Antiviral and Inflammatory Cellular Signaling Associated with Enterovirus 71 Infection

Viruses. 2018 Mar 28;10(4):155. doi: 10.3390/v10040155.

Abstract

Enterovirus 71 (EV71) infection has become a major threat to global public health, especially in infants and young children. Epidemiological studies have indicated that EV71 infection is responsible for severe and even fatal cases of hand, foot, and mouth disease (HFMD). Accumulated evidence indicates that EV71 infection triggers a plethora of interactive signaling pathways, resulting in host immune evasion and inflammatory response. This review mainly covers the effects of EV71 infection on major antiviral and inflammatory cellular signal pathways. EV71 can activate cellular signaling networks including multiple cell surface and intracellular receptors, intracellular kinases, calcium flux, and transcription factors that regulate antiviral innate immunity and inflammatory response. Cellular signaling plays a critical role in the regulation of host innate immune and inflammatory pathogenesis. Elucidation of antiviral and inflammatory cellular signaling pathways initiated by EV71 will not only help uncover the potential mechanisms of EV71 infection-induced pathogenesis, but will also provide clues for the design of therapeutic strategies against EV71 infection.

Keywords: EV71; antiviral innate immunity; cellular signaling; immune evasion; inflammatory response.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Biomarkers
  • Disease Resistance / immunology*
  • Enterovirus A, Human / genetics
  • Enterovirus A, Human / immunology*
  • Enterovirus Infections / immunology*
  • Enterovirus Infections / metabolism*
  • Enterovirus Infections / virology
  • Host-Pathogen Interactions / immunology*
  • Humans
  • Immune Evasion
  • Immunity, Innate*
  • NF-kappa B / metabolism
  • Oxidative Stress
  • Signal Transduction*
  • Toll-Like Receptors / metabolism
  • Viral Proteins / metabolism

Substances

  • Biomarkers
  • NF-kappa B
  • Toll-Like Receptors
  • Viral Proteins