Protective role of LGP2 in influenza virus pathogenesis

J Infect Dis. 2014 Jul 15;210(2):214-23. doi: 10.1093/infdis/jiu076. Epub 2014 Feb 3.


Influenza A virus triggers a contagious respiratory disease that can cause considerable morbidity and mortality. Using an in vitro approach, we previously demonstrated that the pattern recognition receptor retinoic acid-inducible gene I (RIG-I) plays a key role in influenza A virus-mediated immune response. However, the importance of RIG-I signaling in vivo has not been thoroughly examined, because of the lack of an appropriate mouse models. To circumvent this issue, we generated a new transgenic mouse overexpressing LGP2 (hereafter, "LGP2 TG mice"), a major regulator of the RIG-I signaling pathway. The time course of several parameters was compared in infected wild-type and LGP2 TG mice. We found that LGP2 TG mice displayed significantly reduced inflammatory mediators and a lower leukocyte infiltration into the bronchoalveolar airspace. More importantly, LGP2 TG mice had a significant survival advantage. Hence, our in vivo study reveals that LGP2 is a major downregulator of the influenza A virus-triggered detrimental inflammatory response.

Keywords: immunity; inflammation; lung; signal transduction; viral.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • DEAD Box Protein 58
  • DEAD-box RNA Helicases / metabolism
  • Disease Models, Animal
  • Gene Expression
  • Host-Pathogen Interactions*
  • Inflammation Mediators / analysis
  • Influenza A virus / physiology*
  • Leukocytes / immunology
  • Mice
  • Mice, Inbred C57BL
  • Mice, Transgenic
  • Orthomyxoviridae Infections / immunology
  • Orthomyxoviridae Infections / pathology
  • RNA Helicases / metabolism*
  • Signal Transduction
  • Survival Analysis


  • Inflammation Mediators
  • Dhx58 protein, mouse
  • Ddx58 protein, mouse
  • DEAD Box Protein 58
  • DEAD-box RNA Helicases
  • RNA Helicases