Frank T. Vreede

TL;DR: It is shown that RIG-I agonists are exclusively generated by the process of virus replication and correspond to full-length virus genomes, and nongenomic viral transcripts, short replication intermediates, and cleaved self-RNA do not contribute substantially to interferon induction in cells infected with these negative strand RNA viruses.

TL;DR: It is found that in viral ribonucleoprotein (vRNP) reconstitution assays involving only the minimal components required for viral transcription and replication, the relative levels of accumulation of RNA products differed from those observed in infected cells, suggesting a regulatory role for additional viral proteins.

TL;DR: It is suggested that there may be no switch regulating the initiation of RNA synthesis and a model suggesting that nascent cRNA is degraded by host cell nucleases unless it is stabilized by newly synthesized viral RNA polymerase and NP.

TL;DR: The PB2 protein interacts with the mitochondrial antiviral signaling protein, MAVS (also known as IPS-1, VISA, or Cardif), and inhibits MAVS-mediated beta interferon (IFN-β) expression and suggests an important role for the mitochondrial association of the PB2protein in determining virulence.

TL;DR: In vivo evidence, based on the correction of a mutated or deleted residue 1 of a cRNA chloramphenicol acetyltransferase reporter construct, supported this internal initiation and realignment model, and it was concluded that influenza virus RNA polymerase uses different initiation strategies on its cRNA and vRNA promoters.