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".
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Question: Paragraph: Translational stalling of ribosome bound to endoplasmic reticulum (ER) membrane requires an accurate clearance of the associated polypeptides, which is not completely understood in mammals. We characterized in mammalian cells the model of ribosomal stalling at the STOP-codon based on proteins tagged at the C-terminus with the picornavirus 2A peptide followed by a termination codon instead of the Proline (2A*). We exploited the 2A* stalling model to characterize the pathway of degradation of ER-targeted polypeptides. We report that the ER chaperone BiP/GRP78 is a new main factor involved. Moreover, degradation of the ER-stalled polypeptides required the activities of the AAA-ATPase VCP/p97, its associated deubiquitinylase YOD1, the ribosome-associated ubiquitin ligase Listerin and the proteasome. In human proteome, we found two human C-terminal amino acid sequences that cause similar stalling at the STOP-codon. Our data suggest that translational stalling at the ER membrane activates protein degradation at the interface of ribosomal-and ERassociated quality control systems.
Title: BiP/GRP78 Mediates ERAD Targeting of Proteins Produced by Membrane-Bound Ribosomes Stalled at the STOP-Codon

Answer: False

Question: Paragraph: The simian hemorrhagic fever virus (SHFV) genome differs from those of other members of the family Arteriviridae in encoding three papain-like one proteases (PLP1, PLP1 and PLP1) at the 5 end and two adjacent sets of four minor structural proteins at the 3 end. The catalytic Cys and His residues and cleavage sites for each of the SHFV PLP1s were predicted and their functionality was tested in in vitro transcription/translation reactions done with wildtype or mutant polyprotein constructs. Mass spectrometry analyses of selected autoproteolytic products confirmed cleavage site locations. The catalytic Cys of PLP1 is unusual in being adjacent to an Ala instead of a Typ. PLP1 cleaves at both downstream and upstream sites. Intermediate precursor and alternative cleavage products were detected in the in vitro transcription/translation reactions but only the three mature nsp1 proteins were detected in SHFV-infected MA104 cell lysates with SHFV nsp1 protein-specific antibodies. The duplicated sets of SHFV minor structural proteins were predicted to be functionally redundant. A stable, full-length, infectious SHFV-LVR cDNA clone was constructed and a set of mutant infectious clones was generated each with the start codon of one of the minor structural proteins mutated. All eight of the minor structural proteins were found to be required for production of infectious extracellular virus. SHFV causes a fatal hemorrhagic fever in macaques but asymptomatic, persistent infections in natural hosts such as baboons. SHFV infections were compared in macrophages and myeloid dendritic cells from baboons and macaques. Virus yields were higher from macaque cells than from baboon cells. Macrophage cultures from the two types of animals differed dramatically in the percentage of cells infected. In contrast, similar percentages of myeloid dendritic cells were infected but virus replication was efficient in the macaque cells but inefficient in the baboon cells. SHFV infection induced the production of pro-inflammatory cytokines, including IL-1, IL-6, IL-12/23(p40), TNF- and MIP-1, in macaque cells but not baboon cells. (M.A. Brinton). capsid types (coronaviruses-helical and arteriviruses-spherical) and virion sizes. Arteriviruses infect macrophages (M s) and dendritic cells (DCs) and have restricted host ranges; EAV infects horses and donkeys, PRRSV infects pigs, LDV infects mice and SHFV infects nonhuman primates (NHPs) (Snijder and Meulenberg, 1998) . Disease symptoms associated with EAV and PRRSV infections include fever, respiratory disease, tissue necrosis and spontaneous abortions while LDV typically causes an asymptomatic, persistent infection (Snijder and Spaan, 2006) . The majority of research on arteriviruses has focused on EAV and PRRSV due to the significant agricultural impact of the diseases they cause. SHFV was first isolated in 1964 as the causative agent of hemorrhagic fever outbreaks associated with high mortality in macaque colonies in the United States and the USSR http://dx.
Title: Simian hemorrhagic fever virus: Recent advances

Answer: True

Question: 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

Answer:
False