CD163 knockout pigs are fully resistant to highly pathogenic porcine reproductive and respiratory syndrome virus
Porcine reproductive and respiratory syndrome virus (PRRSV) causes severe economic losses to current swine production worldwide. Highly pathogenic PRRSV (HP-PRRSV), originated from a genotype 2 PRRSV, is more virulent than classical PRRSV and further exacerbates the economic impact. HP-PRRSV has bec...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Yang, Huaqiang [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2018transfer abstract |
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| Schlagwörter: |
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| Umfang: |
8 |
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| Übergeordnetes Werk: |
Enthalten in: Modeling and prediction of surface roughness for running-in wear using Gauss-Newton algorithm and ANN - Hanief, M. ELSEVIER, 2015transfer abstract, a multidisciplinary journal of antiviral agents, natural host defence mechanisms, interferons and antiviral vaccines : an official publication of the International Society for Antiviral Research, Amsterdam [u.a.] |
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| Übergeordnetes Werk: |
volume:151 ; year:2018 ; pages:63-70 ; extent:8 |
| Links: |
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| DOI / URN: |
10.1016/j.antiviral.2018.01.004 |
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ELV042164583 |
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| 245 | 1 | 0 | |a CD163 knockout pigs are fully resistant to highly pathogenic porcine reproductive and respiratory syndrome virus |
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| 520 | |a Porcine reproductive and respiratory syndrome virus (PRRSV) causes severe economic losses to current swine production worldwide. Highly pathogenic PRRSV (HP-PRRSV), originated from a genotype 2 PRRSV, is more virulent than classical PRRSV and further exacerbates the economic impact. HP-PRRSV has become the predominant circulating field strain in China since 2006. CD163 is a cellular receptor for PRRSV. The depletion of CD163 whole protein or SRCR5 region (interaction site for the virus) confers resistance to infection of several PRRSV isolates in pigs or cultured host cells. In this study, we described the generation of a CD163 knockout (KO) pig in which the CD163 protein was ablated by using CRISPR/Cas9 gene targeting and somatic cell nuclear transfer (SCNT) technologies. Challenge with HP-PRRSV TP strain showed that CD163 KO pigs are completely resistant to viral infection manifested by the absence of viremia, antibody response, high fever or any other PRRS-associated clinical signs. By comparison, wild-type (WT) controls displayed typical signs of PRRSV infection and died within 2 weeks after infection. Deletion of CD163 showed no adverse effects to the macrophages on immunophenotyping and biological activity as hemoglobin–haptoglobin scavenger. The results demonstrated that CD163 knockout confers full resistance to HP-PRRSV infection to pigs without impairing the biological function associated with the gene. | ||
| 520 | |a Porcine reproductive and respiratory syndrome virus (PRRSV) causes severe economic losses to current swine production worldwide. Highly pathogenic PRRSV (HP-PRRSV), originated from a genotype 2 PRRSV, is more virulent than classical PRRSV and further exacerbates the economic impact. HP-PRRSV has become the predominant circulating field strain in China since 2006. CD163 is a cellular receptor for PRRSV. The depletion of CD163 whole protein or SRCR5 region (interaction site for the virus) confers resistance to infection of several PRRSV isolates in pigs or cultured host cells. In this study, we described the generation of a CD163 knockout (KO) pig in which the CD163 protein was ablated by using CRISPR/Cas9 gene targeting and somatic cell nuclear transfer (SCNT) technologies. Challenge with HP-PRRSV TP strain showed that CD163 KO pigs are completely resistant to viral infection manifested by the absence of viremia, antibody response, high fever or any other PRRS-associated clinical signs. By comparison, wild-type (WT) controls displayed typical signs of PRRSV infection and died within 2 weeks after infection. Deletion of CD163 showed no adverse effects to the macrophages on immunophenotyping and biological activity as hemoglobin–haptoglobin scavenger. The results demonstrated that CD163 knockout confers full resistance to HP-PRRSV infection to pigs without impairing the biological function associated with the gene. | ||
