TASK DEFINITION: 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".
PROBLEM: Paragraph: Background: Infectious laryngotracheitis virus (ILTV; gallid herpesvirus 1) infection causes high mortality and huge economic losses in the poultry industry. To protect chickens against ILTV infection, chicken-embryo origin (CEO) and tissue-culture origin (TCO) vaccines have been used. However, the transmission of vaccine ILTV from vaccinated-to unvaccinated chickens can cause severe respiratory disease. Previously, host cell responses against virulent ILTV infections were determined by microarray analysis. In this study, a microarray analysis was performed to understand host-vaccine ILTV interactions at the host gene transcription level. Results: The 44 K chicken oligo microarrays were used, and the results were compared to those found in virulent ILTV infection. Total RNAs extracted from vaccine ILTV infected chicken embryo lung cells at 1, 2, 3 and 4 days post infection (dpi), compared to 0 dpi, were subjected to microarray assay using the two color hybridization method. Data analysis using JMP Genomics 5.0 and the Ingenuity Pathway Analysis (IPA) program showed that 213 differentially expressed genes could be grouped into a number of functional categories including tissue development, cellular growth and proliferation, cellular movement, and inflammatory responses. Moreover, 10 possible gene networks were created by the IPA program to show intermolecular connections. Interestingly, of 213 differentially expressed genes, BMP2, C8orf79, F10, and NPY were expressed distinctly in vaccine ILTV infection when compared to virulent ILTV infection. Conclusions: Comprehensive knowledge of gene expression and biological functionalities of host factors during vaccine ILTV infection can provide insight into host cellular defense mechanisms compared to those of virulent ILTV. 
 Title: Genome-wide host responses against infectious laryngotracheitis virus vaccine infection in chicken embryo lung cells

SOLUTION: False

PROBLEM: 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

SOLUTION: True

PROBLEM: Paragraph: The new porcine epidemic diarrhea (PED) has caused devastating economic losses to the swine industry worldwide. Despite extensive research on the relationship between autophagy and virus infection, the concrete role of autophagy in porcine epidemic diarrhea virus (PEDV) infection has not been reported. In this study, autophagy was demonstrated to be triggered by the effective replication of PEDV through transmission electron microscopy, confocal microscopy, and Western blot analysis. Moreover, autophagy was confirmed to benefit PEDV replication by using autophagy regulators and RNA interference. Furthermore, autophagy might be associated with the expression of inflammatory cytokines and have a positive feedback loop with the NF-κB signaling pathway during PEDV infection. This work is the first attempt to explore the complex interplay between autophagy and PEDV infection. Our findings might accelerate our understanding of the pathogenesis of PEDV infection and provide new insights into the development of effective therapeutic strategies. Viruses 2017, 9, 53 2 of 16 damaged organelles are delivered to lysosomes for degradation and recycling [8, 9] . Autophagy can be induced by diverse intracellular and extracellular stimuli, such as nutrient starvation, endoplasmic reticulum (ER) stress, pathogen-associated molecular patterns (PAMPs), and virus infection [10] . Increasing evidence indicates that autophagy plays both anti-viral and pro-viral roles in the life cycles and pathogenesis of a broad range of viruses [11] . Specifically, autophagy is an intrinsic host defense mechanism that inhibits viral replication or eliminates viruses by delivering them to the lysosomal compartment for degradation. Meanwhile, viruses develop many mechanisms to block autophagy or even hijack it for their own benefit, such as human cytomegalovirus (HCMV) and herpes simplex virus type 1 (HSV-1) [9, [12] [13] [14] . However, autophagy is also believed to serve as a platform for viral replication, especially for RNA viruses, such as classical swine fever virus (CSFV), porcine reproductive and respiratory syndrome virus (PRRSV), and rotavirus (RV), utilizing the membranes of the autophagosome-like vesicles for their replication [15] [16] [17] . These polar characteristics reveal the complicated relationship between autophagy and viral infection. A previous proteomic study indicated that more differentially expressed proteins were mapped to the autophagy pathway, and the microtubule-associated protein 1B, a useful biomarker protein for autophagy was up-regulated in PEDV-infected Vero cells [18] . In addition, our previous study demonstrated that mTOR (the mammalian target of rapamycin) pathway, which was closely associated with cellular autophagy, was down-regulated, and that the autophagy associated protein ATG5 was up-regulated during PEDV infection [19] . These studies indicated that autophagy might participate in PEDV infection, but the specific function of autophagy in the process of PEDV infection has not been elucidated. In the present study, we demonstrated for the first time that autophagy was triggered in Vero cells during PEDV infection to promote its replication. Moreover, autophagy might mediate the inflammatory responses induced by PEDV infection and have a positive correlation with the NF-κB signaling pathway. Program of China (2016YFD0500702) and the China Agricultural Research System (CARS-36). We thank prof. Xiang Mao from the Shanghai Veterinary Research Institute, for providing the GFP-mRFP-LC3 tandem reporter construct. 
 Title: Porcine Epidemic Diarrhea Virus Induces Autophagy to Benefit Its Replication

SOLUTION:
False