Related Experiment Video
Updated: Aug 13, 2026

Using Reverse Genetics to Manipulate the NSs Gene of the Rift Valley Fever Virus MP-12 Strain to Improve Vaccine Safety and Efficacy
Published on: November 1, 2011
Reovirus µ2 residue 208 drives SRSF2-dependent nuclear hyperaccumulation of IRF9
1Department of Biology, Elon University, Elon, NC, United States.
None:
Mammalian reovirus µ2 antagonizes type I interferon (IFN) signaling and is associated with nuclear hyperaccumulation of IRF9. We tested whether µ2 residue 208, which determines strain-specific IFN-β repression and modulation of host cell mRNA splicing, also controls IRF9 relocalization and whether the splicing factor SRSF2 is required. Recombinant and mutant viruses showed that T1L-like Pro208 is required and sufficient for IRF9 nuclear accumulation in L929 cells. In addition, SRSF2 depletion reduced IFN-mediated induction of Irf7 and Stat1 , but not Isg56/Ifit1 , and abolished T3D-S208P-induced IRF9 nuclear accumulation. Thus, reovirus-induced IRF9 relocalization requires both µ2 residue 208 and host SRSF2.
Related Concept Videos
Regulation of the Unfolded Protein Response
Rous Sarcoma Virus (RSV) and Cancer
RSV is a retrovirus that contains two copies of a plus-strand RNA genome. Its genome consists of four main open...
Conservative Site-specific Recombination and Phase Variation
The recognition sites for Cre recombinase called LoxP...
Leaky Scanning
Respiratory Syncytial Virus Disease