| 650 | 7 | |a SCNT |2 Elsevier | |
| 650 | 7 | |a CD163 |2 Elsevier | |
| 650 | 7 | |a Antiviral breeding |2 Elsevier | |
| 650 | 7 | |a CRISPR/Cas9 |2 Elsevier | |
| 650 | 7 | |a Highly pathogenic PRRSV |2 Elsevier | |
| 650 | 7 | |a Gene-knockout pigs |2 Elsevier | |
| 700 | 1 | |a Zhang, Jian |4 oth | |
| 700 | 1 | |a Zhang, Xianwei |4 oth | |
| 700 | 1 | |a Shi, Junsong |4 oth | |
| 700 | 1 | |a Pan, Yongfei |4 oth | |
| 700 | 1 | |a Zhou, Rong |4 oth | |
| 700 | 1 | |a Li, Guoling |4 oth | |
| 700 | 1 | |a Li, Zicong |4 oth | |
| 700 | 1 | |a Cai, Gengyuan |4 oth | |
| 700 | 1 | |a Wu, Zhenfang |4 oth | |
| 773 | 0 | 8 | |i Enthalten in |n Elsevier Science |a Hanief, M. ELSEVIER |t Modeling and prediction of surface roughness for running-in wear using Gauss-Newton algorithm and ANN |d 2015transfer abstract |d a multidisciplinary journal of antiviral agents, natural host defence mechanisms, interferons and antiviral vaccines : an official publication of the International Society for Antiviral Research |g Amsterdam [u.a.] |w (DE-627)ELV012905879 |
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10.1016/j.antiviral.2018.01.004 doi GBV00000000000154A.pica (DE-627)ELV042164583 (ELSEVIER)S0166-3542(17)30733-7 DE-627 ger DE-627 rakwb eng 610 610 DE-600 670 VZ 530 VZ 660 VZ 000 150 VZ 54.74 bkl Yang, Huaqiang verfasserin aut CD163 knockout pigs are fully resistant to highly pathogenic porcine reproductive and respiratory syndrome virus 2018transfer abstract 8 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Porcine reproductive and respiratory syndrome virus (PRRSV) causes severe economic losses to current swine production worldwide. Highly pathogenic PRRSV (HP-PRRSV), originated from a genotype 2 PRRSV, is more virulent than classical PRRSV and further exacerbates the economic impact. HP-PRRSV has become the predominant circulating field strain in China since 2006. CD163 is a cellular receptor for PRRSV. The depletion of CD163 whole protein or SRCR5 region (interaction site for the virus) confers resistance to infection of several PRRSV isolates in pigs or cultured host cells. In this study, we described the generation of a CD163 knockout (KO) pig in which the CD163 protein was ablated by using CRISPR/Cas9 gene targeting and somatic cell nuclear transfer (SCNT) technologies. Challenge with HP-PRRSV TP strain showed that CD163 KO pigs are completely resistant to viral infection manifested by the absence of viremia, antibody response, high fever or any other PRRS-associated clinical signs. By comparison, wild-type (WT) controls displayed typical signs of PRRSV infection and died within 2 weeks after infection. Deletion of CD163 showed no adverse effects to the macrophages on immunophenotyping and biological activity as hemoglobin–haptoglobin scavenger. The results demonstrated that CD163 knockout confers full resistance to HP-PRRSV infection to pigs without impairing the biological function associated with the gene. Porcine reproductive and respiratory syndrome virus (PRRSV) causes severe economic losses to current swine production worldwide. Highly pathogenic PRRSV (HP-PRRSV), originated from a genotype 2 PRRSV, is more virulent than classical PRRSV and further exacerbates the economic impact. HP-PRRSV has become the predominant circulating field strain in China since 2006. CD163 is a cellular receptor for PRRSV. The depletion of CD163 whole protein or SRCR5 region (interaction site for the virus) confers resistance to infection of several PRRSV isolates in pigs or cultured host cells. In this study, we described the generation of a CD163 knockout (KO) pig in which the CD163 protein was ablated by using CRISPR/Cas9 gene targeting and somatic cell nuclear transfer (SCNT) technologies. Challenge with HP-PRRSV TP strain showed that CD163 KO pigs are completely resistant to viral infection manifested by the absence of viremia, antibody response, high fever or any other