Previous studies have shown that interferon gene-stimulating protein (STING) is essential for IFN-γ-inducible protein 16 (IFI16) as the DNA sensor and RNA sensor to induce transcription of type I interferon (IFN-I) and is essential for IFI16 to synergize with DNA sensor GMP-AMP (cGAMP) synthase (cGAS) in induction of IFN-I transcription. While other and our previous studies have shown that IFI16 enhanced retinoic acid-inducible gene I (RIG-I)-, which was an RNA sensor, and mitochondrial antiviral signaling (MAVS)-, which was the adaptor protein of RIG-I, induced production of IFN-I, so we wonder whether IFI16 regulates the signal pathway of RNA-RIG-I-MAVS-IFN-I in a STING-dependent manner. We used HEK 293T cells, which did not express endogenous STING and were unable to mount an innate immune response upon DNA transfection and found that IFI16 could enhance RIG-I- and MAVS-mediated induction of IFN-I in a STING-independent way. Furthermore, we found that upregulation of the expression of NF-kappa-B essential modulator (NEMO) by IFI16 was not the mechanism that IFI16 regulated the induction of IFN-I. In conclusion, we found that IFI16 regulated the signal pathway of RNA-RIG-I-MAVS-IFN-I in a STING-independent manner.

Humic acid (HA) has an important effect on the environmental behaviors of arsenic. Arsenic has a higher affinity to iron, and arsenic transformation may bring more toxicity to soil’s microbial community. Applying C-rich substrate may affect soil’s functionality. There is few work to uncover the relation among them. So this work aimed to evaluate HA’s impact on arsenic transformation and soil’s functionality in arsenic-contaminated soil during remediation by iron-containing and C-rich material, iron-loaded polyethylene film (Pe-FeLs). Treatments were as follows: (T1) untreated arsenic-contaminated soil; (T2) arsenic-contaminated soil mixed with 0.1%, 0.3%, 0.5%, 1.0% (w/w) of HA; (T3) arsenic-contaminated soil mixed with 50 mg of Pe-FeLs; and (T4) arsenic-contaminated soil mixed with 50 mg of Pe-FeLs and with 0.1%, 0.3%, 0.5%, 1.0% (w/w) of HA. Arsenic and iron from soil were tested by extracting them in soil and measuring the concentration or species by ICP-OES, ICP-MS, or HPLC-ICP-MS. HA was tested by LC-OCD-OND. Soil respiration was measured using the absorption of carbon dioxide by sodium hydroxide. Biochemical properties were valued by measuring microbial biomass C (MBC) and N (MBN), dissolved organic C (DOC), total dissolved N (TDN), studying activities of dehydrogenase (Dehy), β-glucosidase (β-glu) and alkaline phosphatase (Phos), and calculating metabolic potential index (MI). In soil with Pe-FeLs and HA, HA induced the reduction of As(V) and arsenic transformation, due to HA’s competition for adsorption sites or forming HA-Fe-As complex because a higher concentration of HA could enable enough HA contact with Pe-FeLs to form HA-Fe complex. HA induced slightly iron release from Pe-FeLs because of HA’s acidity, which could promote arsenic transformation again. More toxic As(III) induced by arsenic transformation may bring higher toxicity to soil’s microbial community. Treatment with Pe-FeLs and HA induced the C/N cycles in soil higher than other treatments and positively affected soil’s microbial biomass. HA could enhance soil’s C/N cycles and enzymatic activities induced by the addition of Pe-FeLs, which could stimulate the growth of microbial biomass and increase C mineralization and immobilization of available N. Pe-FeLs decreased arsenic concentration in soil, but a lower concentration of HA could negatively affect this process. More toxic As(III) from arsenic transformation negatively affect soil’s microbial community. HA could enhance arsenic transformation induced by Pe-FeLs. Pe-FeLs and HA significantly influenced the soil’s functionality. This work provided another evidence of a strong relation among arsenic transformation, iron-modified and C-rich remediation material, and soil’s functionality in the existence of HA.

