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Related Concept Videos

MicroRNAs01:22

MicroRNAs

MicroRNA (miRNA) are short, regulatory RNA transcribed from introns—non-coding regions of a gene—or intergenic regions—stretches of DNA present between genes. Several processing steps are required to form biologically active, mature miRNA. The initial transcript, called primary miRNA (pri-mRNA), base-pairs with itself forming a stem-loop structure. Within the nucleus, an endonuclease enzyme, called Drosha, shortens the stem-loop structure into hairpin-shaped pre-miRNA. After the pre-miRNA ends...
MicroRNAs01:22

MicroRNAs

MicroRNA (miRNA) are short, regulatory RNA transcribed from introns (non-coding regions of a gene) or intergenic regions (stretches of DNA present between genes). Several processing steps are required to form biologically active, mature miRNA. The initial transcript, called primary miRNA (pri-mRNA), base-pairs with itself, forming a stem-loop structure. Within the nucleus, an endonuclease enzyme, called Drosha, shortens the stem-loop structure into hairpin-shaped pre-miRNA. After the pre-miRNA...
Inhibitors of Viral Protein Synthesis01:30

Inhibitors of Viral Protein Synthesis

Protein synthesis is indispensable for viral replication, as viruses lack the cellular machinery required for this process and must hijack the host's translational apparatus. In response, host cells deploy a critical innate immune defense involving interferons, specialized cytokines that play a central role in inhibiting viral propagation.Upon viral detection, infected cells release interferons that bind to receptors on adjacent uninfected cells, activating the JAK-STAT signaling pathway and...
Inhibitors of Virion Maturation and Assembly01:19

Inhibitors of Virion Maturation and Assembly

As part of their replication cycle, certain viruses synthesize long precursor proteins called polyproteins within infected host cells. In human immunodeficiency virus (HIV), two major polyproteins are produced: Gag and Gag-Pol. The Gag polyprotein supplies the structural components of the virus, while Gag-Pol includes essential viral enzymes such as reverse transcriptase, integrase, and protease. After synthesis, these polyproteins move to the host cell membrane, where they assemble into an...

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Related Experiment Video

Updated: Jul 23, 2026

Stereotactic Injection of MicroRNA-expressing Lentiviruses to the Mouse Hippocampus CA1 Region and Assessment of the Behavioral Outcome
09:06

Stereotactic Injection of MicroRNA-expressing Lentiviruses to the Mouse Hippocampus CA1 Region and Assessment of the Behavioral Outcome

Published on: June 10, 2013

microRNA-219 Reduces Viral Load and Pathologic Changes in Theiler's Virus-Induced Demyelinating Disease.

Ana Lis Moyano1, Jeffrey Steplowski1, Haibo Wang2

  • 1Department of Anatomy and Cell Biology, College of Medicine, University of Illinois at Chicago, Chicago, IL 60612, USA.

Molecular Therapy : the Journal of the American Society of Gene Therapy
|February 14, 2018
PubMed
Summary

MicroRNA-219 (miR-219) loss exacerbates Theiler's murine encephalomyelitis virus (TMEV) infection. Restoring miR-219 reduces neuroinflammation and viral load by impacting cholesterol biosynthesis, offering a potential therapeutic strategy for demyelinating diseases.

Keywords:
anti-viralcholesterolmiRNA-219microgliamyelinoligodendrocytesvirus-induced demyelination

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Published on: August 10, 2018

Area of Science:

  • Neuroimmunology
  • Virology
  • Molecular Biology

Background:

  • Theiler's murine encephalomyelitis virus (TMEV) infection causes demyelinating disease in the central nervous system.
  • MicroRNAs (miRs) play crucial roles in regulating gene expression and cellular processes, including myelin repair and immune responses.
  • miR-219 is a key regulator of myelin assembly and repair, but its role in TMEV-induced demyelination is not fully understood.

Purpose of the Study:

  • To investigate the role of miR-219 in TMEV-induced demyelinating disease.
  • To explore the therapeutic potential of restoring miR-219 expression in TMEV infection.
  • To elucidate the molecular mechanisms by which miR-219 exerts its effects.

Main Methods:

  • Analysis of miR expression in the central nervous system white matter of TMEV-infected SJL mice.
  • Intranasal administration of a synthetic miR-219 mimic before disease onset.
  • RNA sequencing of host lesions to identify miR-219-regulated genes.
  • Assessment of clinical disease, neurogliosis, motor function, and sensorimotor function.
  • Evaluation of cholesterol biosynthesis in infected mice and glial precursor cells.

Main Results:

  • TMEV infection led to a significant reduction of miR-219 in the central nervous system.
  • Restoration of miR-219 ameliorated clinical disease, reduced neurogliosis, and partially recovered motor function.
  • miR-219 negatively regulated proinflammatory cytokines and viral RNA replication.
  • miR-219 downregulated genes involved in cholesterol biosynthesis (Cyp51 and Srebf1), reducing cholesterol production.
  • Interference with cholesterol biosynthesis by miR-219 exhibited anti-inflammatory and anti-viral effects, inhibiting viral RNA replication.

Conclusions:

  • miR-219 plays a protective role in TMEV-induced demyelinating disease.
  • Restoring miR-219 expression is a potential therapeutic strategy for TMEV infection.
  • miR-219 exerts its protective effects through anti-inflammatory and anti-viral mechanisms, partly by modulating cholesterol biosynthesis.