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Ribosomal Protein L13 Participates in Innate Immune Response Induced by Foot-and-Mouth Disease Virus
Junyong Guan1, Shichong Han1, Jin'en Wu1
1State Key Laboratory of Veterinary Etiological Biology, Office International des Epizootie (OIE)/China National Foot-and-Mouth Disease Reference Laboratory, Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Lanzhou, China.
Abstract:
In addition to ribosomal protein synthesis and protein translation, ribosomal proteins also participate in tumorigenesis and tumor progression, immune responses, and viral replication. Here, we show that ribosomal protein L13 (RPL13) participates in the antiviral immune response induced by foot-and-mouth disease virus (FMDV), inhibiting FMDV replication. The overexpression of RPL13 promoted the induction and activation of the promoters of the nuclear factor-κB (NF-κB) and interferon-β (IFN-β) genes, and the expression and protein secretion of the antiviral factor IFN-β and proinflammatory cytokine interleukin-6 (IL-6). The knockdown of RPL13 had the opposite effects. We also found that the FMDV 3Cpro protease interacts with RPL13, and that its activity reduces the expression of RPL13, thus antagonizing the RPL13-mediated antiviral activity. This study extends our knowledge of the extraribosomal functions of ribosomal proteins and provides new scientific information on cellular antiviral defenses and virus-antagonizing mechanisms.
Insights
Ribosomal protein L13 (RPL13) inhibits foot-and-mouth disease virus (FMDV) replication by boosting antiviral gene expression. The FMDV protease antagonizes RPL13’s antiviral activity by reducing its expression.
Area of Science:
- Molecular Biology
- Immunology
- Virology
Background:
- Ribosomal proteins have extraribosomal roles beyond protein synthesis.
- These roles include involvement in immune responses and viral replication.
Purpose of the Study:
- To investigate the role of ribosomal protein L13 (RPL13) in the antiviral immune response against foot-and-mouth disease virus (FMDV).
- To elucidate the mechanism by which RPL13 mediates antiviral activity and how viruses antagonize this defense.
Main Methods:
- Overexpression and knockdown of RPL13 in cellular models.
- Analysis of gene promoter activity (NF-κB, IFN-β).
- Measurement of gene and protein expression (IFN-β, IL-6).
- Investigation of interactions between FMDV 3C protease and RPL13.
Main Results:
- RPL13 overexpression enhanced the expression of antiviral and pro-inflammatory genes (IFN-β, IL-6) and their promoter activity.
- RPL13 knockdown reversed these effects, impairing antiviral response.
- FMDV 3C protease directly interacts with RPL13.
- FMDV 3C protease activity downregulates RPL13 expression, antagonizing its antiviral function.
Conclusions:
- RPL13 plays a significant role in cellular antiviral defense against FMDV.
- FMDV employs a mechanism involving its 3C protease to suppress RPL13-mediated immunity.
- This study highlights novel extraribosomal functions of ribosomal proteins in immunity and viral evasion strategies.
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