This work developed a composite (Pe-FeLs) which loaded ferric lignin on polyethylene film (PE film) by chemical modification and physico-chemically characterized by Microscope, FESEM with elemental mapping analysis, and XRD. Microscope pictures showed that chemical modification did not destroy the appearance of PE film. The FESEM images of Pe-FeLs showed the well-distributed clusters could be clearly seen and most of the particles were spherical morphology. Elemental mapping of individual element on Pe-FeLs clearly indicated the existing of iron. The XRD pattern showed the amorphous hydroxides of iron on Pe-FeLs. In arsenic solution, the total arsenic adsorption capacity of Pe-FeLs was much higher than that of ferric lignin and PE, which showed Pe-FeLs had the ability to adsorb arsenic. For making Pe-FeLs work well in the soil, a Pe-FeLs system was set up with plastic grid plate, PE film with holes, Pe-FeLs, PE film, and plastic grid plate from the upper to bottom in order. With applying Pe-FeLs system under the soil, arsenic was significantly reduced by 25.5 ~ 53.4% in heavily, moderately, and lower arsenic-polluted soils, the biomass of the romaine lettuce increased and arsenic accumulation in the romaine lettuce decreased.

Porcine reproductive and respiratory syndrome (PRRS) is a disease caused by PRRS virus (PRRSV), which seriously harms the pig industry. Revealing the mechanism by which PRRSV inhibits immune response will help prevent and control PRRS. Here, we found that PRRSV-2 may hijack host miR-541-3p to inhibit host innate immune response. Firstly, this work showed that miR-541-3p mimics could facilitate the replication of PRRSV-2 and the results of the quantitative real time polymerase chain reaction (qRT-PCR) showed that PRRSV-2 could up-regulate the expression of miR-541-3p in MARC-145 cells. Since previous studies have shown that type I interferon could effectively inhibit the replication of PRRSV-2, the present work explored whether miR-541-3p regulated the expression of type I interferon and found that miR-541-3p could negatively regulate the transcription of type I interferon by targeting interferon regulatory factor 7 (IRF7). More importantly, PRRSV-2 infection could down-regulate the expression of IRF7 and over-expression of IRF7 could down-regulate the replication of PRRSV-2 in MARC-145 cells. In conclusion, PRRSV-2 infection up-regulated the expression of miR-541-3p to promote its replication in MARC-145 cells, since miR-541-3p can negatively regulate the transcription of type I interferon by targeting IRF7.

In gold-smelting wastewater after the original treatment process of flocculation and precipitation using mainly lime, a mixture of As, Cu, Pb, Mn, Zn, Al, Ni, and Fe existed with an arsenic concentration of 813.07 mg/L and other ions' concentration at ug/L levels. In this work, a new clean process of mainly adsorption with self-made adsorbent Fe-PE, which was synthesized by loading ferric lignin on agricultural mulch film residual, was investigated to purify and remove arsenic from gold-smelting wastewater. A batch of column experiments was investigated to explore the reaction behavior between wastewater and adsorbent Fe-PE. The results showed while operating the adsorption columns at a pilot scale for 68 days, the arsenic concentration in the effluent was below 0.5 mg/L, and there was no significant change in the concentration of co-existing metal ions, indicating that Fe-PE had a good selective adsorption performance for arsenic in wastewater. Furthermore, Fe-PE did not dissolve and release Fe ions in wastewater, and the whole process could not produce sludge. This work first suggested an efficient and potential application for the purification and removal of arsenic from gold-smelting wastewater with agricultural mulch film residual after chemical modification, which will provide a novel strategy for reusing the agricultural mulch film residual.

猪繁殖与呼吸综合征病毒(porcine reproductive and respiratory syndrome virus,PRRSV)严重危害世界养猪业,目前仍无有效防控策略,因此探究宿主内源性蛋白拮抗PRRSV的分子机理意义重大.前期试验发现核因子I/A(nuclear factor I/A,NFIA)可以有效抑制PRRSV复制,故本试验以非洲绿猴胚胎肾细胞Marc-145细胞为模型,对NFIA抑制PRRSV复制的分子机理进行了深入探究.首先,构建NFIA的N末端DNA结合结构城缺失质粒pcD-NA3.1-Flag-ΔN和C末端转录激活结构域缺失质粒pcDNA3.1-Flag-AC并分别转染Marc-145细胞,24 h后感染PRRSV,48 h后用qRT-PCR和Western blot的试验方法分别检测病毒N蛋白的RNA和蛋白表达水平.结果 显示△C仍能有效降低PRRSV的RNA水平和N蛋白水平,但ΔN则不再能降低PRRSV的RNA水平和N蛋白水平,这表明NFIA的N末端结构城是抑制病毒的关键.其次,对NFIA全长质粒pcDNA3.1-Flag-WT进行N末端结构城内不同功能位点的双碱基突变,分别破坏掉NFIA的促腺病毒复制功能(Mut1,YR86～87WL)、DNA结合功能(Mut2,LR119～120VD)和二聚化功能(Mut3,LF135～136VD),将突变质粒分别转染Marc-145细胞,24 h后感染PRRSV,48 h后通过qRT-PCR和Western blot检测发现,Mut2和Mut3不再能降低PRRSV的RNA水平和N蛋白水平,说明N端结构城的DNA结合功能位点和二聚化功能位点是NFIA抑制PRRSV复制的关键.结果 表明,核因子I/A(NFIA)主要依赖其DNA结合结构域的二聚化与DNA结合功能来抑制PRRSV复制.

