Investigation of the anti‐pseudorabies virus activity of interferon lambda 3 in cultured porcine kidney epithelial cells.

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Název: Investigation of the anti‐pseudorabies virus activity of interferon lambda 3 in cultured porcine kidney epithelial cells.
Autoři: Deng, Huidan1,2 (AUTHOR), Jian, Zhijie1 (AUTHOR), Zhu, Ling1,3 (AUTHOR), Li, Fengqin1,4 (AUTHOR), Zhao, Jun1 (AUTHOR), Deng, Junliang1,2,3 (AUTHOR), Sun, Xiangang1 (AUTHOR), Xu, Zhiwen1,2 (AUTHOR) abtcxzw@126.com
Zdroj: Veterinary Medicine & Science. Nov2022, Vol. 8 Issue 6, p2444-2450. 7p.
Druh dokumentu: Article
Témata: Epithelial cells, Gene expression, Aujeszky's disease virus, Protein expression, Kidneys
Author-Supplied Keywords: antiviral activity
IFN‐λ3
IFNLR
PK‐15
PRV
Abstrakt: Background: It has been reported Interferon‐λ (IFN‐λ) has stronger antiviral effect than other interferons. IFN‐λ can induce antiviral interferon stimulated genes (ISGs) in epithelia to protect against virus. Pseudorabies virus (PRV) infection in pigs resulting in fatal encephalitis in newborn piglets, respiratory disorders in finishing pigs, reproductive disorders in sows and other symptoms. Objectives: Since the effect of IFN‐λ on inhibiting PRV proliferation is still unknown. Inthis study, we investigate the relative contribution of porcine IFN‐λ3 toward controlling the infection of PRV in vitro. Our findings may provide a new insight for the prevention and treatment of PRV. Methods: Therefore, the antiviral assay, western blot, qRT‐PCR and ELISA assay were used to investigating the contribution of IFN‐λ against PRV in PK‐15 cells. Results: Here, we demonstrate that the replication of PRV in PK‐15 cells was inhibited after pre‐treatment with IFN‐λ3, and such inhibition was dose dependent. Overexpression of IFN‐λ3 receptor (IFNLR) also restricted virus titre in PK‐15 cells. In addition, IFN‐λ3 also increased the mRNA and protein expression of interferon‐stimulated genes 15 (ISG15), 2′‐5′‐oligoadenylate synthase 1 (OAS1), IFN‐inducible transmembrane 3 (IFITM3) and myxoma resistance protein 1 (Mx1) in PRV‐infected PK‐15 cells. Other than modulation ISGs, IFN‐λ specifically activated IFN‐γ mRNA expression not IFN‐α or IFN‐β. Conclusions: IFN‐λ3 had antiviral activity against PRV and the upregulation of ISGs and IFN‐γ mRNA expression may be the mechanism of IFN‐λ3's antiviral activities. Thus, IFN‐λ3 has a decisive function that greatly limits PRV replication in PK‐15 cells. Our study explores the antiviral activity of IFN‐λ3 on PRV for the first time. [ABSTRACT FROM AUTHOR]
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Author Affiliations: 1College of Veterinary Medicine, Sichuan Agricultural University, Cheng Du Sichuan Province,, China
2Key Laboratory of Animal Diseases and Environmental Hazards of Sichuan Province, Sichuan Agriculture University, Wenjiang Chengdu,, China
3Key Laboratory of Animal Disease and Human Health of Sichuan Province, Sichuan Agricultural University, Cheng Du Sichuan Province,, China
4College of Animal Science, Xichang University, Xichang Sichuan Province,, China
Full Text Word Count: 4343
ISSN: 2053-1095
DOI: 10.1002/vms3.933
Přístupové číslo: 160328637
Databáze: Veterinary Source
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Popis
Abstrakt:Background: It has been reported Interferon‐λ (IFN‐λ) has stronger antiviral effect than other interferons. IFN‐λ can induce antiviral interferon stimulated genes (ISGs) in epithelia to protect against virus. Pseudorabies virus (PRV) infection in pigs resulting in fatal encephalitis in newborn piglets, respiratory disorders in finishing pigs, reproductive disorders in sows and other symptoms. Objectives: Since the effect of IFN‐λ on inhibiting PRV proliferation is still unknown. Inthis study, we investigate the relative contribution of porcine IFN‐λ3 toward controlling the infection of PRV in vitro. Our findings may provide a new insight for the prevention and treatment of PRV. Methods: Therefore, the antiviral assay, western blot, qRT‐PCR and ELISA assay were used to investigating the contribution of IFN‐λ against PRV in PK‐15 cells. Results: Here, we demonstrate that the replication of PRV in PK‐15 cells was inhibited after pre‐treatment with IFN‐λ3, and such inhibition was dose dependent. Overexpression of IFN‐λ3 receptor (IFNLR) also restricted virus titre in PK‐15 cells. In addition, IFN‐λ3 also increased the mRNA and protein expression of interferon‐stimulated genes 15 (ISG15), 2′‐5′‐oligoadenylate synthase 1 (OAS1), IFN‐inducible transmembrane 3 (IFITM3) and myxoma resistance protein 1 (Mx1) in PRV‐infected PK‐15 cells. Other than modulation ISGs, IFN‐λ specifically activated IFN‐γ mRNA expression not IFN‐α or IFN‐β. Conclusions: IFN‐λ3 had antiviral activity against PRV and the upregulation of ISGs and IFN‐γ mRNA expression may be the mechanism of IFN‐λ3's antiviral activities. Thus, IFN‐λ3 has a decisive function that greatly limits PRV replication in PK‐15 cells. Our study explores the antiviral activity of IFN‐λ3 on PRV for the first time. [ABSTRACT FROM AUTHOR]
ISSN:20531095
DOI:10.1002/vms3.933