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: As infectious disease outbreaks emerge, public health agencies often enact vaccination and social distancing measures to slow transmission. Their success depends on not only strategies and resources, but also public adherence. Individual willingness to take precautions may be influenced by global factors, such as news media, or local factors, such as infected family members or friends. Here, we compare three modes of epidemiological decisionmaking in the midst of a growing outbreak using network-based mathematical models that capture plausible heterogeneity in human contact patterns. Individuals decide whether to adopt a recommended intervention based on overall disease prevalence, the proportion of social contacts infected, or the number of social contacts infected. While all strategies can substantially mitigate transmission, vaccinating (or self isolating) based on the number of infected acquaintances is expected to prevent the most infections while requiring the fewest intervention resources. Unlike the other strategies, it has a substantial herd effect, providing indirect protection to a large fraction of the population. misinformation from the "anti-vaxxer" movement [8, [11] [12] [13] . Recently, there have been calls for a special government commission on vaccine safety, despite overwhelming scientific consensus that vaccines are both safe and effective [12, [14] [15] [16] . As outbreaks unfold, people can take a variety precautionary measures to avoid infection, including immunization and social distancing [1, [17] [18] [19] . They often judge personal risk based on their impressions of overall disease prevalence and severity [2, [20] [21] [22] [23] . When infection risk appears low, small risks of adverse effects from the vaccine can seem relatively important and cause vaccine coverage to drop below levels required to control transmission. A variety of other factors can influence the perceived utility of disease prevention, including epidemiological news and rumors, costs of vaccination and other control measures, trust in health professionals, government agencies, media and non-official information sources, as well as societal pressure to ensure the health of one's children [24] [25] [26] [27] [28] [29] . Studies have shown that media reports about outbreaks that specify numbers of cases, hospitalizations or deaths, can influence avoidance behavior and contact patterns at both individual and community levels. In some cases, oversimplified or erroneous media reports regarding flawed vaccines can trigger panic and increases in vaccine hesitancy [30] [31] [32] [33] . For both seasonal and pandemic influenza, such interactions between vaccination decision-making and transmission dynamics can profoundly shape the course of epidemics [20, [34] [35] [36] . Individual intervention decisions can have far-reaching effects. For example, vaccination protects not only the immunized individual, but also social contacts who might have been infected by the individual. Social distancing decisions may break chains of transmission by protecting the decision-maker and more generally disrupting social dynamics. Following [37, 38] , we refer to this indirect protection as a herd effect. Although previously equated to the reduction in incidence in the unimmunized population [38], we quantify the herd effect of an intervention effort by estimating the number of infections averted per vaccine administered (or per individual social distancing action). The general phenomenon in which individual intervention actions reduce the risk of infection to others has also been called vaccination efficiency, vaccination effectiveness, herd immunity, and indirect protection [37] [38] [39] [40] . The magnitude of the herd effect will critically depend on contact patterns [41, 42]. Measures taken by gregarious individuals may have greater immediate benefits than those taken by solitary individuals, with downstream epidemiological consequences modulated by the full social network [43, 44] . Contact patterns may also influence the decision-making process itself, by constraining epidemiological perspectives. When gauging infection risk, individuals may consider global information (e.g., from news media) or local first-hand encounters with disease (e.g., infected acquaintances, friends or family members) [30, 31] . While traditional compartmental models assume homogeneity in both epidemiological risks and intervention benefits, network-based models provide a tractable framework for studying the complex interplay between contact networks, intervention decision making and disease transmission [34, [45] [46] [47] [48] [49] [50] [51] . Here, we investigate the epidemiological impacts of different decision paradigms using a network-based SIR epidemic model, in which individuals also make vaccination or social distancing choices based on their perceived epidemiological risks. Depending on the decision model, they estimate either overall disease prevalence, their number of infected social contacts, or their fraction of infected social contacts. When the perceived threat is sufficiently high, they take a measure that immediately affords full protection for the duration of the epidemic. We compare the efficacy of these three different paradigms across a range of diseases in a realistically heterogeneous network, and show that the most naive model-simply counting one's infected contacts-affords the most epidemiological protection using the least amount of resources (e.g., vaccinations or economic costs associated with social distancing). Local risk perception enhances epidemic control PLOS ONE | https://doi.
Title: Local risk perception enhances epidemic control

Output: True

Input: Consider Input: Paragraph: Besides being a common threat to farm animals and poultry, coronavirus (CoV) was responsible for the human severe acute respiratory syndrome (SARS) epidemic in 2002-4. However, many aspects of CoV behavior, including modes of its transmission, are yet to be fully understood. We show that the amount and the peculiarities of distribution of the protein intrinsic disorder in the viral shell can be used for the efficient analysis of the behavior and transmission modes of CoV. The proposed model allows categorization of the various CoVs by the peculiarities of disorder distribution in their membrane (M) and nucleocapsid (N). This categorization enables quick identification of viruses with similar behaviors in transmission, regardless of genetic proximity. Based on this analysis, an empirical model for predicting the viral transmission behavior is developed. This model is able to explain some behavioral aspects of important coronaviruses that previously were not fully understood. The new predictor can be a useful tool for better epidemiological, clinical, and structural understanding of behavior of both newly emerging viruses and viruses that have been known for a long time. A potentially new vaccine strategy could involve searches for viral strains that are characterized by the evolutionary misfit between the peculiarities of the disorder distribution in their shells and their behavior.
Title: Understanding Viral Transmission Behavior via Protein Intrinsic Disorder Prediction: Coronaviruses

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 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
Output: False