为获得有活性的猪繁殖与呼吸综合征病毒(porcine reproductive and respiratory syndrome virus,PRRSV)BJ-4株GP2a胞外区蛋白,以真核质粒pcDNA3.1-ORF2为模板,设计针对GP2a胞外区(41-208aa)的特异性引物,通过PCR等方法,获得重组表达质粒pET-32a-eORF2,转化宿主菌Rosetta(DE3),并用1 mmol/L异丙基硫代半乳糖苷(IPTG)进行诱导.SDS-PAGE结果表明,重组的GP2a胞外区蛋白以包涵体形式表达,相对分子质量约36 000;将包涵体纯化、复性后,以50μg/只的剂量免疫BALB/c小鼠,三免后,抗体效价达1∶102 400;这表明GP2a胞外区成功表达,且具有良好的免疫原性.

Previous studies have indicated that inhibition of type I interferon production may be an important reason for porcine reproductive and respiratory syndrome virus (PRRSV) to achieve immune escape, revealing the mechanism of inhibiting the production of type I interferon will help design novel strategies for controlling PRRS. Here, we found that PRRSV infection upregulated the expression of miR-382-5p, which in turn inhibited polyI:C-induced the production of type I interferon by targeting heat shock protein 60 (HSP60), thus facilitating PRRSV replication in MARC-145 cells. Furthermore, we found that HSP60 could interact with mitochondrial antiviral signaling protein (MAVS), an important signal transduction protein for inducing production of type I interferon, and promote polyI:C-mediated the production of type I interferon in a MAVS-dependent manner. Finally, we also found that HSP60 could inhibit PRRSV replication in a MAVS-dependent manner, which indicated that HSP60 was a novel antiviral protein against PRRSV replication. In conclusion, the study demonstrated that miR-382-5p was upregulated during PRRSV infection and may promote PRRSV replication by negatively regulating the production of type I interferon, which also indicated that miR-382-5p and HSP60 might be the potential therapeutic targets for anti-PRRSV.

为了研究甲基-CpG结合结构域蛋白2(MBD2)在体外对猪繁殖与呼吸综合征病毒(PRRSV)的复制是否有抑制作用.首先,构建MBD2的3'-UTR报告质粒,通过双荧光素酶报告结果表明MBD2是miR-373靶基因.然后用MOI=1的PRRSV感染MARC-145细胞,在24、36、48 h后分别取样,实时荧光定量PCR(qRT-PCR)和Western blots试验进行检测.结果表明,PRRSV感染下调MBD2的mRNA和蛋白的表达水平.用真核表达载体pcDNA3.1-Flag构建了MBD2的真核表达质粒pcDNA3.1-Flag-MBD2,用pcDNA3.1-Flag-MBD2转染MARC-145细胞,24 h后感染PRRSV,48 h后收获细胞.TCID50的试验结果表明,过表达MBD2能降低PRRSV滴度,而qRT-PCR和Western blots的结果则表明MBD2能降低PRRSV的载量;相反,MBD2的siRNA试验表明,下调表达有利于PRRSV在MARC-145细胞复制.通过基因缺失试验,构建MBD2部分结构域缺失的表达质粒,最终发现MBD2的GR与MBD结构域可能在MBD2抑制PRRSV复制起关键的作用.研究结果表明,MBD2是拮抗PRRSV的宿主内源性蛋白,并发现MBD2的GR与MBD结构域可能在MBD2抑制PRRSV复制中起关键的作用,而PRRSV可能利用miR-373来下调MBD2的表达,从而逃逸宿主对病毒的清除.