PRRS-associated clinical signs. By comparison, wild-type (WT) controls displayed typical signs of PRRSV infection and died within 2 weeks after infection. Deletion of CD163 showed no adverse effects to the macrophages on immunophenotyping and biological activity as hemoglobin–haptoglobin scavenger. The results demonstrated that CD163 knockout confers full resistance to HP-PRRSV infection to pigs without impairing the biological function associated with the gene. SCNT Elsevier CD163 Elsevier Antiviral breeding Elsevier CRISPR/Cas9 Elsevier Highly pathogenic PRRSV Elsevier Gene-knockout pigs Elsevier Zhang, Jian oth Zhang, Xianwei oth Shi, Junsong oth Pan, Yongfei oth Zhou, Rong oth Li, Guoling oth Li, Zicong oth Cai, Gengyuan oth Wu, Zhenfang oth Enthalten in Elsevier Science Hanief, M. ELSEVIER Modeling and prediction of surface roughness for running-in wear using Gauss-Newton algorithm and ANN 2015transfer abstract a multidisciplinary journal of antiviral agents, natural host defence mechanisms, interferons and antiviral vaccines : an official publication of the International Society for Antiviral Research Amsterdam [u.a.] (DE-627)ELV012905879 volume:151 year:2018 pages:63-70 extent:8 https://doi.org/10.1016/j.antiviral.2018.01.004 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 54.74 Maschinelles Sehen VZ AR 151 2018 63-70 8 045F 610 |
| spelling |
10.1016/j.antiviral.2018.01.004 doi GBV00000000000154A.pica (DE-627)ELV042164583 (ELSEVIER)S0166-3542(17)30733-7 DE-627 ger DE-627 rakwb eng 610 610 DE-600 670 VZ 530 VZ 660 VZ 000 150 VZ 54.74 bkl Yang, Huaqiang verfasserin aut CD163 knockout pigs are fully resistant to highly pathogenic porcine reproductive and respiratory syndrome virus 2018transfer abstract 8 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Porcine reproductive and respiratory syndrome virus (PRRSV) causes severe economic losses to current swine production worldwide. Highly pathogenic PRRSV (HP-PRRSV), originated from a genotype 2 PRRSV, is more virulent than classical PRRSV and further exacerbates the economic impact. HP-PRRSV has become the predominant circulating field strain in China since 2006. CD163 is a cellular receptor for PRRSV. The depletion of CD163 whole protein or SRCR5 region (interaction site for the virus) confers resistance to infection of several PRRSV isolates in pigs or cultured host cells. In this study, we described the generation of a CD163 knockout (KO) pig in which the CD163 protein was ablated by using CRISPR/Cas9 gene targeting and somatic cell nuclear transfer (SCNT) technologies. Challenge with HP-PRRSV TP strain showed that CD163 KO pigs are completely resistant to viral infection manifested by the absence of viremia, antibody response, high fever or any other PRRS-associated clinical signs. By comparison, wild-type (WT) controls displayed typical signs of PRRSV infection and died within 2 weeks after infection. Deletion of CD163 showed no adverse effects to the macrophages on immunophenotyping and biological activity as hemoglobin–haptoglobin scavenger. The results demonstrated that CD163 knockout confers full resistance to HP-PRRSV infection to pigs without impairing the biological function associated with the gene. Porcine reproductive and respiratory syndrome virus (PRRSV) causes severe economic losses to current swine production worldwide. Highly pathogenic PRRSV (HP-PRRSV), originated from a genotype 2 PRRSV, is more virulent than classical PRRSV and further exacerbates the economic impact. HP-PRRSV has become the predominant circulating field strain in China since 2006. CD163 is a cellular receptor for PRRSV. The depletion of CD163 whole protein or SRCR5 region (interaction site for the virus) confers resistance to infection of several PRRSV isolates in pigs or cultured host cells. In this study, we described the generation of a CD163 knockout (KO) pig in which the CD163 protein was ablated by using CRISPR/Cas9 gene targeting and somatic cell nuclear transfer (SCNT) technologies. Challenge with HP-PRRSV TP strain showed that CD163 KO pigs are completely resistant to viral infection manifested by the absence of viremia, antibody response, high fever or any other PRRS-associated clinical signs. By comparison, wild-type (WT) controls