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".
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Question: Paragraph: Nasopharyngeal carcinoma (NPC) is a unique malignancy derived from the epithelium of the nasopharynx. Despite great advances in the development of radiotherapy and chemotherapy, relapse and metastasis in NPC patients remain major causes of mortality. Evidence accumulated over recent years indicates that Epstein-Barr virus (EBV) lytic replication plays an important role in the pathogenesis of NPC and inhibition of EBV reactivation is now being considered as a goal for the therapy of EBV-associated cancers. With this in mind, a panel of dietary compounds was screened and emodin was found to have potential anti-EBV activity. Through Western blotting, immunofluorescence, and flow cytometric analysis, we show that emodin inhibits the expression of EBV lytic proteins and blocks virion production in EBV-positive epithelial cell lines. In investigating the underlying mechanism, reporter assays indicated that emodin represses Zta promoter (Zp) and Rta promoter (Rp) activities, triggered by various inducers. Mapping of the Zp construct reveals that the SP1 binding region is important for emodin-triggered repression and emodin is shown to be able to inhibit SP1 expression, suggesting that it likely inhibits EBV reactivation by suppression of SP1 expression. Moreover, we also show that emodin inhibits the tumorigenic properties induced by repeated EBV reactivation, including micronucleus formation, cell proliferation, migration, and matrigel invasiveness. Emodin administration also represses the tumor growth in mice which is induced by EBV activation. Taken together, our results provide a potential chemopreventive agent in restricting EBV reactivation and NPC recurrence. Genetic, environmental, and viral factors have been incriminated in the etiology of NPC and Epstein-Barr virus (EBV) is strongly associated with the occurrence of NPC. EBV is a member of the gamma herpesviruses, with a 172 kb double-stranded DNA genome. The life cycle of EBV includes latency and lytic replication. Eleven gene products, EBNAs 1~6, LMPs 1, 2A, and 2B, and small RNAs EBER 1 and 2, are expressed during latent infection [6] . Upon induction by chemicals or stress, EBV is activated and enters the lytic cycle, known as reactivation. Three subsets of lytic genes, immediate-early, early, and late genes, are expressed sequentially and, subsequently, viral particles are packaged and released [7, 8] . Through years of study, EBV latent infection has been considered to play an important role in NPC carcinogenesis. In recent years, accumulating evidence has suggested that EBV lytic infection also contributes to the tumorigenesis of NPC. Sero-epidemiological surveys indicate that patients with elevated antibody titers against EBV lytic proteins, such as viral capsid antigen (VCA), DNase, DNA polymerase, and early antigen (EA), have a high risk of NPC [9] [10] [11] [12] [13] [14] [15] . Several EBV lytic products have been detected in the NPC biopsies [16] [17] [18] . In addition, EBV lytic proteins, including BARF1, BHRF1, BRLF1, BALF3, BGLF4, and DNase, have been shown to have various tumorigenic functions [16, [19] [20] [21] [22] . In our previous study, we found that EBV reactivated by chemicals promotes cellular genome instability and tumor growth [23, 24] . Collectively, these reports suggest that inhibition of EBV reactivation might be useful for NPC prevention and therapy. Accordingly, for safety and convenience, we have screened several dietary compounds for anti-EBV activity. We reported that the flavonoids have activity against EBV reactivation and through the inhibition of EBV, NPC tumorigenesis has been repressed [25] [26] [27] . Here, we report that the phytochemical emodin has the potential ability to inhibit EBV reactivation. Emodin, a common traditional Chinese medicine, is an anthraquinone derivative present in the roots or rhizomes of rhubarb. Emodin has various medical applications, including anti-cancer, anti-oxidation, anti-inflammation or allergy, anti-diabetes, and anti-viral or bacterial activities [28] . For its anti-viral effect, emodin has the ability to inhibit the SARS coronavirus [29] , and block the replication of HBV [30], Coxsackievirus [31], zika virus [32], and influenza A virus [33] . Moreover, emodin has been suggested to inhibit the replication of herpesviruses [34] [35] [36] . However, the detailed mechanism is not well elucidated. In this study, based on our screening, we show that emodin inhibits EBV reactivation in epithelial cells, through the mechanism of repressing SP1 expression to inhibit the Zta and Rta promoter activities. Moreover, through its anti-EBV activity, NPC tumorigenesis could be relieved, suggesting emodin is a potential agent for therapy of EBV-associated cancer. Results Emodin (1,3,8-trihydroxy-6-methyl-anthraquinone, Figure 1a ) has been shown to be cytotoxic to human cell lines. Before investigating the anti-EBV effect of emodin, two EBV-positive NPC cell lines, NA and HA, and their parental cells TW01 and HONE-1, were assessed for susceptibility to the cytotoxicity of emodin. The cells were seeded into 96-well plates 24 h prior to treatment; then, emodin was added for 48 h to determine its cytotoxic effect on the NPC cell lines NA and HA. Emodin has significant toxicity to TW01 cells, while the derivative NA cells showed little resistance to the compound (Figure 1b) . A similar effect was seen on HONE-1 and HA cells (Figure 1b) . Furthermore, to evaluate these results more precisely, half maximum of cytotoxicity concentrations 50 (CC50) were calculated and are shown in the top panels of Figure 1b . The CC50 values of TW01 and the derivative NA cell lines were 31 and 79 M, while the values for HONE-1 and HA were 58 and 65 M, respectively (Figure 1b) , implying that the cells harboring EBV seemed to be more resistant to emodin (TW01 vs.
Title: Emodin Inhibits EBV Reactivation and Represses NPC Tumorigenesis

Answer: False

Question: 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

Answer: False

Question: Paragraph: Coronavirus infectious bronchitis virus (IBV) encodes a trypsin-like proteinase (3C-like proteinase) by ORF 1a, which has been demonstrated to play a pivotal role in proteolytic processing of gene 1-encoded polyproteins. In our previous studies, the proteinase was identified as a 33-kDa protein in IBV-infected cells, and its catalytic center was shown to consist of H 2820 and C 2922 residues. It is released from the 1a and 1a/1b polyproteins by autoprocessing at two Q-S dipeptide bonds (Q 2779 -S 2780 and Q 3086 -S 3087 ). In this report, further characterization of the two cleavage sites demonstrates that the N-terminal Q 2779 -S 2780 site is tolerant to mutations at the P1 position. Deletion of the C-terminal region of the proteinase shows that a significant amount of the enzymatic activity is maintained upon deletion of up to 67 amino acids, suggesting that the extreme C-terminal region may be dispensable for the proteolytic activity of the proteinase. Analysis of the autoprocessing kinetics in vitro reveals that proteolysis at the Q 2779 -S 2780 site is the first cleavage event mediated by this proteinase. This is followed by cleavage at the Q 3086 -S 3087 site. The occurrence of both cleavage events in intact cells is potentially rapid and efficient, as no intermediate cleavage products covering the proteinase were detected in either IBV-infected or transfected cells. Immunofluorescence microscopy and subcellular fractionation studies further show differential subcellular localization of the proteinase in IBV-infected cells and in cells expressing the 3C-like proteinase alone, indicating that additional roles in viral replication might be played by this protein. Finally, a Q-A (Q 3379 -A 3380 ) dipeptide bond encoded by nucleotides 10,663 to 10,668 was demonstrated to be a cleavage site of the proteinase.
Title: Further Characterization of the Coronavirus Infectious Bronchitis Virus 3C-like Proteinase and Determination of a New Cleavage Site

Answer:
True