TASK DEFINITION: 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".
PROBLEM: Paragraph: Background: To our knowledge, no studies to date demonstrate potential spread of microbes during actual emergency medical service (EMS) activities. Our study introduces a novel approach to identification of contributors to EMS environment contamination and development of infection control strategies, using a bacteriophage surrogate for pathogenic organisms. Methods: Bacteriophage FX174 was used to trace cross-contamination and evaluate current disinfection practices and a hydrogen peroxide (H 2 O 2 ) wipe intervention within emergency response vehicles. Prior to EMS calls, 2 surfaces were seeded with FX174. On call completion, EMS vehicle and equipment surfaces were sampled before decontamination, after decontamination per current practices, and after implementation of the intervention. Results: Current decontamination practices did not significantly reduce viral loads on surfaces (P .3113), but H 2 O 2 wipe intervention did (P .0065). Bacteriophage spread to 56% (27/48) of sites and was reduced to 54% (26/48) and 40% (19/48) with current decontamination practices and intervention practices, respectively. Conclusion: Results suggest firefighters' hands were the main vehicles of microbial transfer. Current practices were not consistently applied or standardized and minimally reduced prevalence and quantity of microbial contamination on EMS surfaces. Although use of a consistent protocol of H 2 O 2 wipes significantly reduced percent prevalence and concentration of viruses, training and promotion of surface disinfection should be provided.
Title: Spread of infectious microbes during emergency medical response

SOLUTION: True

PROBLEM: 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

SOLUTION: True

PROBLEM: Paragraph: Viral infections of the central nervous system (CNS) necessitate rapid, yet tightly controlled responses to contain viral spread while limiting tissue damage. All CNS resident cell types are equipped with pattern recognition receptors (PRRs) to respond to viruses. The resulting activation of IFN-/, proinflammatory cytokines and chemokines is dependent on the virus replication strategy, tropism and PRR distribution. Although IFN-/ induced antiviral mediators are essential to restrict initial viral spread, adaptive immunity promoted by chemokines, cytokines and metalloproteinases is equally critical in lowering viral burden. Recognition of viral antigen presented by MHC molecules is critical for T cell retention and function. Non lytic clearance mechanisms mediated by IFN- and antibodies prevail in providing protection. Targeted intervention can be achieved by PRR stimulation, chemokine-receptor blockade and immune modulation of T cell function. However, due to the extensive positive and negative feedback signaling cascades linking innate and adaptive immune responses, enhanced anti-viral functions will have to be counterbalanced to avoid pathology.
Title: Neuroimmunology of central nervous system viral infections: the cells, molecules and mechanisms involved

SOLUTION:
True