CircPTPN11 inhibits the replication of Coxsackievirus B5 through regulating the IFN-I pathway by targeting

Jingru Gao1, Fan Yang2, Jihong Zhang1

  • 1Medical School, Kunming University of Science and Technology, Kunming, Yunnan Province, China.

Virus Research
|December 8, 2024
PubMed

Insights

Circular RNA CircPTPN11 is upregulated during Coxsackievirus B5 infection, inhibiting viral replication by activating the type-I interferon pathway and targeting SIRPA via miR-152-3p.

Area of Science:

  • Virology
  • Molecular Biology
  • Immunology

Background:

  • Coxsackievirus B5 (CVB5) causes significant diseases like hand-foot-mouth disease, with unclear mechanisms and no specific treatments.
  • Circular RNAs (circRNAs) are implicated in viral infections, but their role in CVB5 is unknown.

Purpose of the Study:

  • To investigate the role and mechanism of circRNAs in CVB5 infection.
  • To identify potential therapeutic targets for CVB5.

Main Methods:

  • CVB5 infection in RD cells to analyze circRNA expression.
  • Quantitative analysis of CircPTPN11 expression.
  • Investigating the interaction between CircPTPN11, miR-152-3p, and SIRPA.
  • Assessing the impact on CVB5 replication and type-I interferon pathway activation.

Main Results:

  • CircPTPN11 expression is significantly upregulated in a time- and dose-dependent manner following CVB5 infection, specifically in intestinal tissue.
  • CircPTPN11 inhibits CVB5 replication by activating IRF3 in the type-I interferon (IFN-I) pathway.
  • CircPTPN11 acts as a molecular sponge for miR-152-3p, which in turn regulates SIRPA expression, ultimately inhibiting CVB5 replication.

Conclusions:

  • CircPTPN11 plays a crucial role in antiviral defense against CVB5 by modulating the miR-152-3p/SIRPA axis and activating the IFN-I pathway.
  • CircPTPN11 represents a potential molecular target for diagnosing and treating CVB5 infections.

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