Skip to main navigation Skip to search Skip to main content

The Interaction between Human Enteroviruses and Type I IFN Signaling Pathway

  • Jing Lu
  • , Lina Yi
  • , Changwen Ke
  • , Yonghui Zhang
  • , Ren Liu
  • , Jinfei Chen
  • , Hsiang-fu Kung
  • , Ming-Liang He*
  • *Corresponding author for this work

Research output: Journal Publications and ReviewsRGC 21 - Publication in refereed journalpeer-review

Abstract

Human enteroviruses (HEV), very common and important human pathogens, cause infections in diverse ways. Recently, the large epidemic of HFMD caused by HEV infection became a growing threat to public health in China. As the first line of immune response, the type I interferon (IFN-α/β) pathway plays an essential role in antiviral infection, particularly in limiting both the early and late stages of infection. Because of co-evolution with the host, the viruses have evolved multiple strategies to evade or subvert the host immunity to ensure their survival. In this paper, we systematically reviewed and summarized the interaction between HEV infections and host type I IFN responses. We firstly described the recent findings of HEV recognition and IFN induction, specifically on host pattern-recognition receptors (PRRs) in HEV infection then we discussed the antiviral effect of IFN in HEV infection. Finally, we timely summarized the mechanisms of HEV to circumvent the IFN responses. Clarification of the complexity in this battle may provide us new strategies for prevention and antiviral treatment. © 2015 Informa Healthcare USA, Inc.
Original languageEnglish
Pages (from-to)201-207
JournalCritical Reviews in Microbiology
Volume41
Issue number2
Online published6 Aug 2013
DOIs
Publication statusPublished - Apr 2015
Externally publishedYes

Research Keywords

  • Antiviral
  • Host-virus interaction
  • Human enterovirus
  • Interferon respons
  • Viral replication

Fingerprint

Dive into the research topics of 'The Interaction between Human Enteroviruses and Type I IFN Signaling Pathway'. Together they form a unique fingerprint.

Cite this