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".

Input: Consider Input: Paragraph: Mouse hepatitis virus, a coronavirus, was rescued from latently infected mouse neuroblastoma cells by polyethylene glyeol-induced fusion to permissive cells. The isolated viruses grew to equal or higher titers than parental JHM virus at 39" but were restricted in replication at 32" and hence were cold-sensitive mutants. Neither isolate synthesized RNA at the nonpermissive temperature (32"), and temperature shift experiments indicated that the restrictive cold-sensitive step in replication occurred during an early viral function. The isolates were unable to complement each other at 32". Although coinfection between each mutant and parental JHM virus often resulted in decreased yields of both infecting viruses, interference could not be convincingly demonstrated. Both mutants were more thermostable than parental JHM virus and could be distinguished from each other and from parental JHM virus by their thermal inactivation kinetics. The isolates were obtained from single cell clones and therefore presumed to be homogeneous; however, thermal inactivation of one (S-3JHM) indicated the possible existence of a second population. Subclones of virus prepared from each isolate were also found to be thermally stable and to retain the cold sensitive defect. No indication of a second ~pulation of S-3JHM virus was detected. 
 Title: Characterization of the Cold-Sensitive Murine Hepatitis Virus Mutants Rescued from Latently Infected Cells by Cell Fusion

Output: True


Input: Consider Input: Paragraph: BACKGROUND-HIV-1-infected mononuclear phagocytes release soluble factors that affect the homeostasis in tissue. HIV-1 can prompt metabolic encephalopathy with the addition of neuronal dysfunction and apoptosis. Recently, we reported that HIV-1 enhances the expression and secretion of bioactive cathepsin B in monocyte-derived macrophages, ultimately contributing to neuronal apoptosis. In this research, we request if microglia respond to HIV infection similarly by modifying the expression, secretion, neurotoxic potential of cathepsin B and the in vivo relevance of these findings. METHODS-HIV-ADA infected human primary microglia and CHME-5 were assessed for expression and activity of cathepsin B, its inhibitors, cystatins B and C, and neurotoxicity associated with these changes. Human primary neurons were exposed to supernatants from HIVinfected and uninfected microglia in the presence of cathepsin B inhibitors and apoptosis was assessed by TUNEL. Microglial expression of cathepsin B was validated in brain tissue from HIVE patients. microglia secreted significantly greater levels of cathepsin B, cystatin B, and cystatin C compared to uninfected cells. Increased apoptosis was observed in neurons exposed to supernatants from HIV-1 infected microglia at days 12 post-infection. The cathepsin B inhibitor CA-074 and cathepsin B antibody prevented neuronal apoptosis. Increased microgliaderived cathepsin B, cystatin B, and cystatin C and caspase-3+ neurons were detected in HIVE brains compared to controls. CONCLUSIONS-Our results suggest that HIV-1-induced cathepsin B production in microglia contributes to neuronal apoptosis and may be an important factor in neuronal death associated with HIVE. Human primary neuron and microglia isolation and culture-Human primary neurons and microglia were provided by Temple University's Comprehensive NeuroAIDS Center. Fetal brain tissue (gestational age 16-18 weeks) was obtained from elective abortion procedures performed in full compliance with National Institutes of Health and Temple University ethical guidelines. The tissue was washed with cold Hanks balanced salt solution (HBSS) and meninges and blood vessels were removed as previously described [Huang et al, 2011; Ghorpade et al, 1998].. For microglia, brain tissue was supplemented with Ca 2+ and Mg 2+ and then digested with 0.25% trypsin (Sigma) for 30 min at 37°C. Trypsin was neutralized with fetal bovine serum (FBS), and the tissue was further dissociated to obtain single-cell suspensions. The cells were cultured in DMEM (Sigma), supplemented with a mixture containing 10% heat-inactivated FBS, 1,000 U of purified recombinant human macrophage colony stimulating factor (MCSF) per ml, penicillin and streptomycin (50 mg/ ml), and 100 mg/ml of neomycin. The mixed culture was maintained under 5% CO 2 for 7 days, and the medium was fully replaced to remove any cell debris. The microglia cells released with further incubation were collected and purified by preferential adhesion. Microglia were seeded as an adherent monolayer at a density of 3 × 10 6 cells/well in a 6well plate and floating cells were removed after 4h. For neurons, tissue in HBSS was digested with papain (Sigma-Aldrich, St. Louis, MO) for 30 min at 37°C. Tissue was then dissociated to obtain single-cell suspensions by repeated pipetting with small bore fire polished glass Pasteur pipettes. Cells were plated in poly-D lysine-coated dishes at a density of ~ 1.8 × 10 6 cells/60mm dish in neurobasal media with B27 supplement, horse serum, and gentamicin (Invitrogen). After 2hr of attachment, media was replaced with fresh complete neurobasal media. Twenty-four hours later, cultures were replaced with neurobasal media without horse serum. Four days later, one fourth of the media was removed and replaced with neurobasal media supplemented with fluorodeoxyuridine (FDU) and uridine. Following FDU treatment, neurons were cultured in neurobasal medium with Glutamax and B27 supplement. One half volume of media was replaced every 48h. Purity of cell type specific cultures was assessed by immunolabeling for cell-type specific markers, including Iba-1 for microglia, GFAP for astrocyte and MAP2, neurofilament, and synaptophysin for neurons. CHME-5 microglia-The microglia cell line CHME-5 was kindly provided by Dr. Randal Davis from Oklahoma State University. It was originally obtained from human fetal microglia (Peudenier et al. 1991) transfected with the T-antigen of SV-40 virus (Janabi et al. 1995). Cells were cultured to 70% confluence in Dulbecco's modified Eagle's medium (DMEM) (Sigma Chemical Company, St. Louis, MO) supplemented with 5% inactivated Zenón et al. 
 Title: HIV-infected microglia mediate cathepsin B induced neurotoxicity

Output: False


Input: Consider Input: Paragraph: Human hepatitis B virus core protein (HBc) is a structural protein of the hepatitis B virus (HBV) and contributes to HBV regulation of host-cell transcription. However, the mechanisms of transcriptional regulation remain poorly characterized. To dissect the function of HBc, a yeast two-hybrid was performed to identify HBc-binding proteins, and the C-terminal of BRG1/hBRM-associated factors 200 (BAF200C) was identified. Then, the existence of HBc interactions with BAF200C and full-length BAF200 was confirmed via co-immunoprecipitation assays in 293T, HepG2 and HepG2-NTCP cells. Furthermore, we show that the binding between HBc and BAF200 was of vital importance to HBc mediated downregulation of interferon-induced transmembrane protein 1 (IFITM1) expression, and the mechanisms for the downregulation were disclosed as follows. Basal level of IFITM1 expression depends on BAF200, rather than the JAK-STAT1 pathway. The interaction of HBc with BAF200 disturbs the stability of the polybromo-associated BAF (PBAF) complex and results in the suppression of IFTM1 transcription. Finally, the antiviral effects of IFITM1 on cell proliferation and HBV replication were found to be partially restored when HBc was co-transfected with BAF200. Collectively, our findings indicate that HBc plays a role in HBV resistance against the antiviral activities of IFNα, providing details about HBV evasion of host innate immunity. Keywords: Human hepatitis B virus core protein (HBc); BRG1/hBRM-associated factors 200 (BAF200); interferon α (IFNα); interferon-induced transmembrane protein 1 (IFITM1) 
 Title: Human Hepatitis B Virus Core Protein Inhibits IFNα-Induced IFITM1 Expression by Interacting with BAF200


Output: False