Instructions: In this task, you're given a paragraph from the research paper and your task is to generate a suitable title for the research paper based on the given paper. Under 100 words is a good title length.
Input: Graphical Abstract Highlights d Catalytic site mutations were introduced in vaccinia virus decapping enzymes, D9 and D10 d D9 and D10 catalytic mutant virus exhibits replication defects and attenuation in mice d Mutant virus increases dsRNA, activates RNase L, and induces PKR phosphorylation d Protein synthesis is inhibited and RNA degraded in absence of functional D9 and D10 SUMMARY Poxvirus replication involves synthesis of doublestranded RNA (dsRNA), which can trigger antiviral responses by inducing phosphorylation-mediated activation of protein kinase R (PKR) and stimulating 2 0 5 0 -oligoadenylate synthetase (OAS). PKR inactivates the translation initiation factor eIF2a via phosphorylation, while OAS induces the endonuclease RNase L to degrade RNA. We show that poxvirus decapping enzymes D9 and D10, which remove caps from mRNAs, inhibit these antiviral responses by preventing dsRNA accumulation. Catalytic site mutations of D9 and D10, but not of either enzyme alone, halt vaccinia virus late protein synthesis and inhibit virus replication. Infection with the D9-D10 mutant was accompanied by massive mRNA reduction, cleavage of ribosomal RNA, and phosphorylation of PKR and eIF2a that correlated with a 15-fold increase in dsRNA compared to wild-type virus. Additionally, mouse studies show extreme attenuation of the mutant virus. Thus, vaccinia virus decapping, in addition to targeting mRNAs for degradation, prevents dsRNA accumulation and anti-viral responses.
Output:
Poxvirus Decapping Enzymes Enhance Virulence by Preventing the Accumulation of dsRNA and the Induction of Innate Antiviral Responses Article Poxvirus Decapping Enzymes Enhance Virulence by Preventing the Accumulation of dsRNA and the Induction of Innate Antiviral Responses