displayed typical signs of PRRSV infection and died within 2 weeks after infection. Deletion of CD163 showed no adverse effects to the macrophages on immunophenotyping and biological activity as hemoglobin–haptoglobin scavenger. The results demonstrated that CD163 knockout confers full resistance to HP-PRRSV infection to pigs without impairing the biological function associated with the gene. SCNT Elsevier CD163 Elsevier Antiviral breeding Elsevier CRISPR/Cas9 Elsevier Highly pathogenic PRRSV Elsevier Gene-knockout pigs Elsevier Zhang, Jian oth Zhang, Xianwei oth Shi, Junsong oth Pan, Yongfei oth Zhou, Rong oth Li, Guoling oth Li, Zicong oth Cai, Gengyuan oth Wu, Zhenfang oth Enthalten in Elsevier Science Hanief, M. ELSEVIER Modeling and prediction of surface roughness for running-in wear using Gauss-Newton algorithm and ANN 2015transfer abstract a multidisciplinary journal of antiviral agents, natural host defence mechanisms, interferons and antiviral vaccines : an official publication of the International Society for Antiviral Research Amsterdam [u.a.] (DE-627)ELV012905879 volume:151 year:2018 pages:63-70 extent:8 https://doi.org/10.1016/j.antiviral.2018.01.004 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 54.74 Maschinelles Sehen VZ AR 151 2018 63-70 8 045F 610 |
| allfields_unstemmed |
10.1016/j.antiviral.2018.01.004 doi GBV00000000000154A.pica (DE-627)ELV042164583 (ELSEVIER)S0166-3542(17)30733-7 DE-627 ger DE-627 rakwb eng 610 610 DE-600 670 VZ 530 VZ 660 VZ 000 150 VZ 54.74 bkl Yang, Huaqiang verfasserin aut CD163 knockout pigs are fully resistant to highly pathogenic porcine reproductive and respiratory syndrome virus 2018transfer abstract 8 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Porcine reproductive and respiratory syndrome virus (PRRSV) causes severe economic losses to current swine production worldwide. Highly pathogenic PRRSV (HP-PRRSV), originated from a genotype 2 PRRSV, is more virulent than classical PRRSV and further exacerbates the economic impact. HP-PRRSV has become the predominant circulating field strain in China since 2006. CD163 is a cellular receptor for PRRSV. The depletion of CD163 whole protein or SRCR5 region (interaction site for the virus) confers resistance to infection of several PRRSV isolates in pigs or cultured host cells. In this study, we described the generation of a CD163 knockout (KO) pig in which the CD163 protein was ablated by using CRISPR/Cas9 gene targeting and somatic cell nuclear transfer (SCNT) technologies. Challenge with HP-PRRSV TP strain showed that CD163 KO pigs are completely resistant to viral infection manifested by the absence of viremia, antibody response, high fever or any other PRRS-associated clinical signs. By comparison, wild-type (WT) controls displayed typical signs of PRRSV infection and died within 2 weeks after infection. Deletion of CD163 showed no adverse effects to the macrophages on immunophenotyping and biological activity as hemoglobin–haptoglobin scavenger. The results demonstrated that CD163 knockout confers full resistance to HP-PRRSV infection to pigs without impairing the biological function associated with the gene. Porcine reproductive and respiratory syndrome virus (PRRSV) causes severe economic losses to current swine production worldwide. Highly pathogenic PRRSV (HP-PRRSV), originated from a genotype 2 PRRSV, is more virulent than classical PRRSV and further exacerbates the economic impact. HP-PRRSV has become the predominant circulating field strain in China since 2006. CD163 is a cellular receptor for PRRSV. The depletion of CD163 whole protein or SRCR5 region (interaction site for the virus) confers resistance to infection of several PRRSV isolates in pigs or cultured host cells. In this study, we described the generation of a CD163 knockout (KO) pig in which the CD163 protein was ablated by using CRISPR/Cas9 gene targeting and somatic cell nuclear transfer (SCNT) technologies. Challenge with HP-PRRSV TP strain showed that CD163 KO pigs are completely resistant to viral infection manifested by the absence of viremia, antibody response, high fever or any other PRRS-associated clinical signs. By comparison, wild-type (WT) controls displayed typical signs of PRRSV infection and died within 2 