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TLR4 signalling: the key to controlling EV71 replication and inflammatory response.

Jinfang Hao1, Hui Wang1, Xiufeng Lu1

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|June 28, 2024
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Summary

Enterovirus 71 (EV71) infection suppresses Toll-like receptor 4 (TLR4) expression, weakening the innate immune response. This down-regulation of TLR4 by EV71 promotes viral replication, aiding its evasion of host defenses.

Keywords:
enterovirus 71immune escapeinflammatory responsetoll-like receptor 4viral replication

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Area of Science:

  • Virology
  • Immunology
  • Cell Biology

Background:

  • Hand, foot, and mouth disease (HFMD) is a common childhood illness caused by enterovirus 71 (EV71).
  • EV71 infection can lead to severe outcomes by potentially inhibiting the host's innate immune system.
  • The role of Toll-like receptor 4 (TLR4), a key immune receptor, in EV71 infection is not well understood.

Purpose of the Study:

  • To investigate the effect of EV71 infection on TLR4 expression and function.
  • To elucidate the mechanism by which EV71 interacts with the host immune system.
  • To determine if TLR4 modulation impacts EV71 replication.

Main Methods:

  • EV71 infection of RD, GES-1, and Vero cells.
  • Quantitative reverse transcription PCR (RT-qPCR) to measure gene expression.
  • Immunofluorescence staining and Western blot to assess protein levels.
  • Interference with TLR4 signaling using agonists, inhibitors, and siRNA.

Main Results:

  • EV71 infection significantly reduced both TLR4 protein and gene transcript levels.
  • Downstream signaling molecules of TLR4 (MYD88, p-NF-κB p65, p-TBK1) and inflammatory cytokines were decreased.
  • Activation of TLR4 inhibited EV71 replication, whereas TLR4 inhibition or knockdown promoted it.

Conclusions:

  • EV71 down-regulates TLR4 expression to suppress the host's innate immune and inflammatory responses.
  • This down-regulation facilitates EV71 replication and represents a novel immune evasion strategy.
  • Targeting TLR4 may offer therapeutic potential against EV71 infections.