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".

Example Input: Paragraph: Dengue virus (DENV) of the Flaviviridae family is a single positive-stranded RNA virus that is transmitted by Aedes aegypti and Aedes albopictus mosquitoes. The objective of this study was to investigate the use of chloroquine (CLQ) as an antiviral drug against dengue virus in monkeys. To analyze the action of the drug in vivo, nonhuman primates groups (Aotus azarai infulatus) were inoculated with a subcutaneous injection of a virulent strain of DENV-2, treated and untreated CLQ. Blood hematological, viremia, and serum biochemical values were obtained from 16 DENV-2-inoculated, treated and untreated; four received only CLQ and one mock-infected Aotus monkeys. Monkey serum samples (day 0-10 post-inoculation) were assayed by reverse transcription polymerase chain reaction and Cytometric Bead Array for determination of viremia and inflammatory cytokines, respectively. Additionally, body temperature and activity levels were determined. In the present work, CLQ was effective on replication of DENV-2 in Aotus monkeys; a time viremia reduction was observed compared with the controls. The concentration of tumor necrosis factor alpha and interferon gamma in the serum of the animals had a statistically significant reduction in the groups treated with CLQ after infection compared with the controls. A significant decrease in systemic levels of the liver enzyme aspartate aminotransferase (AST) was also observed in the animals treated with CLQ after infection compared with the controls. These results suggest that CLQ interferes in DENV-2 replication in Aotus monkeys. 
 Title: Antiviral Activity of Chloroquine Against Dengue Virus Type 2 Replication in Aotus Monkeys
Example Output: False

Example Input: Paragraph: Data are limited regarding 2 new human polyomaviruses, KI polyomavirus (KIPyV) and WU polyomavirus (WUPyV), in immunocompromised patients. We used realtime PCR to test for these and 12 respiratory viruses in 2,732 nasal wash samples collected during the fi rst year after allogeneic hematopoietic cell transplantation from 222 patients. Specimens were collected weekly until day 100; then at least every 3 months. One year after hematopoietic cell transplantation, the cumulative incidence estimate was 26% for KIPyV and 8% for WUPyV. Age <20 years predicted detection of KIPyV (hazard ratio [HR] 4.6) and WUPyV (HR 4.4), and detection of a respiratory virus in the previous 2 weeks predicted KIPyV detection (HR 3.4). Sputum production and wheezing were associated with detection of KIPyV in the past week and WUPyV in the past month. There were no associations with polyomavirus detection and acute graft versus host disease, cytomegalovirus reactivation, neutropenia, lymphopenia, hospitalization, or death. 
 Title: WU and KI Polyomaviruses in Respiratory Samples from Allogeneic Hematopoietic Cell Transplant Recipients
Example Output: False

Example Input: Paragraph: The liver-specific microRNA miR-122, which has essential roles in liver development and metabolism, is a key proviral factor for hepatitis C virus (HCV). Despite its crucial role in the liver and HCV life cycle, little is known about the molecular mechanism of miR-122 expression regulation by HCV infection. Here, we show that the HCV core protein downregulates the abundance of miR-122 by promoting its destabilization via the inhibition of GLD-2, a non-canonical cytoplasmic poly(A) polymerase. The decrease in miR-122 expression resulted in the dysregulation of the known functions of miR-122, including its proviral activity for HCV. By high-throughput sequencing of small RNAs from human liver biopsies, we found that the 22-nucleotide (nt) prototype miR-122 is modified at its 3 0 end by 3 0 -terminal non-templated and templated nucleotide additions. Remarkably, the proportion of miR-122 isomers bearing a single nucleotide tail of any ribonucleotide decreased in liver specimens from patients with HCV. We found that these single-nucleotide-tailed miR-122 isomers display increased miRNA activity and stability over the 22-nt prototype miR-122 and that the 3 0 -terminal extension is catalyzed by the unique terminal nucleotidyl transferase activity of GLD-2, which is capable of adding any single ribonucleotide without preference of adenylate to the miR-122 3 0 end. The HCV core protein specifically inhibited GLD-2, and its interaction with GLD-2 in the cytoplasm was found to be responsible for miR-122 downregulation. Collectively, our results provide new insights into the regulatory role of the HCV core protein in controlling viral RNA abundance and miR-122 functions through miR-122 stability modulation. Viruses may benefit from altering the host cell's normal miRNA milieu, by either lowering or increasing antiviral or proviral miRNA levels. Our results reveal a mechanism by which virus infection can regulate miRNA abundance by modulating the activity of cellular enzymes responsible for miRNA 3 0 -terminal modifications. Hepatitis C virus (HCV) uses microRNA-122 (miR-122) as a proviral host factor to increase viral genome abundance, but HCV infection results in diminished miR-122 levels by unknown mechanisms. We PLOS Pathogens | demonstrated that the HCV core protein plays a role in reprogramming the cellular profile of miR-122 isomers by inhibiting GLD-2, a non-canonical cytoplasmic poly(A) polymerase, to promote miR-122 destabilization. Our results raise several important questions. First, how is only a specific subset of miRNAs in the liver affected by GLD-2 inhibition by the HCV core protein? Second, how does HCV regulate pre-miR-122 processing in its loop region? Third, does GLD-2 inhibition by the HCV core protein affect the translation of a specific group of host mRNAs? With many unanswered questions, our results propose a novel feedback regulatory mechanism for controlling HCV RNA abundance by the viral capsid protein, which is capable of modulating miR-122 activity and stability through the inhibition of GLD-2. GLD-2 Inhibition by the HCV Core Protein PLOS Pathogens | 
 Title: Hepatitis C Virus Core Protein Promotes miR- 122 Destabilization by Inhibiting GLD-2
Example Output:
False