weeks after infection. Deletion of CD163 showed no adverse effects to the macrophages on immunophenotyping and biological activity as hemoglobin–haptoglobin scavenger. The results demonstrated that CD163 knockout confers full resistance to HP-PRRSV infection to pigs without impairing the biological function associated with the gene. SCNT Elsevier CD163 Elsevier Antiviral breeding Elsevier CRISPR/Cas9 Elsevier Highly pathogenic PRRSV Elsevier Gene-knockout pigs Elsevier Zhang, Jian oth Zhang, Xianwei oth Shi, Junsong oth Pan, Yongfei oth Zhou, Rong oth Li, Guoling oth Li, Zicong oth Cai, Gengyuan oth Wu, Zhenfang oth Enthalten in Elsevier Science Hanief, M. ELSEVIER Modeling and prediction of surface roughness for running-in wear using Gauss-Newton algorithm and ANN 2015transfer abstract a multidisciplinary journal of antiviral agents, natural host defence mechanisms, interferons and antiviral vaccines : an official publication of the International Society for Antiviral Research Amsterdam [u.a.] (DE-627)ELV012905879 volume:151 year:2018 pages:63-70 extent:8 https://doi.org/10.1016/j.antiviral.2018.01.004 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 54.74 Maschinelles Sehen VZ AR 151 2018 63-70 8 045F 610 |
| allfieldsGer |
10.1016/j.antiviral.2018.01.004 doi GBV00000000000154A.pica (DE-627)ELV042164583 (ELSEVIER)S0166-3542(17)30733-7 DE-627 ger DE-627 rakwb eng 610 610 DE-600 670 VZ 530 VZ 660 VZ 000 150 VZ 54.74 bkl Yang, Huaqiang verfasserin aut CD163 knockout pigs are fully resistant to highly pathogenic porcine reproductive and respiratory syndrome virus 2018transfer abstract 8 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Porcine reproductive and respiratory syndrome virus (PRRSV) causes severe economic losses to current swine production worldwide. Highly pathogenic PRRSV (HP-PRRSV), originated from a genotype 2 PRRSV, is more virulent than classical PRRSV and further exacerbates the economic impact. HP-PRRSV has become the predominant circulating field strain in China since 2006. CD163 is a cellular receptor for PRRSV. The depletion of CD163 whole protein or SRCR5 region (interaction site for the virus) confers resistance to infection of several PRRSV isolates in pigs or cultured host cells. In this study, we described the generation of a CD163 knockout (KO) pig in which the CD163 protein was ablated by using CRISPR/Cas9 gene targeting and somatic cell nuclear transfer (SCNT) technologies. Challenge with HP-PRRSV TP strain showed that CD163 KO pigs are completely resistant to viral infection manifested by the absence of viremia, antibody response, high fever or any other PRRS-associated clinical signs. By comparison, wild-type (WT) controls displayed typical signs of PRRSV infection and died within 2 weeks after infection. Deletion of CD163 showed no adverse effects to the macrophages on immunophenotyping and biological activity as hemoglobin–haptoglobin scavenger. The results demonstrated that CD163 knockout confers full resistance to HP-PRRSV infection to pigs without impairing the biological function associated with the gene. Porcine reproductive and respiratory syndrome virus (PRRSV) causes severe economic losses to current swine production worldwide. Highly pathogenic PRRSV (HP-PRRSV), originated from a genotype 2 PRRSV, is more virulent than classical PRRSV and further exacerbates the economic impact. HP-PRRSV has become the predominant circulating field strain in China since 2006. CD163 is a cellular receptor for PRRSV. The depletion of CD163 whole protein or SRCR5 region (interaction site for the virus) confers resistance to infection of several PRRSV isolates in pigs or cultured host cells. In this study, we described the generation of a CD163 knockout (KO) pig in which the CD163 protein was ablated by using CRISPR/Cas9 gene targeting and somatic cell nuclear transfer (SCNT) technologies. Challenge with HP-PRRSV TP strain showed that CD163 KO pigs are completely resistant to viral infection manifested by the absence of viremia, antibody response, high fever or any other PRRS-associated clinical signs. By comparison, wild-type (WT) controls displayed typical signs of PRRSV infection and died within 2 weeks after infection. Deletion of CD163 showed no adverse effects to