Modification of African classical swine fever p30 protein with magnetic nanoparticles and establishment of a novel rapid detection method.

African swine fever has caused huge losses to the global pig industry. In the absence of effective vaccines, reliable detection methods are crucial. The p30 protein of ASFV is often used as a target for detection due to its high antigenicity in the early stage of virus replication.

Mass Spectrometry-Based Proteomic Analysis of Potential Host Proteins Interacting with N in PRRSV-Infected PAMs.

One of the most significant diseases in the swine business, porcine reproductive and respiratory syndrome virus (PRRSV) causes respiratory problems in piglets and reproductive failure in sows. The PRRSV nucleocapsid (N) protein is essential for the virus' assembly, replication, and immune evasion. Stages in the viral replication cycle can be impacted by interactions between the PRRSV nucleocapsid protein and the host protein components.

Mass Spectrometry-Based Proteomic Analysis of Potential Host Proteins Interacting with GP5 in PRRSV-Infected PAMs.

Porcine reproductive and respiratory syndrome virus (PRRSV) is a typical immunosuppressive virus causing a large economic impact on the swine industry. The structural protein GP5 of PRRSV plays a pivotal role in its pathogenicity and immune evasion. Virus-host interactions play a crucial part in viral replication and immune escape.

The Molecular and Function Characterization of Porcine MID2.

Midline2 (MID2/TRIM1) is a member of the tripartite motif-containing (TRIM) family, which is involved in a wide range of cellular processes. However, fundamental studies on porcine MID2 (pMID2) are still lacking. In this study, we identified and characterized the full length MID2 gene of pig ().

The Host E3-Ubiquitin Ligase TRIM28 Impedes Viral Protein GP4 Ubiquitination and Promotes PRRSV Replication.

Porcine reproductive and respiratory syndrome (PRRS), caused by the PRRS virus (PRRSV), is a highly pathogenic porcine virus that brings tremendous economic losses to the global swine industry. PRRSVs have evolved multiple elegant strategies to manipulate the host proteins and circumvent against the antiviral responses to establish infection. Therefore, the identification of virus-host interactions is critical for understanding the pathogenesis of PRRSVs.

Immune Molecules' mRNA Expression in Porcine Alveolar Macrophages Co-Infected with Porcine Reproductive and Respiratory Syndrome Virus and Porcine Circovirus Type 2.

Porcine reproductive and respiratory syndrome virus (PRRSV) and porcine circovirus 2 (PCV2) are economically important pathogens in swine, and pigs with dual infections of PCV2 and PRRSV consistently have more severe clinical symptoms and interstitial pneumonia. However, the synergistic pathogenesis mechanism induced by PRRSV and PCV2 co-infection has not yet been illuminated. Therefore, the aim of this study was to characterize the kinetic changes of immune regulatory molecules, inflammatory factors and immune checkpoint molecules in porcine alveolar macrophages (PAMs) in individuals infected or co-infected with PRRSV and/or PCV2.

Proteomic Characterization of PAMs with PRRSV-ADE Infection.

The antibody-dependent enhancement (ADE) effect of a PRRSV infection is that the preexisting sub- or non-neutralizing antibodies specific against PRRSV can facilitate the virus entry and replication, and it is likely to be a great obstacle for the selection of immune strategies and the development of high-efficiency PRRSV vaccines. However, the proteomic characterization of primary alveolar macrophages (PAMs) with a PRRSV-ADE infection has not yet been investigated so far. Therefore, we performed a tandem mass tag (TMT)-based quantitative proteomic analysis of PAMs with a PRRSV-ADE infection in this study.

Activating Fc Gamma Receptors and Viral Receptors Are Required for Antibody-Dependent Enhancement of Porcine Reproductive and Respiratory Syndrome Virus Infection.

Antibody-dependent enhancement (ADE) is an event in preexisting sub-, or non-neutralizing antibodies increasing the viral replication in its target cells. ADE is one crucial factor that intensifies porcine reproductive and respiratory syndrome virus (PRRSV) infection and results in PRRSV-persistent infection. Nevertheless, the exact mechanisms of PRRSV-ADE infection are poorly understood.

Differences in Humoral Immune Response against the Type 2 Porcine Reproductive and Respiratory Syndrome Virus via Different Immune Pathways.

The intramuscular vaccine is the principal strategy to protect pigs from porcine reproductive and respiratory syndrome virus (PRRSV), However, it is still difficult to control PRRSV effectively. This study infected piglets with PRRSV through intramuscular and intranasal inoculation. Subsequently, viral loads, anti-PRRSV antibody levels, and neutralizing antibodies (NAs) titers in both serum and saliva were monitored for 43 days.

