Pseudorabies Virus Tegument Protein UL13 Suppresses RLR-Mediated Antiviral Innate Immunity through Regulating Receptor Transcription

Zhao, Ningning; Wang, Fan; Kong, Zhengjie; Shang, Yue

doi:10.3390/v14071465

Cited by 10 publications

(5 citation statements)

References 50 publications

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“…During reactivation from latency, UL13 might counteract signaling pathway(s) required for efficient reactivation; thus, the phosphorylation-dead mutation at UL13 Tyr-162 that precludes the negative regulation of UL13 activity, might impair reactivation from latency. UL13 homologs inhibit various cellular signaling pathways including JAK/STAT, RIG-I-like receptor, and cGAS/STING [39][40][41][42] . It would be of interest to investigate these pathways regulate reactivation from latency.…”

Section: Discussionmentioning

confidence: 99%

Regulatory Mimicry of Cyclin-Dependent Kinases by Conserved Herpesvirus Protein Kinases

Koyanagi,

Hengphasatporn,

Kato

et al. 2023

Preprint

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Herpesviruses encode conserved protein kinases (CHPKs) that target cellular cyclin-dependent kinase (CDK) phosphorylation sites; thus, they are termed viral CDK-like kinases. Tyrosine 15 in the GxGxxG motifs of CDK1 and CDK2, whose phosphorylation down-regulates their catalytic activities, is conserved in the corresponding motifs of CHPKs. We found that herpes simplex virus 2 (HSV-2) CHPK UL13 mimicked the regulatory mechanism of CDKs. This regulatory mimicry was conserved in CHPKs encoded by herpesviruses subclassified into subfamilies other than HSV-2, suggesting CHPKs have regulatory and functional mimicry with CDKs. Phosphorylation of the corresponding Tyr in HSV-2 UL13 was required for the down-regulation of viral replication and pathogenicity, specifically in the central nervous system of mice, and for efficient viral recurrence in guinea pigs. These data highlight the dual impact of the regulatory mimicry of CDKs by CHPK on the fine-tuned regulation of lytic and latent HSV-2 infectionsin vivo.

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Section: Discussionmentioning

confidence: 99%

Regulatory Mimicry of Cyclin-Dependent Kinases by Conserved Herpesvirus Protein Kinases

Koyanagi,

Hengphasatporn,

Kato

et al. 2023

Preprint

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“…PRV copy numbers were quantified by qPCR using gD gene primers ( Cheng et al, 2020 ) and was performed in triplicated determinants with RealStar Green Fast Mixture (A303, GenStar, USA) on a StepOne plus thermal cycler (ABI, Thermo Fisher Scientific, USA). The primer sequences targeted for the gD gene of PRV were followed as previously described ( Zhao et al, 2022 ).…”

Section: Methodsmentioning

confidence: 99%

Secondary metabolites of Bacillus subtilis L2 show antiviral activity against pseudorabies virus

Wang,

Hao,

Zhou

et al. 2023

Front. Microbiol.

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Bacillus subtilis (B. subtilis) is a commercially important probiotic known to produce secondary metabolites with antibacterial, antifungal and anti-inflammatory activities. However, the potential ability of B. subtilis to combat viruses, especially DNA viruses, has not been extensively investigated. In this study, we identified two distinct B. subtilis strains and examined the efficiency of their secondary metabolites against pseudorabies virus (PRV), a swine herpesvirus resulting in economic losses worldwide. We found that treatment with the secondary metabolites of B. subtilis L2, but not the metabolites of B. subtilis V11, significantly inhibited PRV replication in multiple cells. Notably, the antiviral activity of the metabolites of B. subtilis L2 was thermal stable, resistant to protease digestion. Moreover, these metabolites effectively impeded PRV binding, entry and replication. Importantly, oral administration of the metabolites of B. subtilis L2 protected mice from lethal PRV infection, rescuing weight loss and reducing the viral load in vivo. In summary, our results reveal that the metabolites of B. subtilis L2 exhibit anti-PRV activity both in vitro and in vivo, providing a potential candidate for novel antiviral drugs.

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“…There are 10 glycoproteins encoded by PRV, which are divided into two groups (essential or non-essential glycoproteins) according to the degree to which viral replication depends on them [ 13 , 14 ]. The glycoprotein B (gB) plays a crucial role in membrane fusion during infection and in spreading viruses from cell to cell [ 15 , 16 , 17 ].…”

Section: The Biological Characteristics Of Prvmentioning

confidence: 99%

Recombinant Pseudorabies Virus Usage in Vaccine Development against Swine Infectious Disease

Zhou

Abid

Cao

et al. 2023

Viruses

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Pseudorabies virus (PRV) is the pathogen of pseudorabies (PR), which belongs to the alpha herpesvirus subfamily with a double stranded DNA genome encoding approximately 70 proteins. PRV has many non-essential regions for replication, has a strong capacity to accommodate foreign genes, and more areas for genetic modification. PRV is an ideal vaccine vector, and multivalent live virus-vectored vaccines can be developed using the gene-deleted PRV. The immune system continues to be stimulated by the gene-deleted PRVs and maintain a long immunity lasting more than 4 months. Here, we provide a brief overview of the biology of PRV, recombinant PRV construction methodology, the technology platform for efficiently constructing recombinant PRV, and the applications of recombinant PRV in vaccine development. This review summarizes the latest information on PRV usage in vaccine development against swine infectious diseases, and it offers novel perspectives for advancing preventive medicine through vaccinology.

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Pseudorabies Virus Tegument Protein UL13 Suppresses RLR-Mediated Antiviral Innate Immunity through Regulating Receptor Transcription

Cited by 10 publications

References 50 publications

Regulatory Mimicry of Cyclin-Dependent Kinases by Conserved Herpesvirus Protein Kinases

Regulatory Mimicry of Cyclin-Dependent Kinases by Conserved Herpesvirus Protein Kinases

Secondary metabolites of Bacillus subtilis L2 show antiviral activity against pseudorabies virus

Recombinant Pseudorabies Virus Usage in Vaccine Development against Swine Infectious Disease

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