the macrophages on immunophenotyping and biological activity as hemoglobin–haptoglobin scavenger. The results demonstrated that CD163 knockout confers full resistance to HP-PRRSV infection to pigs without impairing the biological function associated with the gene. SCNT Elsevier CD163 Elsevier Antiviral breeding Elsevier CRISPR/Cas9 Elsevier Highly pathogenic PRRSV Elsevier Gene-knockout pigs Elsevier Zhang, Jian oth Zhang, Xianwei oth Shi, Junsong oth Pan, Yongfei oth Zhou, Rong oth Li, Guoling oth Li, Zicong oth Cai, Gengyuan oth Wu, Zhenfang oth Enthalten in Elsevier Science Hanief, M. ELSEVIER Modeling and prediction of surface roughness for running-in wear using Gauss-Newton algorithm and ANN 2015transfer abstract a multidisciplinary journal of antiviral agents, natural host defence mechanisms, interferons and antiviral vaccines : an official publication of the International Society for Antiviral Research Amsterdam [u.a.] (DE-627)ELV012905879 volume:151 year:2018 pages:63-70 extent:8 https://doi.org/10.1016/j.antiviral.2018.01.004 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 54.74 Maschinelles Sehen VZ AR 151 2018 63-70 8 045F 610 |
| allfieldsSound |
10.1016/j.antiviral.2018.01.004 doi GBV00000000000154A.pica (DE-627)ELV042164583 (ELSEVIER)S0166-3542(17)30733-7 DE-627 ger DE-627 rakwb eng 610 610 DE-600 670 VZ 530 VZ 660 VZ 000 150 VZ 54.74 bkl Yang, Huaqiang verfasserin aut CD163 knockout pigs are fully resistant to highly pathogenic porcine reproductive and respiratory syndrome virus 2018transfer abstract 8 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Porcine reproductive and respiratory syndrome virus (PRRSV) causes severe economic losses to current swine production worldwide. Highly pathogenic PRRSV (HP-PRRSV), originated from a genotype 2 PRRSV, is more virulent than classical PRRSV and further exacerbates the economic impact. HP-PRRSV has become the predominant circulating field strain in China since 2006. CD163 is a cellular receptor for PRRSV. The depletion of CD163 whole protein or SRCR5 region (interaction site for the virus) confers resistance to infection of several PRRSV isolates in pigs or cultured host cells. In this study, we described the generation of a CD163 knockout (KO) pig in which the CD163 protein was ablated by using CRISPR/Cas9 gene targeting and somatic cell nuclear transfer (SCNT) technologies. Challenge with HP-PRRSV TP strain showed that CD163 KO pigs are completely resistant to viral infection manifested by the absence of viremia, antibody response, high fever or any other PRRS-associated clinical signs. By comparison, wild-type (WT) controls displayed typical signs of PRRSV infection and died within 2 weeks after infection. Deletion of CD163 showed no adverse effects to the macrophages on immunophenotyping and biological activity as hemoglobin–haptoglobin scavenger. The results demonstrated that CD163 knockout confers full resistance to HP-PRRSV infection to pigs without impairing the biological function associated with the gene. Porcine reproductive and respiratory syndrome virus (PRRSV) causes severe economic losses to current swine production worldwide. Highly pathogenic PRRSV (HP-PRRSV), originated from a genotype 2 PRRSV, is more virulent than classical PRRSV and further exacerbates the economic impact. HP-PRRSV has become the predominant circulating field strain in China since 2006. CD163 is a cellular receptor for PRRSV. The depletion of CD163 whole protein or SRCR5 region (interaction site for the virus) confers resistance to infection of several PRRSV isolates in pigs or cultured host cells. In this study, we described the generation of a CD163 knockout (KO) pig in which the CD163 protein was ablated by using CRISPR/Cas9 gene targeting and somatic cell nuclear transfer (SCNT) technologies. Challenge with HP-PRRSV TP strain showed that CD163 KO pigs are completely resistant to viral infection manifested by the absence of viremia, antibody response, high fever or any other PRRS-associated clinical signs. By comparison, wild-type (WT) controls displayed typical signs of PRRSV infection and died within 2 weeks after infection. Deletion of CD163 showed no adverse effects to the macrophages on immunophenotyping and biological activity as