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Confocal Imaging of Double-Stranded RNA and Pattern Recognition Receptors in Negative-Sense RNA Virus Infection
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Defective RNA sensing by RIG-I in severe influenza virus infection.

S E Jørgensen1, M Christiansen2, L B Ryø3

  • 1Department of Infectious Diseases, Aarhus University Hospital, Aarhus, Denmark.

Clinical and Experimental Immunology
|February 18, 2018
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Summary

Genetic variants in the RIG-I gene can lead to severe influenza A virus infections. These mutations impair the innate immune response, increasing susceptibility to severe disease and inflammation.

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RIG-Iinfluenzainnate immunityinterferon

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Area of Science:

  • Immunology
  • Virology
  • Genetics

Background:

  • Influenza virus causes seasonal epidemics, with some patients experiencing severe disease.
  • Type I interferon (IFN) plays a role in antiviral responses, but genetic causes of severe influenza are rare.
  • IFN regulatory factor (IRF)7 deficiency is the only known human genetic cause of severe influenza.

Observation:

  • A patient with severe influenza A virus (IAV) H1N1 infection during the 2009 pandemic was studied.
  • Whole exome sequencing identified two variants (p.R71H and p.P885S) in the DDX58 gene, which encodes the RIG-I sensor.
  • These variants are located in critical domains of RIG-I, affecting its signaling.

Findings:

  • The identified RIG-I variants significantly impair its signaling activity.
  • Patient cells showed reduced antiviral responses to RIG-I ligands.
  • Patient cells exhibited increased pro-inflammatory responses to IAV infection.

Implications:

  • Dysregulated innate immune response and increased immunopathology may contribute to severe influenza.
  • These RIG-I variants are suggested as a potential genetic factor contributing to severe influenza in this patient.
  • Future studies should investigate RIG-I variants in genetic factors influencing single-stranded RNA virus infections.