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: 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: Dendritic cells (DCs) link the sensing of the environment by the innate immune system to the initiation of adaptive immune responses. Accordingly, DCs are considered to be a major target in the development of immunomodulating compounds. In this study, the effect of niclosamide, a Food and Drug Administrationapproved antihelminthic drug, on the activation of lipopolysaccharide (LPS)-stimulated murine bone marrow-derived DCs was examined. Our experimental results show that niclosamide reduced the pro-inflammatory cytokine and chemokine expression of LPS-activated DCs. In addition, niclosamide also affected the expression of MHC and costimulatory molecules and influenced the ability of the cells to take up antigens. Therefore, in mixed cell cultures composed of syngeneic OVA-specific T cells and DCs, niclosamide-treated DCs showed a decreased ability to stimulate T cell proliferation and IFN-c production. Furthermore, intravenous injection of niclosamide also attenuated contact hypersensitivity (CHS) in mice during sensitization with 2,4-dinitro-1-fluorobenzene. Blocking the LPS-induced activation of MAPK-ERK, JNK and NF-jB may contribute to the inhibitory effect of niclosamide on DC activation. Collectively, our findings suggest that niclosamide can manipulate the function of DCs. These results provide new insight into the immunopharmacological role of niclosamide and suggest that it may be useful for the treatment of chronic inflammatory disorders or DC-mediated autoimmune diseases. 
 Title: Antihelminthic niclosamide modulates dendritic cells activation and function
[A]: True


[Q]: Paragraph: T cell immunoglobulin mucin domain-1 (TIM-1) is a phosphatidylserine (PS) receptor, mediating filovirus entry into cells through interactions with PS on virions. TIM-1 expression has been implicated in Ebola virus (EBOV) pathogenesis; however, it remains unclear whether this is due to TIM-1 serving as a filovirus receptor in vivo or, as others have suggested, TIM-1 induces a cytokine storm elicited by T cell/virion interactions. Here, we use a BSL2 model virus that expresses EBOV glycoprotein to demonstrate the importance of TIM-1 as a virus receptor late during in vivo infection. Our studies provide evidence that at late times during EBOV GP/rVSV infection, TIM-1 increased virus load and associated mortality, consistent with an important role of this receptor in virus entry. This work suggests that inhibitors which block TIM-1/virus interaction may serve as effective antivirals, reducing virus load at late times during EBOV infection. T cell immunoglobulin mucin domain-1 (TIM-1) is one of a number of phosphatidylserine (PS) receptors that mediate clearance of apoptotic bodies by binding PS on the surface of dead or dying cells. Enveloped viruses mimic apoptotic bodies by exposing PS on the outer leaflet of the viral membrane. While TIM-1 has been shown to serve as an adherence factor/receptor for filoviruses in tissue culture, limited studies have investigated the role of TIM-1 as a receptor in vivo. Here, we sought to determine if TIM-1 was critical for Ebola virus glycoprotein-mediated infection using a BSL2 model virus. We demonstrate that loss of TIM-1 expression results in decreased virus load late during infection and significantly reduced virus-elicited mortality. These findings provide evidence that TIM-1 serves as an important receptor for Ebola virus in vivo. Blocking TIM-1/EBOV interactions may be effective antiviral strategy to reduce viral load and pathogenicity at late times of EBOV infection. TIM-1 enhances Ebola virus pathogenesis PLOS Neglected Tropical Diseases | https://doi.org/10. 
 Title: TIM-1 serves as a receptor for Ebola virus in vivo, enhancing viremia and pathogenesis
[A]:
True