hemoglobin–haptoglobin scavenger. The results demonstrated that CD163 knockout confers full resistance to HP-PRRSV infection to pigs without impairing the biological function associated with the gene. SCNT Elsevier CD163 Elsevier Antiviral breeding Elsevier CRISPR/Cas9 Elsevier Highly pathogenic PRRSV Elsevier Gene-knockout pigs Elsevier Zhang, Jian oth Zhang, Xianwei oth Shi, Junsong oth Pan, Yongfei oth Zhou, Rong oth Li, Guoling oth Li, Zicong oth Cai, Gengyuan oth Wu, Zhenfang oth Enthalten in Elsevier Science Hanief, M. ELSEVIER Modeling and prediction of surface roughness for running-in wear using Gauss-Newton algorithm and ANN 2015transfer abstract a multidisciplinary journal of antiviral agents, natural host defence mechanisms, interferons and antiviral vaccines : an official publication of the International Society for Antiviral Research Amsterdam [u.a.] (DE-627)ELV012905879 volume:151 year:2018 pages:63-70 extent:8 https://doi.org/10.1016/j.antiviral.2018.01.004 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 54.74 Maschinelles Sehen VZ AR 151 2018 63-70 8 045F 610 |
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Enthalten in Modeling and prediction of surface roughness for running-in wear using Gauss-Newton algorithm and ANN Amsterdam [u.a.] volume:151 year:2018 pages:63-70 extent:8 |
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Modeling and prediction of surface roughness for running-in wear using Gauss-Newton algorithm and ANN |
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Yang, Huaqiang @@aut@@ Zhang, Jian @@oth@@ Zhang, Xianwei @@oth@@ Shi, Junsong @@oth@@ Pan, Yongfei @@oth@@ Zhou, Rong @@oth@@ Li, Guoling @@oth@@ Li, Zicong @@oth@@ Cai, Gengyuan @@oth@@ Wu, Zhenfang @@oth@@ |
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CD163 knockout pigs are fully resistant to highly pathogenic porcine reproductive and respiratory syndrome virus |
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Porcine reproductive and respiratory syndrome virus (PRRSV) causes severe economic losses to current swine production worldwide. Highly pathogenic PRRSV (HP-PRRSV), originated from a genotype 2 PRRSV, is more virulent than classical PRRSV and further exacerbates the economic impact. HP-PRRSV has become the predominant circulating field strain in China since 2006. CD163 is a cellular receptor for PRRSV. The depletion of CD163 whole protein or SRCR5 region (interaction site for the virus) confers resistance to infection of several PRRSV isolates in pigs or cultured host cells. In this study, we described the generation of a CD163 knockout (KO) pig in which the CD163 protein was ablated by using CRISPR/Cas9 gene targeting and somatic cell nuclear transfer (SCNT) technologies. Challenge with HP-PRRSV TP strain showed that CD163 KO pigs are completely resistant to viral infection manifested by the absence of viremia, antibody response, high fever or any other PRRS-associated clinical signs. By comparison, wild-type (WT) controls displayed typical signs of PRRSV infection and died within 2 weeks after infection. Deletion of CD163 showed no adverse effects to the macrophages on immunophenotyping and biological activity as hemoglobin–haptoglobin scavenger. The results demonstrated that CD163 knockout confers full resistance to HP-PRRSV infection to pigs without impairing the biological function associated with the gene. |
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Porcine reproductive and respiratory syndrome virus (PRRSV) causes severe economic losses to current swine production worldwide. Highly pathogenic PRRSV (HP-PRRSV), originated from a genotype 2 PRRSV, is more virulent than classical PRRSV and further exacerbates the economic impact. HP-PRRSV has become the predominant circulating field strain in China since 2006. CD163 is a cellular receptor for PRRSV. The depletion of CD163 whole protein or SRCR5 region (interaction site for the virus) confers resistance to infection of several PRRSV isolates in pigs or cultured host cells. In this study, we described the generation of a CD163 knockout (KO) pig in which the CD163 protein was ablated by using CRISPR/Cas9 gene targeting and somatic cell nuclear transfer (SCNT) technologies. Challenge with HP-PRRSV TP strain showed that CD163 KO pigs are completely resistant to viral infection manifested by the absence of viremia, antibody response, high fever or any other PRRS-associated clinical signs. By comparison, wild-type (WT) controls displayed typical signs of PRRSV infection and died within 2 weeks after infection. Deletion of CD163 showed no adverse effects to the macrophages on immunophenotyping and biological activity as hemoglobin–haptoglobin scavenger. The results demonstrated that CD163 knockout confers full resistance to HP-PRRSV infection to pigs without impairing the biological function associated with the gene. |