Porcine reproductive and respiratory syndrome virus (PRRSV) is a single-stranded positive-sense RNA virus, and the current strategies for controlling PRRSV are limited. Interferon gamma-inducible protein 16 (IFI16) has been reported to have a broader role in the regulation of the type I interferons (IFNs) response to RNA and DNA viruses. However, the function of IFI16 in PRRSV infection is unclear. Here, we revealed that IFI16 acts as a novel antiviral protein against PRRSV-2. IFI16 could be induced by interferon-beta (IFN-β). Overexpression of IFI16 could significantly suppress PRRSV-2 replication, and silencing the expression of endogenous IFI16 by small interfering RNAs led to the promotion of PRRSV-2 replication in MARC-145 cells. Additionally, IFI16 could promote mitochondrial antiviral signaling protein (MAVS)-mediated production of type I interferon and interact with MAVS. More importantly, IFI16 exerted anti-PRRSV effects in a MAVS-dependent manner. In conclusion, our data demonstrated that IFI16 has an inhibitory effect on PRRSV-2, and these findings contribute to understanding the role of cellular proteins in regulating PRRSV replication and may have implications for the future antiviral strategies.

以真核质粒pcDNA3.1-flag-nsp1α为模板,利用PCR扩增出nsp1α基因片段,构建原核重组载体pET32a-nsp1α,转化到大肠杆菌BL21(DE3)感受态,1 mmol/L IPTG在37℃诱导表达6 h,成功获得以包涵体形式存在的重组蛋白,能够与小鼠抗His标签单克隆抗体反应;包涵体复性后作为抗原免疫新西兰大白兔,3次免疫后20 d获得兔多抗血清.通过间接ELISA、Western blot、间接免疫荧光、免疫组化等试验获得了高效价的兔多抗血清,该血清能够特异性地识别真核质粒表达的nsp1α以及PRRSV BJ4株.该试验成功表达了pET32a-nsp1α重组蛋白,并制备了高效价、高特异性的兔抗nsp1α多克隆抗体.

Glycoprotein (GP) 2a was a minor structural protein of porcine reproductive and respiratory syndrome virus (PRRSV) and was one of crucial proteins for PRRSV to bind cell receptor, which indicated that there were neutralizing epitopes on GP2a. In the present work, we used mouse anti-GP2a41-208aa serum and one GP2a41-208aa specific monoclonal antibody (McAb) to identify B-cell epitopes of GP2a by peptide-based ELISA. A liner B-cell epitope F194PTPGSRPKLHDFQQ208 was identified. However, the results of virus neutralization experiment showed that the McAb could not reduce the titers of PRRSV, which indicated that the identified epitope was not the neutralizing epitope of PRRSV. While the amino acid sequence of this epitope was conserved in North American (type 2) PRRSV, which suggested that this epitope might be diagnostic potential for type 2 PRRSV strains. In conclusion, our present work identified a new epitope on GP2a and this epitope might be diagnostic potential for type 2 PRRSV strains.

[Objective] Prokaryotic expression and purification of GP4 protein of porcine reproductive and respiratory syndrome virus (PRRSV) were conducted to provide basis for understanding the structure and function of PRRSV GP4.[Method] In this study,the ORF4 gene of PRRSV BJ-4 strain was amplified by RT-PCR and was cloned into the vector pMD19-T.Then,the truncated ORF4 without N and C terminals was amplified by PCR and sub-cloned to pET-32a.The pET-32a-tGP4 was transformed into E.coli BL21(DE3) and induced by IPTG.The solubility of recombinant protein was analyzed and it was purified using urea gradient method.Finally,the recombinant protein immune activity was detected by ELISA.[Result] The ORF4 was 537 bp by RT-PCR.The recombinant plasmid pET-32a-tGP4 was constructed successfully.The induction experiment showed that E.coli could express the recombinant protein GP4 in inclusion body form.Highly pure inclusion body was obtained using urea gradient method and the purified recombinant protein could react well with PRRSV polyclonal anti-serum.[Conclusion] The GP4 protein of PRRSV was successfully expressed using prokaryotic cells and the purified recombinant protein had good immunogenicity.

