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: Fusion of MHV-3-immune splenocytes from MHV-3-resistant A/J murine strain, with NS myeloma cells produced several hybridomas. Among eight hybridoma clones, the 1E7A4H1 clone secreted kappa IgG2a apparently directed against the nucleoprotein of the MHV-3 virion. The monoclonal antibody was able to neutralize tile in vitro cytopathic effect of MHV-3 on cultured L2 cells, and was detected by indirect immunofluorescence on MHV-3-infected cultured Y AC cells. In addition, it conferred a significant protection against MHV-3-induced acute disease, if injected intraperitoneally to C57BL/6 mice before inoculation with MHV-3. , Mouse hepatitis viruses (MHVs), members of the coronavirus family, produce various diseases i n t h e mouse and other animal species [16] . They exhibit different tissue tropisms and patterns of infection [1]. The susceptibility of the animals to the virus-induced diseases appears to be genetically controlled at different levels [16] . Serological neutralization patterns of several of the MHVs are very complex [11, 15] and the three structural proteins demonstrated variable degrees of conservation [4, 13] . Coronaviruses are frequently endemic in laboratory mouse colonies [8] . Neutralizing monoclonal antibodies have been recently prepared against the J H M (MHV-4) [2, 4, 17] and MHV-2 [9] strains. In this brief note, we report on a monoclonaI antibody, apparently specific for the nueleo-* Present address: Instituto Butantan, Laboratoria Especial de Immunologia Viral, S~o Paulo, Brazil. 
 Title: Archives of Virology Protection from mouse hepatitis virus type 3-induced acute disease by an anti-nucleoprotein monoclonal antibody Brief Report

Ex Output:
True


Ex Input:
Paragraph: Background: Pseudomonas aeruginosa (PA) is an opportunistic Gram-negative bacterium that causes serious life threatening and nosocomial infections including pneumonia. PA has the ability to alter host genome to facilitate its invasion, thus increasing the virulence of the organism. Sphingosine-1-phosphate (S1P), a bioactive lipid, is known to play a key role in facilitating infection. Sphingosine kinases (SPHK) 1&2 phosphorylate sphingosine to generate S1P in mammalian cells. We reported earlier that Sphk2 −/− mice offered significant protection against lung inflammation, compared to wild type (WT) animals. Therefore, we profiled the differential expression of genes between the protected group of Sphk2 −/− and the wild type controls to better understand the underlying protective mechanisms related to the Sphk2 deletion in lung inflammatory injury. Whole transcriptome shotgun sequencing (RNA-Seq) was performed on mouse lung tissue using NextSeq 500 sequencing system. Results: Two-way analysis of variance (ANOVA) analysis was performed and differentially expressed genes following PA infection were identified using whole transcriptome of Sphk2 −/− mice and their WT counterparts. Pathway (PW) enrichment analyses of the RNA seq data identified several signaling pathways that are likely to play a crucial role in pneumonia caused by PA such as those involved in: 1. Immune response to PA infection and NF-κB signal transduction; 2. PKC signal transduction; 3. Impact on epigenetic regulation; 4. Epithelial sodium channel pathway; 5. Mucin expression; and 6. Bacterial infection related pathways. Our genomic data suggests a potential role for SPHK2 in PA-induced pneumonia through elevated expression of inflammatory genes in lung tissue. Further, validation by RT-PCR on 10 differentially expressed genes showed 100% concordance in terms of vectoral changes as well as significant fold change. (Continued on next page) 
 Title: Genetic deletion of Sphk2 confers protection against Pseudomonas aeruginosa mediated differential expression of genes related to virulent infection and inflammation in mouse lung

Ex Output:
False


Ex Input:
Paragraph: Viruses readily mutate and gain the ability to infect novel hosts, but few data are available regarding the number of possible host range-expanding mutations allowing infection of any given novel host, and the fitness consequences of these mutations on original and novel hosts. To gain insight into the process of host range expansion, we isolated and sequenced 69 independent mutants of the dsRNA bacteriophage 6 able to infect the novel host, Pseudomonas pseudoalcaligenes. In total, we found at least 17 unique suites of mutations among these 69 mutants. We assayed fitness for 13 of 17 mutant genotypes on P. pseudoalcaligenes and the standard laboratory host, P. phaseolicola. Mutants exhibited significantly lower fitnesses on P. pseudoalcaligenes compared to P. phaseolicola. Furthermore, 12 of the 13 assayed mutants showed reduced fitness on P. phaseolicola compared to wildtype 6, confirming the prevalence of antagonistic pleiotropy during host range expansion. Further experiments revealed that the mechanistic basis of these fitness differences was likely variation in host attachment ability. In addition, using computational protein modeling, we show that host-range expanding mutations occurred in hotspots on the surface of the phage's host attachment protein opposite a putative hydrophobic anchoring domain. 
 Title: Frequency and Fitness Consequences of Bacteriophage 6 Host Range Mutations

Ex Output:

True