MicroRNA-376b-3p Promotes Porcine Reproductive and Respiratory Syndrome Virus Replication by Targeting Viral Restriction Factor TRIM22.

Porcine reproductive and respiratory syndrome virus (PRRSV) is a major economically significant pathogen and has evolved several strategies to evade host antiviral response and provide favorable conditions for survival. In the present study, we demonstrated that a host microRNA, miR-376b-3p, was upregulated by PRRSV infection through the viral components, nsp4 and nsp11, and that miR-376b-3p can directly target tripartite motif-containing 22 (TRIM22) to impair its anti-PRRSV activity, thus facilitating the replication of PRRSV. Meanwhile, we found that TRIM22 induced degradation of the nucleocapsid protein (N) of PRRSV by interacting with N protein to inhibit PRRSV replication, and further study indicated that TRIM22 could enhance the activation of the lysosomal pathway by interacting with LC3 to induce lysosomal degradation of N protein.

Activation of Fc gamma receptor IIb up-regulates the production of interferon-alpha and interferon-gamma in porcine alveolar macrophages during PRRSV infection.

Porcine Fc gamma receptor IIb (FcγRIIb) has been cloned and characterized for many years. However, the role of FcγRIIb in innate antiviral response to porcine reproductive and respiratory syndrome virus (PRRSV) infection has not yet been well investigated. In current study, our results showed that specific activation of FcγRIIb in porcine alveolar macrophages (PAMs) significantly enhanced the production of interferon-alpha (IFN-α) and interferon-gamma (IFN-γ), and significantly repressed the production of transforming growth factor beta 1 (TGF-β1).

Activation of activating Fc gamma receptors down-regulates the levels of interferon β, interferon γ and interferon λ1 in porcine alveolar macrophages during PRRSV infection.

Porcine activating Fc gamma receptors (FcγRI and FcγRIII) have been cloned and characterized for many years. However, their roles in interferon (IFN) antiviral immune response to porcine reproductive and respiratory syndrome virus (PRRSV) infection have not yet been investigated extensively. In this study, PRRSV infection assay showed that PRRSV increased significantly the transcription of IFN-β, IFN-γ and IFN-λ1 in porcine alveolar macrophages (PAMs) in early infection and decreased significantly the transcription of IFN-β, IFN-γ and IFN-λ1 in PAMs in late infection.

Antibody-Mediated Porcine Reproductive and Respiratory Syndrome Virus Infection Downregulates the Production of Interferon-α and Tumor Necrosis Factor-α in Porcine Alveolar Macrophages via Fc Gamma Receptor I and III.

Antibody-dependent enhancement (ADE) contributes to the pathogenesis of porcine reproductive and respiratory syndrome virus (PRRSV)-persistent infection. However, the mechanisms of PRRSV-ADE infection are still confusing. A clear understanding of the event upon virus infection by the ADE pathway has become crucial for developing efficient intervention of the PRRSV infection.

Activation of sialoadhesin down-regulates the levels of innate antiviral cytokines in porcine alveolar macrophages in vitro.

Porcine sialoadhesin (pSn) is a crucial porcine reproductive and respiratory syndrome virus (PRRSV) receptor mediating the attachment and internalization of virus into its major target cells, porcine alveolar macrophages (PAMs). However, the role of pSn in innate antiviral immune response has not yet been investigated. In this study, our results showed that PRRSV down-regulated significantly the mRNA levels of IFN-α, IFN-β, IFN-γ, IFN-λ1, IFN-λ3 and IFN-λ4 and up-regulated significantly the mRNA levels of IL-10 and pSn in infected PAMs in vitro, suggesting that PRRSV infection inhibited the transcription of innate antiviral cytokines in host cells.

Genetic diversity and phylogenetic analysis of the ORF5 gene of PRRSV from central China.

To more fully understand the genetic diversity and molecular epidemiology of prevailing porcine reproductive and respiratory syndrome virus (PRRSV) in Henan province of China, 112 full-length ORF5 gene sequences, originating from Henan province between 2006 and 2015, were subjected to sequence variation and phylogenetic analysis. Phylogenetic analysis revealed that all Henan isolates belonged to the Type 2 genotype and could be further divided into three subgroups. Subgroup 1 and 2 viruses predominated in Henan and subgroup 2 overtook subgroup 1 as the most prevalent PRRSV between 2006 and 2015.

Ligation of porcine Fc gamma receptor III inhibits levels of antiviral cytokine in response to PRRSV infection in vitro.

PRRSV infection ADE facilitates the attachment and internalization of the virus onto macrophages through Fc receptor-mediated endocytosis. FcγR III is the activating receptor with a tyrosine-based activating motif (ITAM) in its cytoplasmic tail, where up-regulates phagocytosis. However, porcine FcγR III's role in the antiviral immune response to PRRSV infection has not been studied.