ABSTRACTMicroRNAs (miRNAs) play an important role in the regulation of immune responses. Previous studies have indicated that dysregulating the miRNAs leads to the immunosuppression of porcine reproductive and respiratory syndrome virus (PRRSV). However, it is not clear how PRRSV regulates the expression of host miRNA, which may lead to immune escape or promote the replication of the virus. The present work suggests that PRRSV upregulated the expression of miR-373 through elevating the expression of specificity protein 1 (Sp1) in MARC-145 cells. Furthermore, this work demonstrated that miR-373 promoted the replication of PRRSV, since miR-373 was a novel negative miRNA for the production of beta interferon (IFN-β) by targeting nuclear factor IA (NFIA), NFIB, interleukin-1 receptor-associated kinase 1 (IRAK1), IRAK4, and interferon regulatory factor 1 (IRF1). We also found that both NFIA and NFIB were novel proteins for inducing the production of IFN-β, and both of them could inhibit the replication of PRRSV. In conclusion, PRRSV upregulated the expression of miR-373 by elevating the expression of Sp1 and hijacked the host miR-373 to promote the replication of PRRSV by negatively regulating the production of IFN-β.IMPORTANCEPRRSV causes one of the most economically devastating diseases of swine, and there is no effective method for controlling PRRSV. It is not clear how PRRSV inhibits the host's immune response and induces persistent infection. Previous studies have shown that PRRSV inhibited the production of type I IFN, and the treatment of type I IFN could efficiently inhibit the replication of PRRSV, so it will be helpful to design new methods of controlling PRRSV by understanding the molecular mechanism by which PRRSV modulated the production of IFN. The current work shows that miR-373, upregulated by PRRSV, promotes PRRSV replication, since miR-373 impaired the production of IFN-β by targeting NFIA, NFIB, IRAK1, IRAK4, and IRF1, and both NFIA and NFIB were antiviral proteins to PRRSV. In conclusion, this paper revealed a novel mechanism of PRRSV that impaired the production of type I IFN by upregulating miR-373 expression in MARC-145 cells.

Porcine reproductive and respiratory syndrome virus (PRRSV) causes one of the most economically devastating and pandemic porcine diseases. Previous study has shown that MARC-145 cells pretreated with recombinant IFN-β (rIFN-β) couldn't develop cytopathic effect (CPE) of PRRSV. However, up to date, it is not clear whether MARC-145 cells post-treated with rIFN-β could develop CPE of PRRSV. The present work showed that the MARC-145 cells didn't develop the CPE at 120 hr post-infection (p.i.) with low-dose of PRRSV when the cells were pre-treated with rIFN-β (Group 1), post-treated with rIFN-β at 4 hr p.i. (Group 2), or post-treated with rIFN-β at 8 hr p.i. (Group 3), while the MARC-145 cells could develop CPE when the cells were infected with high-dose PRRSV and then treated with rIFN-β at 24 hr p.i.. Furthermore, the indirect immunofluorescence assay confirmed that there were a few N protein-positive cells in the high-dose infected cells in Group 1, Group 2 and Group 3, while there were no N protein-positive cells in the low-dose infected cells in all rIFN-β treatment groups. In addition, the numbers of N protein-positive cells in high-dose infected cells (MOI = 10) in Group 1 were lower than that in Group 2 and Group 3. The results above demonstrated that both pre-treatment with rIFN-β and an earlier post-treatment with rIFN-β could inhibit the PRRSV replication and could clear the low-dose infected PRRSV, which indicated that the rIFN-β had efficient antiviral activities when the cells have been infected with PRRSV.

BACKGROUND:Porcine reproductive and respiratory syndrome virus (PRRSV) induces one of most important devastating disease of swine worldwide, and the current methods poorly control it. Previous studies have indicated that the nonstructural protein 11 (nsp11) of PRRSV may be an important protein for the immune escape of PRRSV.RESULTS:Here, we firstly explored the effect of over-expression of nsp11 on PRRSV infection and found that over-expression of nsp11 enhanced the PRRSV titers while the small interfering RNA (siRNAs) specifically targeting nsp11 could reduce the PRRSV titers in MARC-145 cells.CONCLUSION:In conclusion, PRRSV nsp11 promotes PRRSV infection in MARC-145 cells and siRNAs targeting nsp11 may be a potential therapeutic strategy to control PRRSV in future.

