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".

Q: Paragraph: Introduction: Outbreaks of infectious diseases trigger an increase in scientific research and output. Early in outbreaks, evidence is scarce, but it accumulates rapidly. We are continuously facing new disease outbreaks, including the new coronavirus (SARS-nCoV-2) in December 2019.The objective of this study was to describe the accumulation of evidence during the 2013-2016 Zika virus (ZIKV) outbreak in the Pacific and the Americas related to aetiological causal questions about congenital abnormalities and Guillain-Barré syndrome. Methods: We hypothesised that the temporal sequence would follow a pre-specified order, according to study design. We assessed 1) how long it takes before findings from a specific study design appear, 2) how publication of preprints could reduce the time to publication and 3) how time to publication evolves over time. Results: We included 346 publications published between March 6, 2014 and January 1, 2019. In the 2013--2016 ZIKV outbreak, case reports, case series and basic research studies were published first. Case-control and cohort studies appeared between 400-700 days after ZIKV was first detected in the region of the study origin. Delay due to the publication process were lowest at the beginning of the outbreak. Only 4.6% of the publications was available as preprints. Discussion: The accumulation of evidence over time in new causal problems generally followed a hierarchy. Preprints reduced the delay to initial publication. Our methods can be applied to new emerging infectious diseases. 
 Title: Emergence of evidence during disease outbreaks: lessons learnt from the Zika virus outbreak

A: False
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Q: Paragraph: The majority of human emerging infectious diseases (EIDs) are zoonotic, with viruses originating in wild mammals of particular concern (e.g. HIV, Ebola, SARS) 1-3 . Understanding patterns of viral diversity in wildlife and determinants of successful cross-species transmission, or spillover, are therefore key goals for pandemic surveillance programs 4 . However, few analytical tools exist to identify which host species likely harbor the next human virus, or which viruses can cross species boundaries 5-7 . Here we conduct the most comprehensive analysis yet of mammalian hostvirus relationships and show that both the total number of viruses that infect a given species, and the proportion likely to be zoonotic are predictable. After controlling for research effort, the proportion of zoonotic viruses per species is predicted by phylogenetic relatedness to humans, host taxonomy, and human population within a species range -which may reflect human-wildlife contact. We demonstrate for the first time that bats harbor a significantly higher proportion of zoonotic viruses than all other mammalian orders. We identify the taxa and geographic regions with the largest estimated number of 'missing viruses' and 'missing zoonoses' and therefore of highest value for future surveillance. We then show that phylogenetic host breadth and other viral traits are significant predictors of zoonotic potential, providing a novel framework to assess if a newly discovered mammalian virus could infect people. Viral zoonoses are a serious threat to public health and global security, and have caused the majority of recent pandemics in people 4 , yet our understanding of the factors driving viral diversity in mammals, viral host range, and cross-species transmission to humans remain nascent. Recent studies have described broad patterns of pathogen host range 1,3 and various host or microbial factors that facilitate cross-species transmission 5,7,8 , or have focused on Users may view, print, copy, and download text and data-mine the content in such documents, for the purposes of academic research, subject always to the full Conditions of use: http://www.nature. All datasets (host traits, viral traits, full list of host-virus associations and associated references, phylogenetic trees, and phylogenetic distance matrices) along with the R code and R package dependencies needed to fully replicate and evaluate these analyses are provided at http://doi.org/10.5281/zenodo.569079. The top-level README.txt file in the directory details the file structure and metadata provided. 
 Title: Host and viral traits predict zoonotic spillover from mammals HHS Public Access

A: False
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Q: Paragraph: The transposase encoded by insertion sequence IS/ is produced from two out-of-phase reading frames (insA and B'-insB) by translational frameshifting, which occurs within a run of six adenines in the -1 direction. To determine the sequence essential for frameshifting, substitution mutations were introduced within the region containing the run of adenines and were examined for their effects on frameshifting. Substitutions at each of three (2nd, 3rd and 4th) adenine residues in the run, which are recognized by tRNA Lys reading insA, caused serious defects in frameshifting, showing that the three adenine residues are essential for frameshifting. The effects of substitution mutations introduced in the region flanking the run of adenines and in the secondary structures located downstream were, however, small, indicating that such a region and structures are not essential for frameshifting. Deletion of a region containing the termination codon of insA caused a decrease in fi-galactosidase activity specified by the lacZ fusion plasmid in frame with B'-insB. Exchange of the wild-type termination codon of insA for a different one or introduction of an additional termination codon in the region upstream of the native termination codon caused an increase in fi-galactosidase activity, indicating that the termination codon in insA affects the efficiency of frameshifting. 
 Title: DNA sequences required for translational frameshifting in production of the transposase encoded by IS1

A:
False
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