfasserin aut Alonso, M. Carmen verfasserin aut Enthalten in Veterinary research London : BioMed Central, 1993 47(2016), 1 vom: 08. Jan. (DE-627)312853653 (DE-600)2012391-7 1297-9716 nnns volume:47 year:2016 number:1 day:08 month:01 https://dx.doi.org/10.1186/s13567-015-0304-y kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_213 GBV_ILN_230 GBV_ILN_252 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 46.00 ASE AR 47 2016 1 08 01
allfields_unstemmed	10.1186/s13567-015-0304-y doi (DE-627)SPR031820530 (SPR)s13567-015-0304-y-e DE-627 ger DE-627 rakwb eng 630 640 ASE 46.00 bkl Carballo, Carlos verfasserin aut SJNNV down-regulates RGNNV replication in European sea bass by the induction of the type I interferon system 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract European sea bass is highly susceptible to the betanodavirus RGNNV genotype, although the SJNNV genotype has also been detected in this fish species. The coexistence of both genotypes may affect the replication of both viruses by viral interaction or by stimulation of the host antiviral defense system in which the IFN I system plays a key role. IFN I triggers the transcription of interferon-stimulated genes, including Mx genes, whose expression has been used as a reporter of IFN I activity. The present study evaluated the effect of a primary exposure to an SJNNV isolate on a subsequent RGNNV infection and analyzed the role of the IFN I system in controlling VNNV infections in sea bass using different in vivo approaches. VNNV infection and Mx transcription were comparatively evaluated after single infections, superinfection (SJ+RG) and co-infection (poly I:C+RG). The single RGNNV infection resulted in a 24% survival rate, whereas the previous SJNNV or poly I:C inoculation increased the survival rate up to 96 and 100%, respectively. RGNNV replication in superinfection was reduced compared with RGNNV replication after a single inoculation. Mx transcription analysis shows differential induction of the IFN I system by both isolates. SJNNV was a potent Mx inducer, whereas RGNNV induced lower Mx transcription and did not interfere with the IFN I system triggered by SJNNV or poly I:C. This study demonstrates that an antiviral state exists after SJNNV and poly I:C injection, suggesting that the IFN I system plays an important role against VNNV infections in sea bass. Head Kidney (dpeaa)DE-He213 Infectious Hematopoietic Necrosis Virus (dpeaa)DE-He213 Nervous Necrosis Virus (dpeaa)DE-He213 Striped Jack Nervous Necrosis Virus (dpeaa)DE-He213 Viral Nervous Necrosis Virus (dpeaa)DE-He213 Garcia-Rosado, Esther verfasserin aut Borrego, Juan J. verfasserin aut Alonso, M. Carmen verfasserin aut Enthalten in Veterinary research London : BioMed Central, 1993 47(2016), 1 vom: 08. Jan. (DE-627)312853653 (DE-600)2012391-7 1297-9716 nnns volume:47 year:2016 number:1 day:08 month:01 https://dx.doi.org/10.1186/s13567-015-0304-y kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_213 GBV_ILN_230 GBV_ILN_252 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 46.00 ASE AR 47 2016 1 08 01
allfieldsGer	10.1186/s13567-015-0304-y doi (DE-627)SPR031820530 (SPR)s13567-015-0304-y-e DE-627 ger DE-627 rakwb eng 630 640 ASE 46.00 bkl Carballo, Carlos verfasserin aut SJNNV down-regulates RGNNV replication in European sea bass by the induction of the type I interferon system 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract European sea bass is highly susceptible to the betanodavirus RGNNV genotype, although the SJNNV genotype has also been detected in this fish species. The coexistence of both genotypes may affect the replication of both viruses by viral interaction or by stimulation of the host antiviral defense system in which the IFN I system plays a key role. IFN I triggers the transcription of interferon-stimulated genes, including Mx genes, whose expression has been used as a reporter of IFN I activity. The present study evaluated the effect of a primary exposure to an SJNNV isolate on a subsequent RGNNV infection and analyzed the role of the IFN I system in controlling VNNV infections in sea bass using different in vivo approaches. VNNV infection and Mx transcription were comparatively evaluated after single infections, superinfection (SJ+RG) and co-infection (poly I:C+RG). The single RGNNV infection resulted in a 24% survival rate, whereas the previous SJNNV or poly I:C inoculation increased the survival rate up to 96 and 100%, respectively. RGNNV replication in superinfection was reduced compared with RGNNV replication after a single inoculation. Mx transcription analysis shows differential induction of the IFN I system by both isolates. SJNNV was a potent Mx inducer, whereas RGNNV induced lower Mx transcription and did not interfere with the IFN I system triggered by SJNNV or poly I:C. This study demonstrates that an antiviral state exists after SJNNV and poly I:C injection, suggesting that the IFN I system plays an important role against VNNV infections in sea bass. Head Kidney (dpeaa)DE-He213 Infectious Hematopoietic Necrosis Virus (dpeaa)DE-He213 Nervous Necrosis Virus (dpeaa)DE-He213 Striped Jack Nervous Necrosis Virus (dpeaa)DE-He213 Viral Nervous Necrosis Virus (dpeaa)DE-He213 Garcia-Rosado, Esther verfasserin aut Borrego, Juan J. verfasserin aut Alonso, M. Carmen verfasserin aut Enthalten in Veterinary research London : BioMed Central, 1993 47(2016), 1 vom: 08. Jan. (DE-627)312853653 (DE-600)2012391-7 1297-9716 nnns volume:47 year:2016 number:1 day:08 month:01 https://dx.doi.org/10.1186/s13567-015-0304-y kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_213 GBV_ILN_230 GBV_ILN_252 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 46.00 ASE AR 47 2016 1 08 01
