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".

Input: Consider Input: Paragraph: Influenza C virus (ICV) is a common yet under-recognized cause of acute respiratory illness. ICV seropositivity has been found to be as high as 90% by 7-10 years of age, suggesting that most people are exposed to ICV at least once during childhood. Due to difficulty detecting ICV by cell culture, epidemiologic studies of ICV likely have underestimated the burden of ICV infection and disease. Recent development of highly sensitive RT-PCR has facilitated epidemiologic studies that provide further insights into the prevalence, seasonality, and course of ICV infection. In this review, we summarize the epidemiology and clinical characteristics of ICV. 
 Title: viruses Epidemiology and Clinical Characteristics of Influenza C Virus

Output: False


Input: Consider Input: Paragraph: Background: Human papillomavirus 16 (HPV16) is a high-risk DNA tumour virus, which is a major causative agent of cervical cancer. Cellular transformation is associated with deregulated expression of the E6 and E7 oncogenes. E7 has been shown to bind a number of cellular proteins, including the cell cycle control protein pRb. In this study, RNA aptamers (small, singlestranded oligonucleotides selected for high-affinity binding) to HPV16 E7 were employed as molecular tools to further investigate these protein-protein interactions. This study is focused on one aptamer (termed A2). Transfection of this molecule into HPV16-transformed cells resulted in inhibition of cell proliferation (shown using real-time cell electronic sensing and MTT assays) due to the induction of apoptosis (as demonstrated by Annexin V/propidium iodide staining). GST-pull down and bead binding assays were used to demonstrate that the binding of A2 required N-terminal residues of E7 known to be involved in interaction with the cell cycle control protein, pRb. Using a similar approach, A2 was shown to disrupt the interaction between E7 and pRb in vitro. Furthermore, transfection of HPV16-transformed cells with A2 appeared to result in the loss of E7 and rise in pRb levels, as observed by immunoblotting. Conclusions/Significance: This paper includes the first characterisation of the effects of an E7 RNA aptamer in a cell line derived from a cervical carcinoma. Transfection of cells with A2 was correlated with the loss of E7 and the induction of apoptosis. Aptamers specific for a number of cellular and viral proteins have been documented previously; one aptamer (Macugen) is approved for clinical use and several others are in clinical trials. In addition to its role as a molecular tool, A2 could have further applications in the future. 
 Title: An RNA Aptamer Provides a Novel Approach for the Induction of Apoptosis by Targeting the HPV16 E7 Oncoprotein

Output: True


Input: Consider Input: Paragraph: was performed with RdRpSeq-Fwd (similar to the first round) and RdRpSeq-Rnest primer by using MyFi ™ Mix Kit (Bioline, USA) according to the following parameters: 95 °C for 1 min, followed by 35 cycles at 95 °C for 15 seconds, 56 °C for 15 seconds, 72 °C for 20 seconds, and 2 min at 72 °C for terminal elongation[5]. The resulted amplicons were separated by gel electrophoresis, and the DNA fragments were excised, purified and subjected to sequencing in both directions. The obtained sequences were verified by basic local alignment search tool. As for the amplification of complete N gene region, cDNA was synthesized by using SuperScript III First Strand Synthesis System for RT-PCR (Invitrogen, USA) with NR2 primer (Table 1). Two microliters of the generated cDNA was subjected to one round of PCR cycle by using MyFi ™ Mix Kit (Bioline, USA) with NF1 and NR2 (Table 1) primers following the parameters: 95 °C for 1 min followed by 25 cycles at 95 °C for 15 seconds, 52 °C for 15 seconds and 72 °C for 30 seconds and terminal elongation at 72 °C for 5 min. Then, 0.5 μL of the resulted PCR amplicon was further subjected to the second round PCR following the abovementioned parameters. The resulted PCR product was separated by gel electrophoresis while the DNA fragment was excised, purified and subjected to sequencing by using NF1, NR1, NF2, NR2 and N350R primers. The obtained sequences were analyzed by using ChromasPro version 1.7.4 (Technelysium Pty Ltd, Australia). Multiple sequence alignment was performed by using Clustal X (version 2.0.11) with 44 human-derived (including the Malaysian case; MyH010414; GenBank accession No: KP769415) and 3 camel-derived MERS-CoV sequences[6]. Maximum likelihood analysis was conducted by using Molecular Evolutionary Genetics Analysis 6.06[7]. The evolutionary history was computed by using Tamura-Nei model with 1 000 replicates of bootstrap analysis. Extracted RNA from combination of throat and nasal swabs from the case was detected positive both in rRT-PCR and conventional RT-PCR for partial RdRp and N gene. The cycle threshold values for upE, ORF1a and ORF1b were 28.19, 29.16 and 33.36, respectively. Amplification of partial RdRp and N gene regions resulted in DNA fragment of ~240 bp and ~310 bp, respectively (data not shown). Initial sequencing result of these fragments showed highly identical nucleotide sequence (99%) to MERS-CoV strain Jeddah_1_2013 (KJ556336.1), further confirming the MERS-CoV infection. JX869059/Human/Jeddah/HCoV EMC/2012 KC776174/Human/Jordan/Jordan N3/2012 Clade A 0.0005 67 63 63 63 66 50 62 Clade B Figure 1. Phylogenetic analysis of N gene region of Malaysia MERS-CoV case together with 3 camel-derived and 43 human-derived MERS-CoV sequences from 2012-2014. Red diamond: Malaysian case; Blank diamond: sequences from the camel-derived MERS-CoV. 
 Title: Nucleocapsid gene analysis from an imported case of Middle East respiratory syndrome coronavirus, Malaysia Asian Pacific Journal of Tropical Disease


Output: True