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: Interleukin-11 (IL-11), a well-known anti-inflammatory factor, provides protection from intestinal epithelium damage caused by physical or chemical factors. However, little is known of the role of IL-11 during viral infections. In this study, IL-11 expression at mRNA and protein levels were found to be high in Vero cells and the jejunum of piglets during porcine epidemic diarrhea virus (PEDV) infection, while IL-11 expression was found to be positively correlated with the level of viral infection. Pretreatment with recombinant porcine IL-11 (pIL-11) was found to suppress PEDV replication in Vero E6 cells, while IL-11 knockdown promoted viral infection. Furthermore, pIL-11 was found to inhibit viral infection by preventing PEDV-mediated apoptosis of cells by activating the IL-11/STAT3 signaling pathway. Conversely, application of a STAT3 phosphorylation inhibitor significantly antagonized the anti-apoptosis function of pIL-11 and counteracted its inhibition of PEDV. Our data suggest that IL-11 is a newfound PEDV-inducible cytokine, and its production enhances the anti-apoptosis ability of epithelial cells against PEDV infection. The potential of IL-11 to be used as a novel therapeutic against devastating viral diarrhea in piglets deserves more attention and study.
Title: Antiviral activity of interleukin-11 as a response to porcine epidemic diarrhea virus infection
[A]: True

[Q]: Paragraph: Inspired by bioactive biaryl-containing natural products found in plants and the marine 19 environment, a series of synthetic compounds belonging to the azaBINOL chiral ligand family 20 was evaluated for antiviral activity against HIV-1. Testing of 39 unique azaBINOLs in a single-21 round infectivity assay resulted in the identification of three promising antiviral compounds, 22 including 7-isopropoxy-8-(naphth-1-yl)quinoline (azaBINOL B#24), which exhibited low-23 micromolar activity. The active compounds and several close structural analogues were further 24 tested against three different HIV-1 envelope pseudotyped viruses as well as in a full-virus 25 replication system (EASY-HIT). Mode-of-action studies using a time-of-addition assay indicated 26 that azaBINOL B#24 acts after viral entry but before viral assembly and budding. HIV-1 reverse 27 transcriptase (RT) assays that individually test for polymerase and RNase H activity were used to 28 demonstrate that B#24 inhibits RNase H activity, most likely allosterically. Further binding 29 analysis using bio-layer interferometry (BLI) showed that B#24 interacts with HIV-1 RT in a 30 highly specific manner. These results indicate that azaBINOL B#24 is a potentially viable, novel 31
Title: Biological Evaluation of Molecules of the azaBINOL Class as Antiviral Agents: 1 Specific Inhibition of HIV-1 RNase H Activity by 7-Isopropoxy-8-(naphth-1-yl)quinoline 2 3 4 5
[A]: False

[Q]: Paragraph: Among the various respiratory viruses infecting human beings, coronaviruses are important pathogens, which usually infect the upper respiratory tract, where they are mainly associated with common colds. However, in more vulnerable populations, such as newborns, infants, the elderly and immunecompromised individuals, these opportunistic pathogens can also affect the lower respiratory tract, leading to pneumonia, exacerbations of asthma, and various types of respiratory distress syndrome. The respiratory involvement of human coronaviruses has been clearly established since the 1960s. Nevertheless, for almost three decades now, data reported in the scientific literature has also demonstrated that, like it was described for other human viruses, coronaviruses have neuroinvasive capacities since they can spread from the respiratory tract to the central nervous system (CNS). Once there, infection of CNS cells (neurotropism) could lead to human health problems, such as encephalitis and long-term neurological diseases. Neuroinvasive coronaviruses could damage the CNS as a result of misdirected host immune responses that could be associated with autoimmunity in susceptible individuals (virusinduced neuroimmunopathology) and/or viral replication, which directly induces damage to CNS cells (virus-induced neuropathology). Given all these properties, it has been suggested that these opportunistic human respiratory pathogens could be associated with the triggering or the exacerbation of neurologic diseases for which the etiology remains poorly understood. Herein, we present host and viral factors that participate in the regulation of the possible pathogenic processes associated with CNS infection by human coronaviruses and we try to decipher the intricate interplay between virus and host target cells in order to characterize their role in the virus life cycle as well as in the capacity of the cell to respond to viral invasion.
Title: Human coronaviruses: Viral and cellular factors involved in neuroinvasiveness and neuropathogenesis
[A]:
True