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".

Paragraph: Profiles of antibodies to the nucleocapsid protein of the severe acute respiratory syndrome (SARS)-associated coronavirus in 445 probable SARS patients and 3,749 healthy people or non-SARS patients were analyzed by antigen-capturing enzyme-linked immunosorbent assay. Antinucleocapsid antibodies were elucidated in 17.5% of the probable SARS patients 1 to 7 days after the onset of symptoms and in 80% of the patients 8 to 14 days after the onset. About 90% of the probable SARS patients were positive 15 or more days after illness. Antibody titers increased up to 70 days, and high antibody titers were maintained at least for another 3 months. Of the healthy people and non-SARS patients, only seven (0.187%) were weakly positive. FIG. 1. Development of anti-N protein antibody titers over time in 445 patients who probably had SARS. 228 NOTES CLIN. DIAGN. LAB. IMMUNOL. 
 Title: Profile of Antibodies to the Nucleocapsid Protein of the Severe Acute Respiratory Syndrome (SARS)-Associated Coronavirus in Probable SARS Patients
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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
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Paragraph: Many viruses have been implicated in utilizing or modulating the Ubiquitin Proteasome System (UPS) to enhance viral multiplication and/or to sustain a persistent infection. The mosquito-borne Venezuelan equine encephalitis virus (VEEV) belongs to the Togaviridae family and is an important biodefense pathogen and select agent. There are currently no approved vaccines or therapies for VEEV infections; therefore, it is imperative to identify novel targets for therapeutic development. We hypothesized that a functional UPS is required for efficient VEEV multiplication. We have shown that at non-toxic concentrations Bortezomib, a FDAapproved inhibitor of the proteasome, proved to be a potent inhibitor of VEEV multiplication in the human astrocytoma cell line U87MG. Bortezomib inhibited the virulent Trinidad donkey (TrD) strain and the attenuated TC-83 strain of VEEV. Additional studies with virulent strains of Eastern equine encephalitis virus (EEEV) and Western equine encephalitis virus (WEEV) demonstrated that Bortezomib is a broad spectrum inhibitor of the New World alphaviruses. Time-of-addition assays showed that Bortezomib was an effective inhibitor of viral multiplication even when the drug was introduced many hours post exposure to the virus. Mass spectrometry analyses indicated that the VEEV capsid protein is ubiquitinated in infected cells, which was validated by confocal microscopy and immunoprecipitation assays. Subsequent studies revealed that capsid is ubiquitinated on K48 during early stages of infection which was affected by Bortezomib treatment. This study will aid future investigations in identifying host proteins as potential broad spectrum therapeutic targets for treating alphavirus infections. 
 Title: The Ubiquitin Proteasome System Plays a Role in Venezuelan Equine Encephalitis Virus Infection

False