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".

[Q]: Paragraph: Broad-spectrum antiviral drugs are urgently needed to treat individuals infected with new and reemerging viruses, or with viruses that have developed resistance to antiviral therapies. Mammalian natural host defense peptides (mNHP) are short, usually cationic, peptides that have direct antimicrobial activity, and which in some instances activate cell-mediated antiviral immune responses. Although mNHP have potent activity in vitro, efficacy trials in vivo of exogenously provided mNHP have been largely disappointing, and no mNHP are currently licensed for human use. Mastoparan is an invertebrate host defense peptide that penetrates lipid bilayers, and we reasoned that a mastoparan analog might interact with the lipid component of virus membranes and thereby reduce infectivity of enveloped viruses. Our objective was to determine whether mastoparan-derived peptide MP7-NH 2 could inactivate viruses of multiple types, and whether it could stimulate cell-mediated antiviral activity. We found that MP7-NH 2 potently inactivated a range of enveloped viruses. Consistent with our proposed mechanism of action, MP7-NH 2 was not efficacious against a non-enveloped virus. Pre-treatment of cells with MP7-NH 2 did not reduce the amount of virus recovered after infection, which suggested that the primary mechanism of action in vitro was direct inactivation of virus by MP7-NH 2 . These results demonstrate for the first time that a mastoparan derivative has broad-spectrum antiviral activity in vitro and suggest that further investigation of the antiviral properties of mastoparan peptides in vivo is warranted. 
 Title: A mastoparan-derived peptide has broad-spectrum antiviral activity against enveloped viruses
[A]: True


[Q]: Paragraph: The spread of the COVID-19 caused by the SARS-CoV-2 outbreak has been growing since its first identification in December 2019. The publishing of the first SARS-CoV-2 genome made a valuable source of data to study the details about its phylogeny, evolution, and interaction with the host. Protein-protein binding assays have confirmed that Angiotensin-converting enzyme 2 (ACE2) is more likely to be the cell receptor via which the virus invades the host cell. In the present work, we provide an insight into the interaction of the viral spike Receptor Binding Domain (RBD) from different coronavirus isolates with host ACE2 protein. By calculating : bioRxiv preprint 2 the binding energy between RBD and ACE2, we highlighted the putative jump in the affinity from a progenitor form of SARS-CoV-2 to the current virus responsible for COVID-19 outbreak. Our result was consistent with the phylogeny analysis and corroborates the opinion that the interface segment of the spike protein RBD might be acquired by SARS-CoV-2 via a complex evolutionary process rather than mutation accumulation. We also highlighted the relevance of Q493 and P499 amino acid residues of SARS-CoV-2 RBD for binding to hACE2 and maintaining the stability of the interface. Moreover, we show from the structural analysis that it is unlikely for the interface residues to be the result of human engineering. Finally, we studied the impact of eight different variants located at the interaction surface of ACE2, on the complex formation with SARS-CoV-2 RBD. We found that none of them is likely to disrupt the interaction with the viral RBD of SARS-CoV-2. 
 Title: Interaction of the spike protein RBD from SARS-CoV-2 with ACE2: similarity with SARS-CoV, hot-spot analysis and effect of the receptor polymorphism
[A]: False


[Q]: Paragraph: So far, there has been scarce information about the status of immunoglobulins (Ig) and the gene expression of inflammatory cytokines in buffaloes showing digestive troubles. The purpose of the present study was to explore the modulation of gene expression of some immuneinflammatory markers in buffaloes suffered from various digestive disorders. For this reason, 50 native breed water buffaloes were studied. Forty of these buffaloes showed various symptoms of digestive disorders and were allocated into 4 groups of equal sizes (group 1: uncategorized stomatitis; group 2: acute traumatic reticuloperitonitis [TRR]; group 3: acute rumen impaction; and group 4: undifferentiated enteritis). Ten apparently healthy buffaloes were randomly selected and considered as a control group. RNA was firstly extracted from the whole blood then a reverse transcription kits was used to convert the RNA to cDNA. Real-time PCR was used to measure the expression of mRNAs of interleukin (IL)-1β, IL-6, IL-10, and tumor necrosis factor (TNF)-α, IgG, and IgA, while glyceraldehyde-3-phosphate dehydrogenase (GAPDH) used as an internal reference. The results of realtime PCR revealed a significant (P ≤ 0.05) upregulation of the gene expression of IL-1β, IL-6, IL-10, and TNF-α in blood of diseased buffaloes compared with those of controls. Animals showing acute TRP had peak values of both IL-6 and IL-10; while those exhibiting enteritis and rumen impaction had the highest values of IL-1β and TNF-α, respectively. The results of qPCR also revealed a significant (P ≤ 0.05) downregulation of both IgG and IgA gene expression in blood of all diseased buffaloes compared with controls. The lowest values of both genes were recorded in buffaloes showing acute TRP. The results herein suggest that the tested genes could have a pivotal role in the pathophysiologic mechanism of the underlying diseases. 
 Title: Modulation of immunity and inflammatory gene expression in buffalo (Bubalus bubalis) with some digestive disorders
[A]:
True