instruction:
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".
question:
Paragraph: Severe acute respiratory syndrome (SARS) is caused by a novel coronavirus (CoV), SARS-CoV. In previous studies, we showed that a SARS-CoV spike (S) glycoproteinbased modified vaccinia Ankara (MVA-S) vaccine could induce strong neutralizing antibody (Nab) response which might have played a critical role in protecting Chinese rhesus monkeys from the pathogenic viral challenge. To date, however, it remains unknown what the minimal level of Nab is required to achieve sterile immunity in humans. It is therefore important to explore techniques to maximize the level of Nab response in vivo. Here, we evaluate various vaccination regimens using combinations of DNA-S, MVA-S, and adenovirus type 5 (Ad5-S) vaccines. We show that in vaccinated mice and rabbits, a heterologous MVA-S prime with Ad5-S boost regimen induces the highest and most persistent level of Nab response when compared with other combinations. Interestingly, the initial level of Nab after prime does not necessarily predict the magnitude of the secondary response after the boost. Thus, our data provides a promising optimal regimen for vaccine development in humans against SARS-CoV infection.
Title: Heterologous MVA-S prime Ad5-S boost regimen induces high and persistent levels of neutralizing antibody response against SARS coronavirus
answer:
False

question:
Paragraph: In ostriches, the population densities resulting from intensive rearing increases susceptibility to pathogens such as mycoplasmas. In addition to good management practices, vaccination offers an attractive alternative for controlling mycoplasma infections in food animals, instead of using antibiotics, which often leave unacceptable residues. The use of live attenuated vaccines, however, carry the concern of reversion to virulence or genetic recombination with field strains. Currently there are no commercially available vaccines against ostrich-infecting mycoplasmas and this study therefore set out to develop and evaluate the use of a DNA vaccine against mycoplasma infections in ostriches using an OppA protein as antigen. To this end, the oppA gene of "Mycoplasma nasistruthionis sp. nov." str. Ms03 was cloned into two DNA vaccine expression vectors after codon correction by site-directed mutagenesis. Three-months-old ostriches were then vaccinated intramuscularly at different doses followed by a booster vaccination after 6 weeks. The ability of the DNA vaccines to elicit an anti-OppA antibody response was evaluated by ELISA using the recombinant OppA protein of Ms03 as coating antigen. A statistically significant anti-OppA antibody response could be detected after administration of a booster vaccination indicating that the OppA protein was successfully immunogenic. The responses were also both dose and vector dependent. In conclusion, the DNA vaccines were able to elicit an immune response in ostriches and can therefore be viewed as an option for the development of vaccines against mycoplasma infections.
Title: DNA Vaccines Against Mycoplasma Elicit Humoral Immune Responses in Ostriches
answer:
False

question:
Paragraph: Background: The interplay between IFN-, IL-17 and neutrophils during CNS inflammatory disease is complex due to cross-regulatory factors affecting both positive and negative feedback loops. These interactions have hindered the ability to distinguish the relative contributions of neutrophils, Th1 and Th17 cell-derived effector molecules from secondary mediators to tissue damage and morbidity. Methods: Encephalitis induced by a gliatropic murine coronavirus was used as a model to assess the direct contributions of neutrophils, IFN- and IL-17 to virus-induced mortality. CNS inflammatory conditions were selectively manipulated by adoptive transfer of virus-primed wild-type (WT) or IFN- deficient (GKO) memory CD4 + T cells into infected SCID mice, coupled with antibody-mediated neutrophil depletion and cytokine blockade. Results: Transfer of GKO memory CD4 + T cells into infected SCID mice induced rapid mortality compared to recipients of WT memory CD4 + T cells, despite similar virus control and demyelination. In contrast to recipients of WT CD4 + T cells, extensive neutrophil infiltration and IL-17 expression within the CNS in recipients of GKO CD4 + T cells provided a model to directly assess their contribution(s) to disease. Recipients of WT CD4 + T cells depleted of IFN- did not express IL-17 and were spared from mortality despite abundant CNS neutrophil infiltration, indicating that mortality was not mediated by excessive CNS neutrophil accumulation. By contrast, IL-17 depletion rescued recipients of GKO CD4 + T cells from rapid mortality without diminishing neutrophils or reducing GM-CSF, associated with pathogenic Th17 cells in CNS autoimmune models. Furthermore, co-transfer of WT and GKO CD4 + T cells prolonged survival in an IFN- dependent manner, although IL-17 transcription was not reduced. Conclusions: These data demonstrate that IL-17 mediates detrimental clinical consequences in an IFN--deprived environment, independent of extensive neutrophil accumulation or GM-CSF upregulation. The results also suggest that IFN- overrides the detrimental IL-17 effector responses via a mechanism downstream of transcriptional regulation.
Title: IFN- protects from lethal IL-17 mediated viral encephalomyelitis independent of neutrophils
answer:
True