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".

Example Input: Paragraph: Background: Detection of respiratory viruses by time-resolved fluoroimmunoassay based on monoclonal antibodies were developed in our laboratories in the late 1980s and they have been successfully used in daily diagnosis for more than seven years. Later, similar Biotin-EIAs were developed but the sensitivities were unsatisfactory. Objectives: Further optimization of monoclonal Biotin-EIAs and comparison of the optimized assays with TR-FIAs. Study design: Variations in test format, diluents, incubation times and temperatures, and different monoclonal antibodies were tested, and the final comparisons were made with TR-FIA using stored nasopharyngeal aspirates. Results: The improvements in Biotin-EIA featured four changes which increased sensitivity in the assay: (a) test diluent contained diethylenetriamino-pentaacetic acid; (b) antigen and biotinylated detector antibody were added simultaneously; (c) reaction time was extended from 1 h at 37°C to overnight at 4°C; (d) from the thirteen monoclonal antibodies used in TR-FIA, ten were optimal also in Biotin-EIA, but in the parainfluenza 1 and 2 assays other monoclonals proved more sensitive. Out of 257 originally positive specimens tested in the comparison studies, 192 (74.7%) were again positive and 54 (21.0%) were negative in both assays; nine were negative in TR-FIA but positive in Biotin-EIA, while two specimens were negative in Biotin-EIA but positive in TR-FIA. The overall agreement between the two assays was 95.7%. 
 Title: Clinical and Diagnostic Virology Comparison of monoclonal biotin-avidin enzyme immunoassay and monoclonal time-resolved fluoroimmunoassay in detection of respiratory virus antigens
Example Output: False

Example 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
Example Output: True

Example Input: Paragraph: Genome-wide analysis of the mode of action of GSK983, a potent antiviral agent, led to the identification of dihydroorotate dehydrogenase (DHODH) as its target, along with the discovery that knockdown of genes in pyrimidine salvage pathways sensitized cells to GSK983. Because GSK983 is an ineffective antiviral in the presence of physiological uridine concentrations, we explored combining GSK983 with pyrimidine salvage inhibitors. We synthesized and evaluated analogs of cyclopentenyl uracil (CPU), an inhibitor of uridine salvage. We found that CPU was efficiently converted into its triphosphates in cells. When combined with GSK983, it led to large drops in cellular UTP and CTP pools. Consequently, CPU-GSK983 suppressed dengue virus replication in the presence of physiological concentrations of uridine. In addition, the CPU-GSK983 combination markedly enhanced the effect of RNA-dependent RNA polymerase (RdRp) inhibition on viral genome infection. Our findings highlight a new host-targeting strategy for potentiating the antiviral activities of RdRp inhibitors. 
 Title: Enhancing the Antiviral Efficacy of RNA-Dependent RNA Polymerase Inhibition by Combination with Modulators of Pyrimidine Metabolism
Example Output:
False