allfieldsSound	10.1186/s13567-015-0304-y doi (DE-627)SPR031820530 (SPR)s13567-015-0304-y-e DE-627 ger DE-627 rakwb eng 630 640 ASE 46.00 bkl Carballo, Carlos verfasserin aut SJNNV down-regulates RGNNV replication in European sea bass by the induction of the type I interferon system 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract European sea bass is highly susceptible to the betanodavirus RGNNV genotype, although the SJNNV genotype has also been detected in this fish species. The coexistence of both genotypes may affect the replication of both viruses by viral interaction or by stimulation of the host antiviral defense system in which the IFN I system plays a key role. IFN I triggers the transcription of interferon-stimulated genes, including Mx genes, whose expression has been used as a reporter of IFN I activity. The present study evaluated the effect of a primary exposure to an SJNNV isolate on a subsequent RGNNV infection and analyzed the role of the IFN I system in controlling VNNV infections in sea bass using different in vivo approaches. VNNV infection and Mx transcription were comparatively evaluated after single infections, superinfection (SJ+RG) and co-infection (poly I:C+RG). The single RGNNV infection resulted in a 24% survival rate, whereas the previous SJNNV or poly I:C inoculation increased the survival rate up to 96 and 100%, respectively. RGNNV replication in superinfection was reduced compared with RGNNV replication after a single inoculation. Mx transcription analysis shows differential induction of the IFN I system by both isolates. SJNNV was a potent Mx inducer, whereas RGNNV induced lower Mx transcription and did not interfere with the IFN I system triggered by SJNNV or poly I:C. This study demonstrates that an antiviral state exists after SJNNV and poly I:C injection, suggesting that the IFN I system plays an important role against VNNV infections in sea bass. Head Kidney (dpeaa)DE-He213 Infectious Hematopoietic Necrosis Virus (dpeaa)DE-He213 Nervous Necrosis Virus (dpeaa)DE-He213 Striped Jack Nervous Necrosis Virus (dpeaa)DE-He213 Viral Nervous Necrosis Virus (dpeaa)DE-He213 Garcia-Rosado, Esther verfasserin aut Borrego, Juan J. verfasserin aut Alonso, M. Carmen verfasserin aut Enthalten in Veterinary research London : BioMed Central, 1993 47(2016), 1 vom: 08. Jan. (DE-627)312853653 (DE-600)2012391-7 1297-9716 nnns volume:47 year:2016 number:1 day:08 month:01 https://dx.doi.org/10.1186/s13567-015-0304-y kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_213 GBV_ILN_230 GBV_ILN_252 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 46.00 ASE AR 47 2016 1 08 01
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source	Enthalten in Veterinary research 47(2016), 1 vom: 08. Jan. volume:47 year:2016 number:1 day:08 month:01
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author	Carballo, Carlos
spellingShingle	Carballo, Carlos ddc 630 bkl 46.00 misc Head Kidney misc Infectious Hematopoietic Necrosis Virus misc Nervous Necrosis Virus misc Striped Jack Nervous Necrosis Virus misc Viral Nervous Necrosis Virus SJNNV down-regulates RGNNV replication in European sea bass by the induction of the type I interferon system
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topic_title	630 640 ASE 46.00 bkl SJNNV down-regulates RGNNV replication in European sea bass by the induction of the type I interferon system Head Kidney (dpeaa)DE-He213 Infectious Hematopoietic Necrosis Virus (dpeaa)DE-He213 Nervous Necrosis Virus (dpeaa)DE-He213 Striped Jack Nervous Necrosis Virus (dpeaa)DE-He213 Viral Nervous Necrosis Virus (dpeaa)DE-He213
topic	ddc 630 bkl 46.00 misc Head Kidney misc Infectious Hematopoietic Necrosis Virus misc Nervous Necrosis Virus misc Striped Jack Nervous Necrosis Virus misc Viral Nervous Necrosis Virus
topic_unstemmed	ddc 630 bkl 46.00 misc Head Kidney misc Infectious Hematopoietic Necrosis Virus misc Nervous Necrosis Virus misc Striped Jack Nervous Necrosis Virus misc Viral Nervous Necrosis Virus
topic_browse	ddc 630 bkl 46.00 misc Head Kidney misc Infectious Hematopoietic Necrosis Virus misc Nervous Necrosis Virus misc Striped Jack Nervous Necrosis Virus misc Viral Nervous Necrosis Virus
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title	SJNNV down-regulates RGNNV replication in European sea bass by the induction of the type I interferon system
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title_full	SJNNV down-regulates RGNNV replication in European sea bass by the induction of the type I interferon system
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author_browse	Carballo, Carlos Garcia-Rosado, Esther Borrego, Juan J. Alonso, M. Carmen
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title_sort	sjnnv down-regulates rgnnv replication in european sea bass by the induction of the type i interferon system
title_auth	SJNNV down-regulates RGNNV replication in European sea bass by the induction of the type I interferon system
