ZAP, a CCCH-Type Zinc Finger Protein, Inhibits Porcine Reproductive and Respiratory Syndrome Virus Replication and Interacts with Viral Nsp9 (Q92340084)

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scientific article published on 01 May 2019

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English	ZAP, a CCCH-Type Zinc Finger Protein, Inhibits Porcine Reproductive and Respiratory Syndrome Virus Replication and Interacts with Viral Nsp9	scientific article published on 01 May 2019

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scholarly article

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29 April 2020

ZAP, a CCCH-Type Zinc Finger Protein, Inhibits Porcine Reproductive and Respiratory Syndrome Virus Replication and Interacts with Viral Nsp9 (English)

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29 April 2020

porcine reproductive and respiratory syndrome

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based on heuristic

inferred from title

porcine reproductive and respiratory syndrome virus

object named as

Porcine Reproductive and Respiratory Syndrome Virus

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based on heuristic

inferred from title

2

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29 April 2020

author name string

Yongxiang Zhao

1

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29 April 2020

Juan Bai

3

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29 April 2020

Xuewei Liu

4

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29 April 2020

Hans Nauwynck

5

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29 April 2020

Ping Jiang

6

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publication date

1 May 2019

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29 April 2020

Journal of Virology

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93

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10

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29 April 2020

Nsp1α of Porcine Reproductive and Respiratory Syndrome Virus Strain BB0907 Impairs the Function of Monocyte-Derived Dendritic Cells via the Release of Soluble CD83

1 reference

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Cholesterol 25-hydroxylase is an interferon-inducible factor that protects against porcine reproductive and respiratory syndrome virus infection.

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CG dinucleotide suppression enables antiviral defence targeting non-self RNA.

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Cholesterol 25-Hydroxylase Inhibits Porcine Reproductive and Respiratory Syndrome Virus Replication through Enzyme Activity-Dependent and -Independent Mechanisms

1 reference

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The Nucleocapsid Protein and Nonstructural Protein 10 of Highly Pathogenic Porcine Reproductive and Respiratory Syndrome Virus Enhance CD83 Production via NF-κB and Sp1 Signaling Pathways

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Nuclear export signal of PRRSV NSP1α is necessary for type I IFN inhibition

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Highly Pathogenic Porcine Reproductive and Respiratory Syndrome Virus Nsp4 Cleaves VISA to Impair Antiviral Responses Mediated by RIG-I-like Receptors.

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Monkey Viperin Restricts Porcine Reproductive and Respiratory Syndrome Virus Replication

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Porcine Reproductive and Respiratory Syndrome Virus Nucleocapsid Protein Interacts with Nsp9 and Cellular DHX9 To Regulate Viral RNA Synthesis

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Porcine Reproductive and Respiratory Syndrome Virus (PRRSV): Pathogenesis and Interaction with the Immune System.

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The Interferon-Induced Mx2 Inhibits Porcine Reproductive and Respiratory Syndrome Virus Replication

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Porcine reproductive and respiratory syndrome virus 3C protease cleaves the mitochondrial antiviral signalling complex to antagonize IFN-β expression

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The N-N non-covalent domain of the nucleocapsid protein of type 2 porcine reproductive and respiratory syndrome virus enhances induction of IL-10 expression

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The DEAD-box RNA helicase 5 positively regulates the replication of porcine reproductive and respiratory syndrome virus by interacting with viral Nsp9 in vitro

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The interaction of nonstructural protein 9 with retinoblastoma protein benefits the replication of genotype 2 porcine reproductive and respiratory syndrome virus in vitro

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Porcine reproductive and respiratory syndrome virus nonstructural protein 4 antagonizes beta interferon expression by targeting the NF-κB essential modulator

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The interaction between host Annexin A2 and viral Nsp9 is beneficial for replication of porcine reproductive and respiratory syndrome virus

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Poly(I:C) inhibits porcine reproductive and respiratory syndrome virus replication in MARC-145 cells via activation of IFIT3.

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ZAPS electrifies RIG-I signaling.

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ZAPS is a potent stimulator of signaling mediated by the RNA helicase RIG-I during antiviral responses

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ZAP-mediated mRNA degradation

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Identifiers

10.1128/JVI.00001-19

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29 April 2020

1 reference

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29 April 2020

1 reference

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29 April 2020

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