Molecular evolution of porcine reproductive and respiratory syndrome virus isolates from central China.

To investigate the genetic diversity of prevailing porcine reproductive and respiratory syndrome virus (PRRSV) in Henan Province of China, 61 ORF5 gene sequences, originating from Henan Province during 2003-2010, were subjected to amino acid variation and phylogenetic analysis. The analyzed PRRSV ORF5 sequences carried evidence of one unique recombination event. Phylogenetic analysis revealed that all Henan isolates belonged to type 2 genotype and were divided into two subgroups.

Ligation of porcine Fc gamma receptor I inhibits levels of antiviral cytokine in response to PRRSV infection in vitro.

PRRSV infection ADE facilitates the attachment and internalization of the virus onto macrophages through Fc receptor-mediated endocytosis. FcγRI is the activating receptor with a tyrosine-based activating motif (ITAM) in its cytoplasmic tail, where up-regulates phagocytosis. However, porcine FcγRI's role in the antiviral immune response to PRRSV infection has not been studied.

Genetic variation and phylogenetic analysis of porcine circovirus type 2 infections in central China.

Porcine circovirus type 2 (PCV2) infection causes postweaning multisystemic wasting syndrome and porcine circovirus-associated diseases in many regions. A total of 77 sequences, including 31 sampled from Henan province of China, were retrieved from GenBank and subjected to amino acid variation and phylogenetic analyses. The two PCV genotypes prevailing in Henan were PCV-2a and PCV-2b with PCV-2b accounting for 93.

Ligation of Fc gamma receptor IIB enhances levels of antiviral cytokine in response to PRRSV infection in vitro.

PRRSV infection ADE facilitates the attachment and internalization of the virus onto its host cells, such as monocytes and macrophages, through Fc receptor-mediated endocytosis. FcγRIIB is the only inhibitory receptor with a tyrosine-based inhibitory motif (ITIM) in its cytoplasmic tail, where counters the "ITAM triggered" activation signals and down-regulates phagocytosis. However, porcine FcγRIIB's role in the antiviral immune response to PRRSV infection has not been studied.

Porcine Fc gamma RIIb sub-isoforms are generated by alternative splicing.

Receptors for the Fc portion of IgG (FcγRs) are expressed on various leukocytes and they modulate both humoral and cell-mediated immune responses with different capacities for IgG binding and phagocytosis. Four different types of FcγRs, FcγRI (CD64), FcγRII (CD32), FcγRIII (CD16) and FcγRIV, have been identified. There are three FcγRII isoforms (activating FcγRIIa and FcγRIIc, and inhibitory FcγRIIb) in humans, one isoform (inhibitory FcγRIIb) in mice, and two isoforms (inhibitory FcγRIIb and activating FcγRIIc) in cattle.

Molecular cloning and characterization of a porcine Fc gamma RIIb sub-isoform(FcγRIIb1).

Receptors for the Fc fragment of IgG (FcγRs) constitute one of the main effector mechanisms through which IgG immune complexes exert their action. Four FcγRs, FcγRI (CD64) with high affinity, FcγRI with intermediate affinity, FcγRII (CD32) and FcγRIII (CD16) with low affinity, have been identified. There are three FcγRII isoforms (activating FcγRIIa and FcγRIIc, and inhibiting FcγRIIb) existing in humans, one isoform in mice (inhibiting FcγRIIb), and two isoforms in cattle (inhibiting FcγRIIb, activating FcγRIIc).

Enhancement of the immunogenicity of an infectious laryngotracheitis virus DNA vaccine by a bicistronic plasmid encoding glycoprotein B and interleukin-18.

A DNA vaccine against infectious laryngotracheitis virus (ILTV) can induce specific humoral and cell-mediated immunity. However, compared to conventional vaccines, DNA vaccines usually induce poor antibody responses. To determine if co-expression of a cytokine can result in a more potent ILTV DNA vaccine, immunogenicity and protective efficacy of a monocistronic vector encoding the glycoprotein B (gB) of ILTV was compared to that of a bicistronic vector separately encoding the gB and chicken interleukin-18.

Up-regulation of the MyD88-dependent pathway of TLR signaling in spleen and caecum of young chickens infected with Salmonella serovar Pullorum.

TLR signaling plays a role in Salmonella infection, but less information is available in chickens infected with Salmonella serovar Pullorum. The present study with young chickens, experimentally infected with S. Pullorum, has used real-time quantitative RT-PCR to investigate the relative expression of genes of the TLR4 signaling pathway (TLR4, MyD88, TRAF6 and NF-kappaB) in the spleen and caecum at 1, 3, 7 and 14 days post-infection (dpi).