abstract	Abstract European sea bass is highly susceptible to the betanodavirus RGNNV genotype, although the SJNNV genotype has also been detected in this fish species. The coexistence of both genotypes may affect the replication of both viruses by viral interaction or by stimulation of the host antiviral defense system in which the IFN I system plays a key role. IFN I triggers the transcription of interferon-stimulated genes, including Mx genes, whose expression has been used as a reporter of IFN I activity. The present study evaluated the effect of a primary exposure to an SJNNV isolate on a subsequent RGNNV infection and analyzed the role of the IFN I system in controlling VNNV infections in sea bass using different in vivo approaches. VNNV infection and Mx transcription were comparatively evaluated after single infections, superinfection (SJ+RG) and co-infection (poly I:C+RG). The single RGNNV infection resulted in a 24% survival rate, whereas the previous SJNNV or poly I:C inoculation increased the survival rate up to 96 and 100%, respectively. RGNNV replication in superinfection was reduced compared with RGNNV replication after a single inoculation. Mx transcription analysis shows differential induction of the IFN I system by both isolates. SJNNV was a potent Mx inducer, whereas RGNNV induced lower Mx transcription and did not interfere with the IFN I system triggered by SJNNV or poly I:C. This study demonstrates that an antiviral state exists after SJNNV and poly I:C injection, suggesting that the IFN I system plays an important role against VNNV infections in sea bass.
abstractGer	Abstract European sea bass is highly susceptible to the betanodavirus RGNNV genotype, although the SJNNV genotype has also been detected in this fish species. The coexistence of both genotypes may affect the replication of both viruses by viral interaction or by stimulation of the host antiviral defense system in which the IFN I system plays a key role. IFN I triggers the transcription of interferon-stimulated genes, including Mx genes, whose expression has been used as a reporter of IFN I activity. The present study evaluated the effect of a primary exposure to an SJNNV isolate on a subsequent RGNNV infection and analyzed the role of the IFN I system in controlling VNNV infections in sea bass using different in vivo approaches. VNNV infection and Mx transcription were comparatively evaluated after single infections, superinfection (SJ+RG) and co-infection (poly I:C+RG). The single RGNNV infection resulted in a 24% survival rate, whereas the previous SJNNV or poly I:C inoculation increased the survival rate up to 96 and 100%, respectively. RGNNV replication in superinfection was reduced compared with RGNNV replication after a single inoculation. Mx transcription analysis shows differential induction of the IFN I system by both isolates. SJNNV was a potent Mx inducer, whereas RGNNV induced lower Mx transcription and did not interfere with the IFN I system triggered by SJNNV or poly I:C. This study demonstrates that an antiviral state exists after SJNNV and poly I:C injection, suggesting that the IFN I system plays an important role against VNNV infections in sea bass.
abstract_unstemmed	Abstract European sea bass is highly susceptible to the betanodavirus RGNNV genotype, although the SJNNV genotype has also been detected in this fish species. The coexistence of both genotypes may affect the replication of both viruses by viral interaction or by stimulation of the host antiviral defense system in which the IFN I system plays a key role. IFN I triggers the transcription of interferon-stimulated genes, including Mx genes, whose expression has been used as a reporter of IFN I activity. The present study evaluated the effect of a primary exposure to an SJNNV isolate on a subsequent RGNNV infection and analyzed the role of the IFN I system in controlling VNNV infections in sea bass using different in vivo approaches. VNNV infection and Mx transcription were comparatively evaluated after single infections, superinfection (SJ+RG) and co-infection (poly I:C+RG). The single RGNNV infection resulted in a 24% survival rate, whereas the previous SJNNV or poly I:C inoculation increased the survival rate up to 96 and 100%, respectively. RGNNV replication in superinfection was reduced compared with RGNNV replication after a single inoculation. Mx transcription analysis shows differential induction of the IFN I system by both isolates. SJNNV was a potent Mx inducer, whereas RGNNV induced lower Mx transcription and did not interfere with the IFN I system triggered by SJNNV or poly I:C. This study demonstrates that an antiviral state exists after SJNNV and poly I:C injection, suggesting that the IFN I system plays an important role against VNNV infections in sea bass.
collection_details	GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_213 GBV_ILN_230 GBV_ILN_252 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700
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title_short	SJNNV down-regulates RGNNV replication in European sea bass by the induction of the type I interferon system
url	https://dx.doi.org/10.1186/s13567-015-0304-y
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author2	Garcia-Rosado, Esther Borrego, Juan J. Alonso, M. Carmen
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up_date	2024-07-04T01:23:19.284Z
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SJNNV down-regulates RGNNV replication in European sea bass by the induction of the type I interferon system

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