In this task, you're given a paragraph and title from the research paper. Your task is to classify whether the given title is suitable or not for the research paper based on the given paragraph. Return "True" if title is proper according to paragraph else "False".

Ex Input:
Paragraph: Dengue virus (DENV) emerged from the sylvatic environment and colonized urban settings, being sustained in a human-Aedes-human transmission chain, mainly by the bites of females of the anthropophilic species Aedes aegypti. Herein, we sought evidence for fine-tuning in viral codon usage, possibly due to viral adaptation to human transmission. We compared the codon adaptation of DENV serotype 2 (DENV-2) genotypes from urban and sylvatic habitats and tried to correlate the findings with key evolutionary determinants. We found that DENV-2 codons of urban and sylvatic genotypes had a higher CAI to humans than to Ae. aegypti. Remarkably, we found no significant differences in codon adaptation to human between urban American/Asian and sylvatic DENV-2 genotypes. Moreover, CAI values were significantly different, when comparing all genotypes to Ae. aegypti codon preferences, with lower values for sylvatic than urban genotypes. In summary, our findings suggest the presence of a molecular signature among the genotypes that circulate in sylvatic and urban environments, and may help explain the trafficking of DENV-2 strains to an urban cycle.
Title: Codon adaptation biases among sylvatic and urban genotypes of Dengue virus type 2

Ex Output:
False

Ex Input:
Paragraph: The present study was undertaken to evaluate chikungunya virus (CHIKV) proteins for RNAi suppressor activity. We systematically analyzed all nine CHIKV proteins for RNAi suppressor activity using Sf21 RNAi sensor cell line based assay. Two non-structural proteins, namely, nsP2 and nsP3 were found to exhibit RNAi suppressor activity. We further validated the findings in natural hosts, namely in Aedes and in mammalian cell lines and further through EMSA and Agrobacterium infiltration in GFP silenced transgenic tobacco plants. Domains responsible for maximum RNAi suppressor activity were also identified within these proteins. RNA binding motifs in these domains were identified and their participation in RNAi suppression evaluated using site directed mutagenesis. Sequence alignment of these motifs across all species of known alphaviruses revealed conservation of these motifs emphasizing on a similar role of action in other species of alphaviruses as well. Further validation of RNAi suppressor activity of these proteins awaits establishment of specific virus infection models. RNA interference (RNAi) is a conserved evolutionary mechanism designed to impart an antiviral defence system across organisms ranging from plants, fungi, arthropods and nematodes 1-4 . The phenomenon, triggered by the production of double stranded RNA (dsRNA) by the pathogen upon infection, leads to the activation of the RNA interference silencing complex (RISC) by loading of dsRNA/siRNA into the complex ultimately leading to cleavage of the viral RNA 5,6,7 . Several components of RISC participate in the cleavage, most important being ribonuclease III Dicer (DCR) and Argonaute protein (AGO). Dicer acts on dsRNA to generate small RNA (sRNA) that are loaded into the AGO, resulting in cleavage 8,9 ; however, some RNAi pathways are independent of Dicer and other components like RNA-dependent RNA polymerase (RdRP) produce short RNA transcripts that directly bind to AGO 10 . Similarly, much is now known about the Piwi pathway that is specifically active in the germline 11 . In response to RNAi in plants and insects, viruses infecting these systems utilise some of their own proteins/sequence elements that counteract the antiviral RNAi pathway 12 . These viral suppressors of RNAi (VSRs) act through different mechanisms, either by binding to long dsRNA and protecting them from Dicer 7,13 or short RNAs 14 or through multi-mode mechanisms 15,16 . Recently it has been shown that some viruses encode host-specific VSRs due to co-evolution of the virus and the host, emphasising on the importance of analysing suppressor activity in relevant host 17 . Amongst medically important pathogenic viruses, arboviruses form an important subset of viruses due to the complexity of their host preferences 18 . These viruses, mainly constituted by genera flavivirus and alphavirus,
Title: Analysis of chikungunya virus proteins reveals that non-structural proteins nsP2 and nsP3 exhibit RNA interference (RNAi) suppressor activity OPEN

Ex Output:
False

Ex Input:
Paragraph: Background: Mice lacking the type I interferon receptor (IFNAR 2/2 mice) reproduce relevant aspects of Crimean-Congo hemorrhagic fever (CCHF) in humans, including liver damage. We aimed at characterizing the liver pathology in CCHF virusinfected IFNAR 2/2 mice by immunohistochemistry and employed the model to evaluate the antiviral efficacy of ribavirin, arbidol, and T-705 against CCHF virus. Methodology/Principal Findings: CCHF virus-infected IFNAR 2/2 mice died 2-6 days post infection with elevated aminotransferase levels and high virus titers in blood and organs. Main pathological alteration was acute hepatitis with extensive bridging necrosis, reactive hepatocyte proliferation, and mild to moderate inflammatory response with monocyte/macrophage activation. Virus-infected and apoptotic hepatocytes clustered in the necrotic areas. Ribavirin, arbidol, and T-705 suppressed virus replication in vitro by $3 log units (IC 50 0.6-2.8 mg/ml; IC 90 1.2-4.7 mg/ml). Ribavirin [100 mg/(kg6d)] did not increase the survival rate of IFNAR 2/2 mice, but prolonged the time to death (p,0.001) and reduced the aminotransferase levels and the virus titers. Arbidol [150 mg/(kg6d)] had no efficacy in vivo. Animals treated with T-705 at 1 h [15, 30, and 300 mg/(kg6d)] or up to 2 days [300 mg/(kg6d)] post infection survived, showed no signs of disease, and had no virus in blood and organs. Co-administration of ribavirin and T-705 yielded beneficial rather than adverse effects. Conclusions/Significance: Activated hepatic macrophages and monocyte-derived cells may play a role in the proinflammatory cytokine response in CCHF. Clustering of infected hepatocytes in necrotic areas without marked inflammation suggests viral cytopathic effects. T-705 is highly potent against CCHF virus in vitro and in vivo. Its in vivo efficacy exceeds that of the current standard drug for treatment of CCHF, ribavirin.
Title: Evaluation of Antiviral Efficacy of Ribavirin, Arbidol, and T-705 (Favipiravir) in a Mouse Model for Crimean-Congo Hemorrhagic Fever

Ex Output:
False