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: There is an urgent need to project how transmission of the novel betacoronavirus SARS-CoV-2 will unfold in coming years. These dynamics will depend on seasonality, the duration of immunity, and the strength of cross-immunity to/from the other human coronaviruses. Using data from the United States, we measured how these factors affect transmission of human betacoronaviruses HCoV-OC43 and HCoV-HKU1. We then built a mathematical model to simulate transmission of SARS-CoV-2 through the year 2025. We project that recurrent wintertime outbreaks of SARS-CoV-2 will probably occur after an initial pandemic wave. We summarize the full range of plausible transmission scenarios and identify key data still needed to distinguish between them, most importantly longitudinal serological studies to determine the duration of immunity to SARS-CoV-2. Main text. The ongoing SARS-CoV-2 epidemic has caused nearly 80,000 detected cases of COVID-19 illness and claimed over 2,500 lives as of 24 Feb 2020 (1). With sustained transmission reported in China, Japan, Iran, Italy, and South Korea (1), the outbreak is on the verge of becoming a pandemic. The required intensity, duration, and urgency of public health responses will depend on how the initial pandemic wave unfolds and on the subsequent transmission dynamics of SARS-CoV-2. One possibility is that SARS-CoV-2 will follow its closest genetic relative, SARS-CoV, and be eradicated by intensive public health measures after causing a brief but intense epidemic (2). Increasingly, public health authorities consider this scenario unlikely (3). Alternatively, the transmission of SARS-CoV-2 could resemble that of pandemic influenza by circulating seasonally after causing an initial global wave of infection (4). Such a scenario could reflect the previous emergence of known human coronaviruses from zoonotic origins e.g. human coronavirus (HCoV) OC43 (5). This paper identifies viral, environmental, and immunologic factors which in combination will determine which scenarios in fact play out, and identifies key data needed to distinguish between them. The transmission dynamics of the SARS-CoV-2 epidemic will depend on factors including the degree of seasonal variation in transmission strength, the duration of immunity, and the degree of cross-immunity between SARS-CoV-2 and other coronaviruses. SARS-CoV-2 belongs to the betacoronavirus genus, which includes the SARS coronavirus, MERS coronavirus, and two other human coronaviruses, HCoV-OC43 and HCoV-HKU1. The SARS and MERS coronaviruses cause severe illness with case fatality rates of 9 and 36% respectively, but the transmission of both has remained limited (6). HCoV-OC43 and HCoV-HKU1 infections may be asymptomatic or associated with mild to moderate upper respiratory tract illness; these HCoVs are considered the second most common cause of the common cold (6). While investigations into the spectrum of illness caused by SARS-CoV-2 are ongoing, recent evidence indicates the majority of cases experience mild illness with more limited occurrence of severe lower respiratory infection (7). Current COVID-19 case fatality rates in China are estimated at 2.9% within Hubei province, and 0.4% outside (8), suggesting lower severity than SARS and MERS but higher severity than HCoV-OC43 and HCoV-HKU1. In terms of transmission, the ability of SARS-CoV-2 to cause widespread infection is more reflective of HCoV-OC43 and HCoV-HKU1 than of its more clinically severe relatives. HCoV-OC43 and HCoV-HKU1 cause annual wintertime outbreaks of respiratory illness in temperate regions (9, 10), suggesting that wintertime climate and host behaviors may facilitate transmission, as is true for influenza (11) (12) (13) . Immunity to HCoV-OC43 and HCoV-HKU1 appears to wane appreciably within one year (14), while SARS infection can induce longer-lasting immunity (15). The . CC-BY-NC-ND 4.0 International license It is made available under a author/funder, who has granted medRxiv a license to display the preprint in perpetuity. is the (which was not peer-reviewed) The copyright holder for this preprint . 
 Title: Projecting the transmission dynamics of SARS-CoV-2 through the post-pandemic period

A: False
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Q: Paragraph: Introduction: Novel immune globulin (IG) products (RI-002, RI-001) have been designed to provide protection against respiratory syncytial virus (RSV) mediated respiratory illness while at the same time meeting the manufacturing requirements established by FDA for antibody supplementation in immunocompromised subjects. Areas covered: This review covers the manufacture and development of both RI-001 and RI-002, including the selection of plasma donors for IG preparation with high-titers of anti-RSV antibody, in vitro, and preclinical data in the cotton rat model S. hispidus, and clinical trials including Phase II and compassionate use studies of RI-001 and a multi-center, pivotal Phase III study of RI-002 in PIDD patients. Expert commentary: The data demonstrate that RI-002 is efficacious in the prevention and treatment of RSV in preclinical normal and immune suppressed animal models and is safe and efficacious in the treatment of patients with various forms of primary immunodeficiency disease (PIDD). This product offers potential advantages over other available IG's for prophylaxis in immunocompromised patients requiring polyclonal immunoglobulin supplementation because of its unique antibody composition. In addition to its enhanced neutralizing anti-RSV activity and its polyclonal IG composition, there is preclinical data to support the use of RI-002 for humoral protection against other respiratory pathogens. ARTICLE HISTORY 
 Title: RI-002, an intravenous immunoglobulin containing high titer neutralizing antibody to RSV and other respiratory viruses for use in primary immunodeficiency disease and other immune compromised populations

A: True
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Q: Paragraph: Background: Entry of Severe Acute Respiratory Syndrome coronavirus (SARS-CoV) and its envelope fusion with host cell membrane are controlled by a series of complex molecular mechanisms, largely dependent on the viral envelope glycoprotein Spike (S). There are still many unknowns on the implication of cellular factors that regulate the entry process. Methodology/Principal Findings: We performed a yeast two-hybrid screen using as bait the carboxy-terminal endodomain of S, which faces the cytosol during and after opening of the fusion pore at early stages of the virus life cycle. Here we show that the ezrin membrane-actin linker interacts with S endodomain through the F1 lobe of its FERM domain and that both the eight carboxy-terminal amino-acids and a membrane-proximal cysteine cluster of S endodomain are important for this interaction in vitro. Interestingly, we found that ezrin is present at the site of entry of S-pseudotyped lentiviral particles in Vero E6 cells. Targeting ezrin function by small interfering RNA increased S-mediated entry of pseudotyped particles in epithelial cells. Furthermore, deletion of the eight carboxy-terminal amino acids of S enhanced S-pseudotyped particles infection. Expression of the ezrin dominant negative FERM domain enhanced cell susceptibility to infection by SARS-CoV and S-pseudotyped particles and potentiated S-dependent membrane fusion. Conclusions/Significance: Ezrin interacts with SARS-CoV S endodomain and limits virus entry and fusion. Our data present a novel mechanism involving a cellular factor in the regulation of S-dependent early events of infection. 
 Title: Ezrin Interacts with the SARS Coronavirus Spike Protein and Restrains Infection at the Entry Stage

A:
True
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