Toll-like receptor 3 is involved in detection of enterovirus a71 infection and targeted by viral 2a protease

Kuan Ru Chen, Chun Keung Yu, Szu Hao Kung, Shun Hua Chen, Chuan Fa Chang, Tzu Chuan Ho, Yi Ping Lee, Hung Chuan Chang, Lan Yin Huang, Shih Yen Lo, Jui Chung Chang, Pin Ling

Research output: Contribution to journalArticlepeer-review

11 Citations (Scopus)


Enterovirus A71 (EV-A71) has emerged as a major pathogen causing hand, foot, and mouth disease, as well as neurological disorders. The host immune response affects the outcomes of EV-A71 infection, leading to either resolution or disease progression. However, the mechanisms of how the mammalian innate immune system detects EV-A71 infection to elicit antiviral immunity remain elusive. Here, we report that the Toll-like receptor 3 (TLR3) is a key viral RNA sensor for sensing EV-A71 infection to trigger antiviral immunity. Expression of TLR3 in HEK293 cells enabled the cells to sense EV-A71 infection, leading to type I, IFN-mediated antiviral immunity. Viral double-stranded RNA derived from EV-A71 infection was a key ligand for TLR3 detection. Silencing of TLR3 in mouse and human primary immune cells impaired the activation of IFN-β upon EV-A71 infection, thus reinforcing the importance of the TLR3 pathway in defending against EV-A71 infection. Our results further demonstrated that TLR3 was a target of EV-A71 infection. EV-A71 protease 2A was implicated in the downregulation of TLR3. Together, our results not only demonstrate the importance of the TLR3 pathway in response to EV-A71 infection, but also reveal the involvement of EV-A71 protease 2A in subverting TLR3-mediated antiviral defenses.

Original languageEnglish
Article number689
Issue number12
Publication statusPublished - 2018 Dec

All Science Journal Classification (ASJC) codes

  • Infectious Diseases
  • Virology


Dive into the research topics of 'Toll-like receptor 3 is involved in detection of enterovirus a71 infection and targeted by viral 2a protease'. Together they form a unique fingerprint.

Cite this