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. Author manuscript; available in PMC: 2013 May 1.
Published in final edited form as: Virus Res. 2011 Oct 21;162(0):12–18. doi: 10.1016/j.virusres.2011.10.017

Figure 1. Induction of IFN by influenza virus.

Figure 1

Influenza virus enters the cell through the endocytic pathway. Fusion of the envelope of the virus to that of the endosome results in the release of the segmented genome of the virus, which is transported to the nucleus where replication takes place. During this entry process, some virions may not escape the endosome and expose the viral RNA to TLR3/7/8 present in specialized cells, which recognize double stranded and single stranded RNA. At late times of infection, the newly synthesized viral RNA segments move to the cytoplasm, where they can encounter the ubiquitously expressed cytoplasmic sensor RIG-I before assembly of new virions takes place. The presence of a 5′-triphospate and of a partial double strand structure makes the influenza virus RNAs optimal substrates for RIG-I activation. Viral RNAs in the cytoplasm can also enter the endosome through autophagic processes. TLR signaling by the adaptors TRIF or MyD88, and RIG-I signaling by the adaptor MAVS triggers signal transduction cascade that results in activation of IRF3/7 and NF-kB factors that translocates to the nucleus where they promote the synthesis of type I and type III IFN mRNAs.