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".

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 37C. 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 37C. 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 Zenon et al.
Title: HIV-infected microglia mediate cathepsin B induced neurotoxicity
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Paragraph: Contact patterns among hosts are considered as one of the most critical factors contributing to unequal pathogen transmission. Consequently, networks have been widely applied in infectious disease modeling. However most studies assume static network structure due to lack of accurate observation and appropriate analytic tools. In this study we used high temporal and spatial resolution animal position data to construct a high-resolution contact network relevant to infectious disease transmission. The animal contact network aggregated at hourly level was highly variable and dynamic within and between days, for both network structure (network degree distribution) and individual rank of degree distribution in the network (degree order). We integrated network degree distribution and degree order heterogeneities with a commonly used contact-based, directly transmitted disease model to quantify the effect of these two sources of heterogeneity on the infectious disease dynamics. Four conditions were simulated based on the combination of these two heterogeneities. Simulation results indicated that disease dynamics and individual contribution to new infections varied substantially among these four conditions under both parameter settings. Changes in the contact network had a greater effect on disease dynamics for pathogens with smaller basic reproduction number (i.e. R 0 , 2).
Title: Highly dynamic animal contact network and implications on disease transmission
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Paragraph: IAV and the host Crm1-dependent nuclear export machinery requires further exploration. Recently, Chase and collaborators showed that the interaction between vRNPs and the nuclear export machinery takes place in dense chromatin domains that allow IAV to "snatch" Crm1-RanGTP nuclear export complexes to the detriment of cellular substrates 13 . These results, together with other observations, highlight the involvement of host nuclear compartmentalization and chromatin territories in regulating nuclear traffic of IAV vRNPs [14] [15] [16] [17] . Several investigations, including ours, have revealed that IAV induce a strong remodeling of nuclear architecture with marked modifications of the nucleoli ultrastructure and compartments 3,17-20 . The nucleolus, known as the site of ribosome biogenesis, is also a sensor of cellular stresses and is involved in several cellular pathways, such as cell-cycle regulation or apoptosis 21-23 . Several DNA and RNA viruses, including cytoplasmic viruses are known to induce nucleolar alterations that contribute towards optimal infection 24-26 . In the context of IAV, their interplay with nucleolus and selective interactions with several nucleolar components appears to be decisive in the outcome of infection 17, 20 . Ozawa and colleagues demonstrated that dynamic nucleolar localization of NP is functionally significant by contributing to efficient viral replication and transcription 27 . Moreover, different studies have demonstrated a subtype dependent interaction between viral non-structural protein (NS1) and cellular nucleolin, suggesting a role of the nucleolar targeting functions of NS1 in IAV pathogenesis 28, 29 . Proteomics-based approaches have revealed changes in the nucleolar proteome of IAV infected cells 5,30 and identified several nucleolar components, such as nucleolin, nucleophosmin (B23) and ribosomal proteins, as putative interactants of reconstituted IAV vRNPs 7 . In addition, high-throughput RNAi approaches have highlighted the functional requirement of several of these nucleolar components in viral replication 31-33 . Nucleolin is a multifunctional protein that contributes extensively to DNA and RNA regulatory mechanisms, including ribosome biogenesis, chromatin remodeling, mRNA stability and translation, nuclear export of RNA and protein complexes, and microRNA processing 34, 35 . In this way, nucleolin takes part in several cellular functions, such as gene silencing, senescence, cell proliferation and growth 23,35-37 , and continuously shuttles between nucleolar/nuclear compartments and the cytoplasm up to the cell surface 38,39 . Moreover, through its ability to associate with diverse target RNAs, nucleolin is implicated in various pathological processes, particularly cancer and viral infection 40 . In this context, different functional interactions with nucleolin have been described for several DNA viruses, such as poliovirus 41 , adenovirus 42 , HSV 43, 44 or CMV 45, 46 , and several RNA viruses, such as hepatitis C and delta viruses 47,48 , coronavirus 49 , hPIV-3 50 , papillomavirus HPV9 51 , Crimean-Congo hemorrhagic fever virus 52 , HIV1 53 , noroviruses 54 and notably the infectious salmon anemia virus (ISAV) which belongs to the family Orthomyxoviridae, as IAV 55 . Altogether, these studies highlight nucleolin as a key interacting factor that is crucial, in some cases, for viral replication and involved in nucleo-cytoplasmic export of viral genome or viral egress 44 . At first, we observed the dynamic redistribution of nucleolin from a nucleolar to a very specific nuclear polarized pattern during infection. The aim of this study was therefore to investigate the functional relationship between IAV and nucleolin with regards to the nuclear traffic of vRNPs and their targeting to the dense chromatin compartment 13 and in the context of the viral remodeling of the host nuclear architectures 17,20 . We first characterized NP, the main component of IAV vRNP, as co-localizing and interacting with endogenous nucleolin during infection. Moreover, using cell fractionation and RNAi approaches, we suggest that nucleolin contributes to efficient vRNP trafficking and viral replication. Based on our results, we propose nucleolin as an essential host factor for the chromatin targeting of the nucleocytoplasmic export complex of vRNPs during infection.
Title: Nucleolin interacts with influenza A nucleoprotein and contributes to viral ribonucleoprotein complexes nuclear trafficking and efficient influenza viral replication OPEN
False