Porcine reproductive and respiratory syndrome virus activates inflammasomes of porcine alveolar macrophages via its small envelope protein E

Zhang, Kao; Hou, Qiang; Zhong, Zhenyu; Li, Xiujin; Chen, Huihui; Li, Wenyan; Wen, Jiexia; Wang, Liyue; Liu, Weiquan; Zhong, Fei

doi:10.1016/j.virol.2013.04.007

Cited by 57 publications

(40 citation statements)

References 32 publications

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“…We speculated that there may be other mechanisms involved in NLRP3-independent inflammasome activation during HP-PRRSV infection. Recently, PRRSV structural protein E was found to activate inflammasome and induce IL-1B secretion (49). However, the underlying mechanism was not characterized.…”

Section: Discussionmentioning

confidence: 99%

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DDX19A Senses Viral RNA and Mediates NLRP3-Dependent Inflammasome Activation

Liu

et al. 2015

The Journal of Immunology

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The NLRP3 inflammasome plays a major role in innate immune responses by activating caspase-1, resulting in secretion of IL-1β and inflammatory pathologic responses. Viral RNA can induce NLRP3 inflammasome activation. However, none of the components of NLRP3 inflammasome has the ability to bind viral RNA. Therefore, it had been proposed that there might have been some unidentified cytosolic RNA sensors that could bind viral RNA and NLRP3 to initiate NLRP3 inflammasome activation. In this study, DDX19A, a member of the DEAD/H-box protein family, was identified as a novel component of NLRP3 inflammasome using arterivirus infection as a model. We found that DDX19A interacted with viral RNA and NLRP3. Knockdown of DDX19A expression efficiently inhibited procaspase-1 cleavage and IL-1β secretion in porcine reproductive and respiration syndrome virus (PRRSV)–infected or PRRSV RNA-stimulated primary porcine alveolar macrophages. Overall, DDX19A was identified as a novel cytosolic RNA sensor that bridged PRRSV RNA and NLRP3 to activate NLRP3 inflammasome.

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Section: Discussionmentioning

confidence: 99%

“…IL-1b level was closely correlated with persistent infection and pathogenesis of PRRSV (48). Recently, it has been reported that PRRSV structural protein E was involved in IL-1b secretion (49), and HP-PRRSV infection can induce IL-1b secretion, which depends on the TLR4/MyD88 pathway and NLRP3 inflammasome activation (50).…”

mentioning

confidence: 99%

DDX19A Senses Viral RNA and Mediates NLRP3-Dependent Inflammasome Activation

Liu

et al. 2015

The Journal of Immunology

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“…More recently, several members of the picornaviridae family were shown to similarly activate NLRP3 through their 2B protein ion channel including encephalomyocarditis virus, poliovirus, enterovirus 71, and human rhinovirus [41,42]. The SH protein of human respiratory syncytial virus (RSV) also mediates NLRP3 inflammasome activation, as does the E protein of porcine reproductive and respiratory syndrome virus (PRRSV) [43,44]. Clearly, ion flux is a key feature for NLRP3 sensing of viral infection.…”

Section: Nlrp3 Inflammasomementioning

confidence: 99%

Inflammasome control of viral infection

Lupfer

Malik

Kanneganti

2015

Current Opinion in Virology

134

122

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The inflammasome is a caspase-1 containing complex that activates the proinflammatory cytokines IL-1β and IL-18 and results in the proinflammatory cell death known as pyroptosis. Numerous recent publications have highlighted the importance of inflammasome activation in the control of virus infection. Inflammasome activation during viral infection is dependent on a variety of upstream receptors including the NOD-Like receptor, RIG-I-Like receptor and AIM2-Like receptor families. Various receptors also function in inflammasome activation in different cellular compartments, including the cytoplasm and the nucleus. The effectiveness of inflammasomes at suppressing virus replication is highlighted by the prevalence and diversity of virus encoded inflammasome inhibitors. Also, the host has a myriad of regulatory mechanisms in place to prevent unwanted inflammasome activation and overt inflammation. Finally, recent reports begin to suggest that inflammasome activation and inflammasome modulation may have important clinical applications. Herein, we highlight recent advances and discuss potential future directions toward understanding the role of inflammasomes during virus infection.

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“…GFP-PRRSV generation was performed as described previously [3, 10, 35]. The 5′-capped GFP-PRRSV mRNA (Figure 2(a)) was first transcripted by T7 DNA polymerase in vitro with the transcription kit using Acl I-linearized FL12-GFP plasmid as a template (there is a T7 promoter upstream PRRSV genome in FL12 plasmid).…”

Section: Resultsmentioning

confidence: 99%

Preparation of North American Type II PRRSV Infectious Clone Expressing Green Fluorescent Protein

Wang

Zhang

Lin

et al. 2014

BioMed Research International

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Porcine reproductive and respiratory syndrome virus (PRRSV) is still one of the most important infectious diseases threatening the swine industry. To construct North American type II PRRSV infectious clone containing green fluorescent protein (GFP) gene, we amplify gfp gene, flanked by PRRSV Nsp2 gene fragments upstream and downstream, using overlap PCR method from pcDNA-EF1-GFP plasmid and FL12 plasmid containing PRRSV infectious genome as the templates. The Nsp2 fragment-flanked gfp gene was inserted into Nsp2 gene of the FL12 plasmid by Spe I and Xho I sites to generate PRRSV infectious recombinant plasmid (FL12-GFP) containing gfp gene. The recombinant PRRSV expressing GFP (PRRSV-GFP) was rescued in baby hamster kidney-21 (BHK-21) cells by transfecting PRRSV mRNA synthesized in vitro and amplified in Marc-145 cells. The PRRSV-GFP infectivity and replication capacity were identified. Results showed that, by adopting overlap PCR strategy, the gfp gene was successfully inserted into and fused with PRRSV Nsp2 gene in the PRRSV infectious clone plasmid FL-12 to generate FL12-GFP plasmid. The recombinant PRRSV-GFP was generated through transfecting PRRSV mRNA in BHK-2 cells. Like its parental virus, the recombinant PRRSV-GFP maintains its infectivity to Marc-145 cells and porcine alveolar macrophages (PAMs). This study provides essential conditions for further investigation on PRRSV.

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Porcine reproductive and respiratory syndrome virus activates inflammasomes of porcine alveolar macrophages via its small envelope protein E

Cited by 57 publications

References 32 publications

DDX19A Senses Viral RNA and Mediates NLRP3-Dependent Inflammasome Activation

DDX19A Senses Viral RNA and Mediates NLRP3-Dependent Inflammasome Activation

Inflammasome control of viral infection

Preparation of North American Type II PRRSV Infectious Clone Expressing Green Fluorescent Protein

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