Viral RNA Decay

We believe that the cellular mRNA decay machinery can act as an antiviral defense mechanism. After all, many viral RNAs have evolved to mimic cellular transcripts and should therefore be ideal targets for degradation. A degraded genome cannot be replicated or translated, and therefore presents no threat (Sokoloski et al, 2006; Dickson and Wilusz, 2011). Several projects in the lab focus on characterizing the interactions between viral RNAs and cellular mRNA decay factors. One virus we have investigated extensively is the alphavirus Sindbis Virus (SINV). We have discovered that SINV RNAs are actually quite resistant to decay, and this is likely because they usurp cellular RNA-binding proteins that act as stabilizing factors (Garneau et al 2008, Sokoloski et al, 2010). We have also shown that the rabies virus glycoprotein mRNA can interact with a poly(C) binding protein to enhance its stability (Palusa et al, 2012). We hypothesize that other RNA viruses (e.g. Dengue, Rabies, Ebola) will have evolved similar, or novel mechanisms to protect their genomes from the mRNA decay machinery. Moreover, by interfering with these interactions we should be able to induce viral RNA decay and prevent infection.