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: MRNA2 of the arteriviruses lactate dehydrogenase-elevating virus (LDV) and equine arteritis virus (EAV) encodes two proteins that are read in different frames, an about 26 kDa minor envelope glycoprotein and an about 8 kDa protein that lacks N-glycosylation sites and a signal peptide, but possesses a central hydrophobic segment. Recent studies have shown that both proteins of EAV are translated from mRNA 2 in EAV infected BHK cells, that the 8 kDa protein is membrane associated and that small amounts of it are recovered in purified virions (Snijder, E.J., van Tol, H., Pederson, K.W., Raamsman, M.J.B., de Vries, A.A.F., 1999. Identification of a novel structural protein of arteriviruses. J. Virol. 73, 6335-6345). The authors concluded that the 8 kDa protein is another arterivirus envelope protein and designated it E protein. However, we have not detected a significant level of an 8 kDa protein in LDV virions and thus conclude that it is not a structural virion component.
Title: An ORF-2a protein is not present at a significant level in virions of the arterivirus lactate dehydrogenase-elevating virus

SOLUTION: True

PROBLEM: Paragraph: The observations that Lymphopenia is common in severe acute respiratory syndrome (SARS) patients and that peripheral blood mononuclear cell (PBMC) could be infected by SARS-CoV indicate that PBMC could be useful in identifying the gene expression profile in convalescent patients and tracing the host response to SARS-CoV infection. In this study, the altered genes expressions in the PBMC of convalescent SARS patients were investigated with suppression subtractive hybridization (SSH). We found that genes encoded by mitochondrial DNA (mtDNA) were obviously upregulated, while mitochondria were now found to be closely connected with antiviral immunity. The identification of a viral gene, M, in SSH cDNA library shows the long-term existence of SARS-CoV in vivo. In addition, some oxidative stress sensitive genes, heat shock proteins, transcription factors, and cytokines showed remarkable elevation. Thin-section electron microscope shows increased lysosome-like granule and mitochondria in PBMC of patients. These results provide important intracellular clue for tracing host response to SARS-CoV infection and suggest a role of mitochondria in that process.
Title: Upregulation of Mitochondrial Gene Expression in PBMC from Convalescent SARS Patients

SOLUTION: True

PROBLEM: Paragraph: Multiple pathogens, such as bacteria, fungi, and viruses, have been frequently found in asthmatic airways and are associated with the pathogenesis and exacerbation of asthma. Among these pathogens, Alternaria alternata (Alt), a universally present fungus, and human rhinovirus have been extensively studied. However, their interactions have not been investigated. In the present study, we tested the effect of Alt exposure on virus-induced airway epithelial immunity using live virus and a synthetic viral mimicker, double-stranded RNA (dsRNA). Alt treatment was found to significantly enhance the production of proinflammatory cytokines (e.g., IL-6 and IL-8) induced by virus infection or dsRNA treatment. In contrast to this synergistic effect, Alt significantly repressed type I and type III IFN production, and this impairment led to elevated viral replication. Mechanistic studies suggested the positive role of NF-kB and mitogen-activated protein kinase pathways in the synergism and the attenuation of the TBK1-IRF3 pathway in the inhibition of IFN production. These opposite effects are caused by separate fungal components. Proteasedependent and -independent mechanisms appear to be involved. Thus, Alt exposure alters the airway epithelial immunity to viral infection by shifting toward more inflammatory but less antiviral responses.
Title: Modulation of Airway Epithelial Antiviral Immunity by Fungal Exposure

SOLUTION:
True