Recent Advances in PRRS Virus Receptors and the Targeting of Receptor–Ligand for Control

Su, Chih-Chung; Rowland, Raymond R. R.; Yoo, Dongwan

doi:10.3390/vaccines9040354

Cited by 23 publications

(25 citation statements)

References 134 publications

(196 reference statements)

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“…Many of the genes in the list are natively expressed in uninfected porcine liver and lung at detectable levels ( 18 ). Some key upregulated genes of interest included the most overexpressed gene in the MLV-129p-IFNmix analysis, CD209 molecule ( CD209 ), a known receptor for PRRSV ( 9 , 21 ). The gene is an innate and adaptive immunity C-type lectin receptor involved in recognizing various viral pathogens, regulating virus life cycles, and promoting T-cell proliferation.…”

Section: Resultsmentioning

confidence: 99%

Transcriptomic Analysis of Liver Indicates Novel Vaccine to Porcine Reproductive and Respiratory Virus Promotes Homeostasis in T-Cell and Inflammatory Immune Responses Compared to a Commercial Vaccine in Pigs

Fleming

Miller

et al. 2022

Front. Vet. Sci.

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One of the largest impediments for commercial swine production is the presence of Porcine Reproductive and Respiratory Syndrome Virus (PRRSV), a devastating RNA viral infection that is responsible for over $1 billion in loss in the U.S. annually. The challenge with combating PRRSV is a combination of the effect of an extraordinary rate of mutation, the ability to infect macrophages, and subversion of host immune response through a series of actions leading to both immunomodulation and immune evasion. Currently there are a handful of commercial vaccines on the market that have been shown to be effective against homologous infections, but struggle against heterologous or mixed strain infections. However, vaccination is the current best strategy for combating PRRSV, making research into new vaccine technology key. To address these issues with PRRSV and host antiviral functions a novel modified-live vaccine (MLV) able to stimulate known antiviral interferons was created and examined for its ability to potentiate effective immunity and better protection. Here, we examine gene expression in the liver of pigs vaccinated with our novel vaccine, given the liver's large role in antiviral responses and vaccine metabolism. Our study indicated that pigs administered the novel vaccine experience homeostatic gene expression consistent with less inflammation and T-cell depletion risk than pigs administered the commercial vaccine.

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Section: Resultsmentioning

confidence: 99%

Transcriptomic Analysis of Liver Indicates Novel Vaccine to Porcine Reproductive and Respiratory Virus Promotes Homeostasis in T-Cell and Inflammatory Immune Responses Compared to a Commercial Vaccine in Pigs

Fleming

Miller

et al. 2022

Front. Vet. Sci.

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show abstract

“…As an intracellular obligate pathogen, PRRSV exploits host cellular machinery to establish infection. PRRSV infection is initiated by attachment to host cell receptors/factors on the plasma membrane ( 13 ). Upon internalization, PRRSV utilizes the host machinery to finish its translation, transcription, and replication ( 14 ).…”

Section: Introductionmentioning

confidence: 99%

Tumor Susceptibility Gene 101 (TSG101) Contributes to Virion Formation of Porcine Reproductive and Respiratory Syndrome Virus via Interaction with the Nucleocapsid (N) Protein along with the Early Secretory Pathway

Zhang

Geng

et al. 2022

J Virol

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Porcine reproductive and respiratory syndrome virus (PRRSV) has caused huge economic losses to global swine industry. As an intracellular obligate pathogen, PRRSV exploits host cellular machinery to establish infection. The endocytic sorting complex required for transport (ESCRT) system has been shown to participate in different life cycle stages of multiple viruses. In the current study, a systematic small interference RNA (siRNA) screening assay identified that certain ESCRT components contributed to PRRSV infection. Among them, tumor susceptibility gene 101 (TSG101) was demonstrated to be important for PRRSV infection by knockdown and overexpression assays. TSG101 was further revealed to be involved in virion formation rather than viral attachment, internalization, RNA replication and nucleocapsid (N) protein translation within the first round of PRRSV life cycle. In detail, TSG101 was determined to specially interact with PRRSV N protein and take effect on its subcellular localization along with the early secretory pathway. Taken together, these results provide evidence that TSG101 is a pro-viral cellular factor for PRRSV assembly, which will be a promising target to interfere with the viral infection. IMPORTANCE PRRSV infection results in a serious swine disease affecting pig farming in the world. However, efficient prevention and control of PRRSV is hindered by its complicated infection process. Up to now, our understanding of PRRSV assembly during infection is especially limited. Here, we identified that TSG101, an ESCRT-I subunit, facilitated virion formation of PRRSV via interaction with the viral N protein along with the early secretory pathway. Our work actually expands the knowledge of PRRSV infection and provides a novel therapeutic target for prevention and control of the virus.

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“…PRRSV mainly replicates in porcine PAMs, resulting in the polarization of PAMs toward the M2 phenotype characterized by the high-level expression of CD163, which serves as a functional receptor for virus entry (Wang et al, 2017;Su et al, 2021). The viral protein(s) essential for regulating macrophage polarization remain(s) unknown, but a study has been implied that PRRSV induces M2-polarized macrophages for efficient growth while simultaneously counteracting the antiviral responses of M1-polarized macrophages (Wang et al, 2017).…”

Section: Exploitation Of Surface Markers On M2 Macrophages For Virus ...mentioning

confidence: 99%

Modulation of Macrophage Polarization by Viruses: Turning Off/On Host Antiviral Responses

et al. 2022

Front. Microbiol.

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Macrophages are professional antigen-presenting cells and serve as the first line of defense against invading pathogens. Macrophages are polarized toward the proinflammatory classical (M1) or anti-inflammatory alternative (M2) phenotype upon viral infections. M1-polarized macrophages exert critical roles in antiviral responses via different mechanisms. Within the long competitive history between viruses and hosts, viruses have evolved various immune evasion strategies, inhibiting macrophage acquisition of an antiviral phenotype, impairing the antiviral responses of activated macrophages, and/or exploiting macrophage phenotypes for efficient replication. This review focuses on the sophisticated regulation of macrophage polarization utilized by viruses and is expected to provide systematic insights into the regulatory mechanisms of macrophage polarization by viruses and further facilitate the design of therapeutic targets for antivirals.

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Recent Advances in PRRS Virus Receptors and the Targeting of Receptor–Ligand for Control

Cited by 23 publications

References 134 publications

Transcriptomic Analysis of Liver Indicates Novel Vaccine to Porcine Reproductive and Respiratory Virus Promotes Homeostasis in T-Cell and Inflammatory Immune Responses Compared to a Commercial Vaccine in Pigs

Transcriptomic Analysis of Liver Indicates Novel Vaccine to Porcine Reproductive and Respiratory Virus Promotes Homeostasis in T-Cell and Inflammatory Immune Responses Compared to a Commercial Vaccine in Pigs

Tumor Susceptibility Gene 101 (TSG101) Contributes to Virion Formation of Porcine Reproductive and Respiratory Syndrome Virus via Interaction with the Nucleocapsid (N) Protein along with the Early Secretory Pathway

Modulation of Macrophage Polarization by Viruses: Turning Off/On Host Antiviral Responses

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