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: Using sequence data to infer population dynamics is playing an increasing role in the analysis of outbreaks. The most common methods in use, based on coalescent inference, have been widely used but not extensively tested against simulated epidemics. Here, we use simulated data to test the ability of both parametric and non-parametric methods for inference of effective population size (coded in the popular BEAST package) to reconstruct epidemic dynamics. We consider a range of simulations centred on scenarios considered plausible for pandemic influenza, but our conclusions are generic for any exponentially growing epidemic. We highlight systematic biases in non-parametric effective population size estimation. The most prominent such bias leads to the false inference of slowing of epidemic spread in the recent past even when the real epidemic is growing exponentially. We suggest some sampling strategies that could reduce (but not eliminate) some of the biases. Parametric methods can correct for these biases if the infected population size is large. We also explore how some poor sampling strategies (e.g. that over-represent epidemiologically linked clusters of cases) could dramatically exacerbate bias in an uncontrolled manner. Finally, we present a simple diagnostic indicator, based on coalescent density and which can easily be applied to reconstructed phylogenies, that identifies time-periods for which effective population size estimates are less likely to be biased. We illustrate this with an application to the 2009 H1N1 pandemic. Pandemic growth rates from sequences E. de Silva et al. 1799 Pandemic growth rates from sequences E. de Silva et al. 1807  
 Title: Inferring pandemic growth rates from sequence data

Answer: True


Question: Paragraph: Porcine epidemic diarrhea virus (PEDV), an enteropathogenic Alphacoronavirus, has caused enormous economic losses in the swine industry. p53 protein exists in a wide variety of animal cells, which is involved in cell cycle regulation, apoptosis, cell differentiation and other biological functions. In this study, we investigated the effects of PEDV infection on the cell cycle of Vero cells and p53 activation. The results demonstrated that PEDV infection induces cell cycle arrest at G0/G1 phase in Vero cells, while UV-inactivated PEDV does not cause cell cycle arrest. PEDV infection up-regulates the levels of p21, cdc2, cdk2, cdk4, Cyclin A protein and down-regulates Cyclin E protein. Further research results showed that inhibition of p53 signaling pathway can reverse the cell cycle arrest in G0/G1 phase induced by PEDV infection and cancel out the up-regulation of p21 and corresponding Cyclin/cdk mentioned above. In addition, PEDV infection of the cells synchronized in various stages of cell cycle showed that viral subgenomic RNA and virus titer were higher in the cells released from G0/G1 phase synchronized cells than that in the cells released from the G1/S phase and G2/M phase synchronized or asynchronous cells after 18 h p.i.. This is the first report to demonstrate that the p53-dependent pathway plays an important role in PEDV induced cell cycle arrest and beneficially contributes to viral infection. 
 Title: Porcine epidemic diarrhea virus through p53-dependent pathway causes cell cycle arrest in the G0/G1 phase

Answer: False


Question: Paragraph: An oligonucteotide containing multiple AP-1 binding sites was introduced into the regulatory sequence in the long terminal repeat (LTR) of feline immunodeficiency virus (FIV). Chloramphenicol acetyltransferase assay revealed that basal promoter activity of the mutated LTR was higher than that of the wildtype LTR in Crandell feline kidney (CRFK) cells. The mutated LTR was introduced into an infectious molecular clone of FIV and the clone was transfected into CRFK cells. The virus production of the mutant in the cells was as high as that of the wildtype when determined by the reverse transcriptase activity assay. The growth of the mutant virus obtained from the transfected CRFK cells was examined in feline T lymphoblastoid cell lines (MYA-1 and FeL-039 cells) and primary feline peripheral blood mononuclear cells (fPBMCs). The growth was delayed when compared with that of the wild-type virus in all the cells used. Upon examination by polymerase chain reaction, the length of the LTR of the mutant virus was shortened in both MYA-1 cells and fPBMCs. Sequence analysis revealed that the insertion was completely deleted 39 days after infection in the MYA-1 cells. T. Miyazawa et al. several putative binding sites for enhancer proteins such as AP-1, AP-4, C/EBP are present [13, 14, 26] . Previously we reported that by deletion of AP-1 and AP-4 related sequences in the LTR, promoter activity was reduced in Crandell feline kidney (CRFK) andfelis catus whole foetus-4 (fcwf-4) cells using the chloramphenicol acetyltransferase (CAT) assay [11, 19] . Recently, Thompson et al. [29] reported that protein(s) present in the nuclear extract from feline T cells (F422 cells) which are permissive for FIV replication bind to the putative AP-1 and AP-4 binding sites. These findings suggest that the AP-1 in feline cells can bind to the AP-1 binding site in the L T R and is critical for the basal promoter activity of the LTR. Conversely, a m u t a n t virus which lacks the AP-1 and AP-4 binding sites replicated in feline T lymphoblastoid cell lines (MYA-1 and FeL-039 cells) [19] and primary feline peripheral blood mononuclear cells (fPBMCs) [17] . These data indicate that the AP-1 and AP-4 binding sites are not necessary for the efficient replication of FIV in feline T lymphocytes. In this study, we introduced an oligonucleotide containing multiple AP-1 binding sites adjacent to the original AP-1 binding site in the U3 region of the L T R and examined the effects of the insertion on the promoter and growth activities of the mutant. Cell culture CRFK cells [3] and fcwf-4 [9] were maintained in Dulbecco's modified Eagle's medium supplemented with 10% heat-inactivated foetal calf serum (FCS). fPBMCs obtained from a specific pathogen-free cat were isolated as described previously [15, 16] . 21] and FeL-039 [30] cells, and fPBMCs were maintained in the RPMI 1640 growth medium supplemented with 10% FCS, antibiotics, 50 gM 2-merecaptoethanol, 2 g g/ml polybrene and 100 units/ml of recombinant human interleukin-2 at 37°C in a humidified atmosphere of 5% CO 2 in air. DNA constructs 
 Title: Effects of insertion of multiple AP-1 binding sites into the U3 region of the long terminal repeat of feline immunodeficiency virus

Answer:
True