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.

Example input: The severe acute respiratory syndrome (SARS) epidemic originating from China in 2002 was caused by a previously uncharacterized coronavirus that could be identified by specific RT-PCR amplification. Efforts to control future SARS outbreaks depend on the accurate and early identification of SARS-CoV infected patients. A real-time fluorogenic RT-PCR assay based on the 3 -noncoding region (3 -NCR) of SARS-CoV genome was developed as a quantitative SARS diagnostic tool. The ideal amplification efficiency of a sensitive SARS-CoV RT-PCR assay should yield an E value (PCR product concentration increase per amplification cycle) equal to 2.0. It was demonstrated that the 3 -NCR SARS-CoV based RT-PCR reactions could be formulated to reach excellent E values of 1.81, or 91% amplification efficacy. The SARS-CoV cDNA preparations derived from viral RNA extract and the cloned recombinant plasmid both exhibit the identical amplification characteristics, i.e. amplification efficacy using the same PCR formulation developed in this study. The viral genomic copy (or genomic equivalences, GE) per infectious unit (GE/pfu) of SARS-CoV used in this study was also established to be approximate 1200-1600:1. The assay's detection sensitivity could reach 0.005 pfu or 6-8 GE per assay. It was preliminarily demonstrated that the assay could efficiently detect SARS-CoV from clinical specimens of SARS probable and suspected patients identified in Taiwan. The 3 -NCR based SARS-CoV assay demonstrated 100% diagnostic specificity testing samples of patients with acute respiratory disease from a non-SARS epidemic region.
Example output: Development and evaluation of an efficient 3 -noncoding region-based SARS coronavirus (SARS-CoV) RT-PCR assay for detection of SARS-CoV
Example explanation: It's a correct title because the paragraph described the development of 3 -noncoding region of SARS-CoV genome and assay efficiently detecting SARS-CoV from clinical specimens.
Q: The mammalian reoviruses and rotaviruses have evolved specifi c mechanisms to evade the Type I interferon (IFN) antiviral response. Rotavirus likely represses the IFN response by at least 4 mechanisms. First, the rotavirus protein NSP1, most likely functioning as an E3 ligase, can induce proteasome-dependent degradation of the transcription factors IRF3, IRF5, and IRF7 to prevent their induction of IFN. Second, NSP1 can induce proteasome-dependent degradation of the ubiquitin ligase complex protein -TrCP, resulting in stabilization of IB and concomitant failure of virus to activate NF-B for induction of IFN. Third, rotavirus may sequester NF-B in viroplasms. And fourth, rotavirus can prevent STAT1 and STAT2 nuclear translocation. The predominant mechanism for rotavirus inhibition of the IFN response is likely both rotavirus strain-specifi c and cell type-specifi c. The mammalian reoviruses also display strain-specifi c differences in their modulation of the IFN response. Reovirus activates RIG-I and IPS-1 for phosphorylation of IRF3. Reovirus-induced activation of MDA5 also participates in induction if IFN-, perhaps through activation of NF-B. Reovirus likely inhibits the IFN response by at least 3 virus strain-specifi c mechanisms. First, the reovirus 2 protein can induce an unusual nuclear accumulation of IRF9 and repress IFN-stimulated gene (ISG) expression, most likely by disrupting IRF9 function as part of the heterotrimeric transcription factor complex, ISGF3. Second, the reovirus 3 protein can bind dsRNA and prevent activation of the latent antiviral effector protein PKR. And third, genetic approaches have identifi ed the reovirus 2 and 2 proteins in virus strain-specifi c modulation of the IFN response, but the signifi cance remains unclear. In sum, members of the family Reoviridae have evolved a variety of mechanisms to subvert the host's innate protective response. Yue Z, Shatkin AJ. 1997. Double-stranded RNA-dependent protein kinase (PKR) is regulated by reovirus structural proteins. Virology 234(2):364-371. Zurney J, Howard KE, Sherry B. 2007. Basal expression levels of IFNAR and Jak-STAT components are determinants of celltype-specifi c differences in cardiac antiviral responses. J Virol 81(24):13668-13680. Zurney J, Kobayashi T, Holm GH, Dermody TS, Sherry B. 2009. Reovirus mu2 protein inhibits interferon signaling through a novel mechanism involving nuclear accumulation of interferon regulatory factor 9. J Virol 83 (5):2178-2187.
A:
Rotavirus and Reovirus Modulation of the Interferon Response