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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".

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
Output:
False