IL-1β induced by PRRSV co-infection inhibited CSFV C-strain proliferation via the TLR4/NF-κB/MAPK pathways and the NLRP3 inflammasome

Genetic Diversity of Porcine Reproductive and Respiratory Syndrome Virus (PRRSV) From 1996 to 2017 in China

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Overexpression of RACK1 enhanced the replication of porcine reproductive and respiratory syndrome virus in Marc-145 cells and promoted the NF-κB activation via upregulating the expression and phosphorylation of TRAF2

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TNF-α induced by porcine reproductive and respiratory syndrome virus inhibits the replication of classical swine fever virus C-strain

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Activation of Interleukin-1β Release by the Classical Swine Fever Virus Is Dependent on the NLRP3 Inflammasome, Which Affects Virus Growth in Monocytes

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An Antiviral Branch of the IL-1 Signaling Pathway Restricts Immune-Evasive Virus Replication

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Canonical Stimulation of the NLRP3 Inflammasome by Fungal Antigens Links Innate and Adaptive B-Lymphocyte Responses by Modulating IL-1β and IgM Production

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Cleaved c-FLIP mediates the antiviral effect of TNF-α against hepatitis B virus by dysregulating hepatocyte nuclear factors

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Nonstructural Protein 4 of Porcine Reproductive and Respiratory Syndrome Virus Modulates Cell Surface Swine Leukocyte Antigen Class I Expression by Downregulating β2-Microglobulin Transcription

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Up-regulation of IL-10 upon PRRSV vaccination impacts on the immune response against CSFV

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Targeting Swine Leukocyte Antigen Class I Molecules for Proteasomal Degradation by the nsp1α Replicase Protein of the Chinese Highly Pathogenic Porcine Reproductive and Respiratory Syndrome Virus Strain JXwn06

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(2015) Christopher A Hunter et al.   NATURE IMMUNOLOGY

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Porcine Reproductive and Respiratory Syndrome Virus Induces IL-1βProduction Depending on TLR4/MyD88 Pathway and NLRP3 Inflammasome in Primary Porcine Alveolar Macrophages

(2014) Jing Bi et al.   MEDIATORS OF INFLAMMATION

Classical swine fever in China: A minireview

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Comparative expression of Toll-like receptors and inflammatory cytokines in pigs infected with different virulent porcine reproductive and respiratory syndrome virus isolates

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Activation of the NLRP3 Inflammasome by IAV Virulence Protein PB1-F2 Contributes to Severe Pathophysiology and Disease

(2013) Julie L. McAuley et al.   PLoS Pathogens

TLR2/MyD88/NF-κB Pathway, Reactive Oxygen Species, Potassium Efflux Activates NLRP3/ASC Inflammasome during Respiratory Syncytial Virus Infection

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(2012) Louise Lohse et al.   VETERINARY MICROBIOLOGY

Stress-activated protein kinases are involved in porcine reproductive and respiratory syndrome virus infection and modulate virus-induced cytokine production

(2012) Yoo Jin Lee et al.   VIROLOGY

Induction of interleukin-10 is dependent on p38 mitogen-activated protein kinase pathway in macrophages infected with porcine reproductive and respiratory syndrome virus

(2012) Jun Hou et al.   Virology Journal

Activation of c-Jun NH(2)-terminal kinase is required for porcine reproductive and respiratory syndrome virus-induced apoptosis but not for virus replication

(2012) Shutao Yin et al.   VIRUS RESEARCH

Toll-like Receptors and Their Crosstalk with Other Innate Receptors in Infection and Immunity

(2011) Taro Kawai et al.   IMMUNITY

Hepatitis C virus activates interleukin-1  via caspase-1-inflammasome complex

(2011) D. Burdette et al.   JOURNAL OF GENERAL VIROLOGY

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Toll-like receptors and innate immunity

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The Intracellular Sensor NLRP3 Mediates Key Innate and Healing Responses to Influenza A Virus via the Regulation of Caspase-1

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