猪繁殖与呼吸综合征（PRRS）是严重危害养猪业的病毒性传染病之一,其致病原猪繁殖与呼吸综合征病毒（PRRSV）抑制宿主的天然免疫和特异性免疫反应,引起机体免疫抑制,造成持续性感染,从而给该病的防控带来困难。NLRP3炎症小体作为先天性免疫的重要组分在机体抗病毒中发挥重要作用。前期研究发现PRRSV能够激活NLRP3炎症小体,但PRRSV是否存在拮抗NLRP3炎症小体的组分还未见报道。本研究首先在缺失内源性炎症小体的HEK293T细胞中,共转染NLRP3、ASC、procaspase-1和pro-IL-1β四个真核表达质粒,建立NLRP3炎症小体的体外研究模型。然后,在该炎症小体模型细胞和猪肺泡巨噬细胞中,转染PRRSV nsp1α的真核表达质粒,结果表明nsp1α能够明显拮抗炎症小体的活化,而进一步的突变试验表明缺失N端锌指（ZF）结构或者突变ZF结构的nsp1α均不能抑制NLRP3炎症小体活化。本研究不仅首次发现了拮抗NLRP3炎症小体活化的PRRSV蛋白——nsp1α,而且发现nsp1α的N端锌指结构是其抑制NLRP3炎症小体活性所必需。本研究进一步发现了PRRSV拮抗天然免疫的新机制,并为PRRSV的防控提供了潜在的分子靶点和理论指导。

Porcine reproductive and respiratory syndrome virus (PRRSV) is one of the most economically devastating and pandemic diseases of swine, which is poorly controlled by current methods. The inhibition of specific genes by small interfering RNA (siRNA) has been proven to be a potential therapeutic strategy against viral infection. Previous studies have indicated that the nonstructural protein 1α (nsp1α) of PRRSV may take an important role in virulence of PRRSV. The present work was involved to explore the effect of siRNA targeting nsp1α on the replication of PRRSV in MARC-145 cells, and the results showed that over-expression of nsp1α enhanced the replication of PRRSV and that siRNAs specifically targeting nsp1α significantly inhibited the replication of PRRSV in MARC-145 cells. In conclusion, this work indicated that nsp1α may be a viral pathogenicity factor of PRRSV and that siRNAs specifically targeting nsp1α may be a new strategy to control PRRSV in the future.

In order to obtain activated nonstructural protein 1α( nsp1α) of porcine reproductive and res-piratory syndrome virus (PRRSV),the nsp1α gene was amplified from the expression plasmid pcDNA3. 1-nsp1α of PRRSV BJ-4 strain and was subcloned into prokaryotic expression vector pET-28a. Then the pET-28a-nsp1α was transformed into E. coli BL21 (DE3). The E. coli BL21 (DE3) was induced by 1 mmol/L IPTG. SDS-PAGE result showed that the nsp1αwas mainly expressed in form of inclusion body and the molecular weight was 20 ku. Western blot result showed that nsp1αcould recognized with His-tag mouse Mcab. ELISA result showed that nspld could react with the PRRSV porcine positive serum which was diluted to 1∶6 400 . In this research the PRRSV nsp1α was expressed successfully and had good im- munological activity.

NLRP3 inflammasome, which is multiprotein complex that induces the maturity and secretion of proinflammatory interleukin-1β (IL-1β), takes a bridge between the innate and adaptive immune responses to the invading pathogens. It has been shown that porcine reproductive and respiratory syndrome virus (PRRSV) could activate the NLRP3 inflammasome but induce the host's immunosuppression. This study aims to explore whether PRRSV could encode the component to antagonize the NLRP3 inflammasome. The obtained results showed that PRRSV could induce the expression and secretion of IL-1β in early infection through the pathway of NLRP3 inflammasome in porcine alveolar macrophages (PAMs), but the levels of pro-IL-1β mRNA and IL-1β protein decreased to a degree that was similar to the level of the mock-infected group in later infection. This work also found that PRRSV nonstructural protein (nsp) 11 could inhibit the expression of pro-IL-1β mRNA induced by lipopolysaccharide (LPS) and the secretion of IL-1β induced by LPS plus nigericin in PAMs. Furthermore, the mutation studies showed that the endoribonuclease activity was essential for nsp11 to inhibit the secretion of IL-1β. Therefore, it could be indicated that PRRSV could induce the activation of NLRP3 inflammasome, but the virus encoded nsp11 to inhibit this action.