ArticlePLoS pathogens2020
Feline calicivirus strain 2280 p30 antagonizes type I interferon-mediated antiviral innate immunity through directly degrading IFNAR1 mRNA.
Article in PLoS pathogens, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 23 citations in OpenAlex.
- A novel replication-deficient feline herpesvirus type 1 vector-based vaccine provides strong immune protection in cats.Journal of virology · 2026Article
- Feline calicivirus VP1-based mRNA vaccine protects cats against FCV challenge.Virologica Sinica · 2026Article
- Construction of Reverse Genetics System for Feline Calicivirus FCV-BJ616 and Proteomic Analysis.MicrobiologyOpen · 2026Article
- A novel replication-deficient FCV vaccine provides strong immune protection in cats.Journal of virology · 2025Article
- The African swine fever virus p22 inhibits the JAK-STAT signaling pathway by promoting the TAX1BP1-mediated degradation of the type I interferon receptor.PLoS pathogens · 2025Article
- Unlocking the secrets of Feline calicivirus: advances in structural and nonstructural proteins and its role as a key model for other Caliciviruses.Virology journal · 2025Review
- Decitabine Increases the Transcription ofMicroorganisms · 2025Article
- Analysis of Genetic Diversity Based on Sequences of Feline Calicivirus Strains Isolated in China.Transboundary and emerging diseases · 2025Article
- A Virulent Systemic Feline Calicivirus Strain Isolated in China Could Produce Broadly Neutralizing Antibodies Against Multiple Strains.Transboundary and emerging diseases · 2025Article
- Update on feline calicivirus: viral evolution, pathogenesis, epidemiology, prevention and control.Frontiers in microbiology · 2024Review
- An Outbreak of Limping Syndrome Associated with Feline Calicivirus.Animals : an open access journal from MDPI · 2023Article
- Article
- Extracellular Vesicles (EVs) Are Copurified with Feline Calicivirus, yet EV-Enriched Fractions Remain Infectious.Microbiology spectrum · 2022Article
- Calicivirus Infection in Cats.Viruses · 2022Review
- Feline Calicivirus Proteinase-Polymerase Protein Degrades mRNAs To Inhibit Host Gene Expression.Journal of virology · 2021Article
- Calicivirus Non-structural Proteins: Potential Functions in Replication and Host Cell Manipulation.Frontiers in microbiology · 2021Review
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Feline calicivirus (FCV) belongs to the Caliciviridae, which comprises small RNA viruses of both medical and veterinary importance. Once infection has occurred, FCV can persist in the cat population, but the molecular mechanism of how it escapes the innate immune response is still unknown. In this study, we found FCV strain 2280 to be relatively resistant to treatment with IFN-β. FCV 2280 infection inhibited IFN-induced activation of the ISRE (Interferon-stimulated response element) promoter and transcription of ISGs (Interferon-stimulated genes). The mechanistic analysis showed that the expression of IFNAR1, but not IFNAR2, was markedly reduced in FCV 2280-infected cells by inducing the degradation of IFNAR1 mRNA, which inhibited the phosphorylation of downstream adaptors. Further, overexpression of the FCV 2280 nonstructural protein p30, but not p30 of the attenuated strain F9, downregulated the expression of IFNAR1 mRNA. His-p30 fusion proteins were produced in Escherichia coli and purified, and an in vitro digestion assay was performed. The results showed that 2280 His-p30 could directly degrade IFNAR1 RNA but not IFNAR2 RNA. Moreover, the 5'UTR of IFNAR1 mRNA renders it directly susceptible to cleavage by 2280 p30. Next, we constructed two chimeric viruses: rFCV 2280-F9 p30 and rFCV F9-2280 p30. Compared to infection with the parental virus, rFCV 2280-F9 p30 infection displayed attenuated activities in reducing the level of IFNAR1 and inhibiting the phosphorylation of STAT1 and STAT2, whereas rFCV F9-2280 p30 displayed enhanced activities. Animal experiments showed that the virulence of rFCV 2280-F9 p30 infection was attenuated but that the virulence of rFCV F9-2280 p30 was increased compared to that of the parental viruses. Collectively, these data show that FCV 2280 p30 could directly and selectively degrade IFNAR1 mRNA, thus blocking the type I interferon-induced activation of the JAK-STAT signalling pathway, which may contribute to the pathogenesis of FCV infection.
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