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Porcine reproductive and respiratory syndrome virus (PRRSV) causes severe economic losses to current swine production worldwide. Highly pathogenic PRRSV (HP-PRRSV), originated from a genotype 2 PRRSV, is more virulent than classical PRRSV and further exacerbates the economic impact. HP-PRRSV has become the predominant circulating field strain in China since 2006. CD163 is a cellular receptor for PRRSV. The depletion of CD163 whole protein or SRCR5 region (interaction site for the virus) confers resistance to infection of several PRRSV isolates in pigs or cultured host cells. In this study, we described the generation of a CD163 knockout (KO) pig in which the CD163 protein was ablated by using CRISPR/Cas9 gene targeting and somatic cell nuclear transfer (SCNT) technologies. Challenge with HP-PRRSV TP strain showed that CD163 KO pigs are completely resistant to viral infection manifested by the absence of viremia, antibody response, high fever or any other PRRS-associated clinical signs. By comparison, wild-type (WT) controls displayed typical signs of PRRSV infection and died within 2 weeks after infection. Deletion of CD163 showed no adverse effects to the macrophages on immunophenotyping and biological activity as hemoglobin–haptoglobin scavenger. The results demonstrated that CD163 knockout confers full resistance to HP-PRRSV infection to pigs without impairing the biological function associated with the gene. |
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In this study, we described the generation of a CD163 knockout (KO) pig in which the CD163 protein was ablated by using CRISPR/Cas9 gene targeting and somatic cell nuclear transfer (SCNT) technologies. Challenge with HP-PRRSV TP strain showed that CD163 KO pigs are completely resistant to viral infection manifested by the absence of viremia, antibody response, high fever or any other PRRS-associated clinical signs. By comparison, wild-type (WT) controls displayed typical signs of PRRSV infection and died within 2 weeks after infection. Deletion of CD163 showed no adverse effects to the macrophages on immunophenotyping and biological activity as hemoglobin–haptoglobin scavenger. 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ELSEVIER</subfield><subfield code="t">Modeling and prediction of surface roughness for running-in wear using Gauss-Newton algorithm and ANN</subfield><subfield code="d">2015transfer abstract</subfield><subfield code="d">a multidisciplinary journal of antiviral agents, natural host defence mechanisms, interferons and antiviral vaccines : an official publication of the International Society for Antiviral Research</subfield><subfield code="g">Amsterdam [u.a.]</subfield><subfield code="w">(DE-627)ELV012905879</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:151</subfield><subfield code="g">year:2018</subfield><subfield code="g">pages:63-70</subfield><subfield code="g">extent:8</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.1016/j.antiviral.2018.01.004</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ELV</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_U</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">54.74</subfield><subfield code="j">Maschinelles Sehen</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">151</subfield><subfield code="j">2018</subfield><subfield code="h">63-70</subfield><subfield code="g">8</subfield></datafield><datafield tag="953" ind1=" " ind2=" "><subfield code="2">045F</subfield><subfield code="a">610</subfield></datafield></record></collection>
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