In this section
@article{Rehwinkel:2010:10.1016/j.cell.2010.01.020,
author = {Rehwinkel, J and Tan, CP and Goubau, D and Schulz, O and Pichlmair, A and Bier, K and Robb, N and Vreede, F and Barclay, W and Fodor, E and Reis, e Sousa C},
doi = {10.1016/j.cell.2010.01.020},
journal = {Cell},
pages = {397--408},
title = {RIG-I detects viral genomic RNA during negative-strand RNA virus infection.},
url = {http://dx.doi.org/10.1016/j.cell.2010.01.020},
volume = {140},
year = {2010}
}
TY - JOUR
AB - RIG-I is a key mediator of antiviral immunity, able to couple detection of infection by RNA viruses to the induction of interferons. Natural RIG-I stimulatory RNAs have variously been proposed to correspond to virus genomes, virus replication intermediates, viral transcripts, or self-RNA cleaved by RNase L. However, the relative contribution of each of these RNA species to RIG-I activation and interferon induction in virus-infected cells is not known. Here, we use three approaches to identify physiological RIG-I agonists in cells infected with influenza A virus or Sendai virus. We show that RIG-I agonists are exclusively generated by the process of virus replication and correspond to full-length virus genomes. Therefore, 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. Rather, single-stranded RNA viral genomes bearing 5'-triphosphates constitute the natural RIG-I agonists that trigger cell-intrinsic innate immune responses during infection.
AU - Rehwinkel,J
AU - Tan,CP
AU - Goubau,D
AU - Schulz,O
AU - Pichlmair,A
AU - Bier,K
AU - Robb,N
AU - Vreede,F
AU - Barclay,W
AU - Fodor,E
AU - Reis,e Sousa C
DO - 10.1016/j.cell.2010.01.020
EP - 408
PY - 2010///
SP - 397
TI - RIG-I detects viral genomic RNA during negative-strand RNA virus infection.
T2 - Cell
UR - http://dx.doi.org/10.1016/j.cell.2010.01.020
VL - 140
ER -