instruction:
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".
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 µM, while the values for HONE-1 and HA were 58 and 65 µM, 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: Background: Host genetic factors may play a role in susceptibility and resistance to SARS associated coronavirus (SARS-CoV) infection. The study was carried out to investigate the association between the genetic polymorphisms of 2',5'-oligoadenylate synthetase 1 (OAS1) gene as well as myxovirus resistance 1 (MxA) gene and susceptibility to SARS in Chinese Han population. A hospital-based case-control study was conducted. A collective of 66 SARS cases and 64 close contact uninfected controls were enrolled in this study. End point real time polymerase chain reaction (PCR) and PCR-based Restriction Fragment Length Polymorphism (RFLP) analysis were used to detect the single nucleic polymorphisms (SNPs) in OAS1 and MxA genes. Information on other factors associated with SARS infection was collected using a pre-tested questionnaire. Univariate and multivariate logistic analyses were conducted. Results: One polymorphism in the 3'-untranslated region (3'-UTR) of the OAS1 gene was associated with SARS infection. Compared to AA genotype, AG and GG genotypes were found associated with a protective effect on SARS infection with ORs (95% CI) of 0.42 (0.20~0.89) and 0.30 (0.09~0.97), respectively. Also, a GT genotype at position 88 in the MxA gene promoter was associated with increased susceptibility to SARS infection compared to a GG genotype (OR = 3.06, 95% CI: 1.25~7.50). The associations of AG genotype in OAS1 and GT genotype in MxA remained significant in multivariate analyses after adjusting for SARS protective measures (OR = 0.38, 95% CI: 0.14~0.98 and OR = 3.22, 95% CI: 1.13~9.18, respectively). Conclusion: SNPs in the OAS1 3'-UTR and MxA promoter region appear associated with host susceptibility to SARS in Chinese Han population. 
 Title: BMC Infectious Diseases Association of SARS susceptibility with single nucleic acid polymorphisms of OAS1 and MxA genes: a case-control study
answer:
True


question:
Paragraph: Attenuated, live viral vaccines have been extraordinarily successful in protecting against many diseases. The main drawbacks in their development and use have been reliance on an unpredictable method of attenuation and the potential for evolutionary reversion to high virulence. Methods of genetic engineering now provide many safer alternatives to live vaccines, so if live vaccines are to compete with these alternatives in the future, they must either have superior immunogenicity or they must be able to overcome these former disadvantages. Several live vaccine designs that were historically inaccessible are now feasible because of advances in genome synthesis. Some of those methods are addressed here, with an emphasis on whether they enable predictable levels of attenuation and whether they are stable against evolutionary reversion. These new designs overcome many of the former drawbacks and position live vaccines to be competitive with alternatives. Not only do new methods appear to retard evolutionary reversion enough to prevent vaccine-derived epidemics, but it may even be possible to permanently attenuate live vaccines that are transmissible but cannot evolve to higher virulence under prolonged adaptation. 
 Title: Evolutionary reversion of live viral vaccines: Can genetic engineering subdue it?
answer:

False