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Related Concept Videos

Exon Recombination02:32

Exon Recombination

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The evolution of new genes is critical for speciation. Exon recombination, also known as exon shuffling or domain shuffling, is an important means of new gene formation. It is observed across vertebrates, invertebrates, and in some plants such as potatoes and sunflowers. During exon recombination, exons from the same or different genes recombine and produce new exon-intron combinations, which might evolve into new genes. 
Exon shuffling follows “splice frame rules.” Each exon...
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During most eukaryotic translation processes, the small 40S ribosome subunit scans an mRNA from its 5' end until it encounters the first start AUG codon. The large 60S ribosomal subunit then joins the smaller one to initiate protein synthesis. The location of the translation initiation is largely determined by the nucleotides near the start codon as there may be multiple translation initiation sites present on the mRNA.  Marilyn Kozak discovered that the sequence RCCAUGG (where R...
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Related Experiment Video

Updated: Jan 16, 2026

A Murine Model of Dengue Virus-induced Acute Viral Encephalitis-like Disease
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Integrative Mechanistic Studies Identify Reticulon-3 as a Critical Modulator of Infectious Exosome-Driven Dengue

Razieh Bitazar1,2, Clinton Njinju Asaba1, Saina Shegefti1

  • 1Armand-Frappier Santé Biotechnologie Research Center, Institut National de la Recherche Scientifique, Laval, QC H7V 1B7, Canada.

Viruses
|September 27, 2025
PubMed
Summary

Dengue virus (DENV) uses Reticulon 3 isoform S (RTN3S) to create infectious exosomes for spread. RTN3S is crucial for viral release and immune evasion, offering a new target for antiviral therapies.

Keywords:
antiviralsdengueendoplasmicflavivirusimmunoevasioninfectious exosomesmonocytesmultivesicularpathogenesisreticulon 3trafficking

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Area of Science:

  • Virology
  • Cell Biology
  • Immunology

Background:

  • Dengue virus (DENV) utilizes host exosome pathways for dissemination and immune evasion.
  • Host factors facilitating DENV exosome biogenesis are not well understood.

Purpose of the Study:

  • To investigate the role of host factors in DENV-mediated exosome production and viral release.
  • To identify novel mechanisms of DENV pathogenesis and potential therapeutic targets.

Main Methods:

  • Investigated Reticulon 3 isoform S (RTN3S) expression in DENV-infected hepatic and monocytic cells.
  • Assessed the physical association of RTN3S with viral components (dsRNA, NS3).
  • Quantified exosome production and viral export upon RTN3S manipulation (knockdown/overexpression).
  • Analyzed monocyte phenotype (CD16 expression) and cytokine secretion in DENV-infected cells and patient samples.

Main Results:

  • DENV infection induces RTN3S expression, which binds to viral RNA and NS3.
  • RTN3S is essential for efficient exosome production and the release of infectious viral particles.
  • Overexpression of RTN3S enhances infectious exosome release, dependent on its C-terminal domain.
  • DENV-infected monocytes show altered CD16 expression, upregulated vesicle trafficking genes, and increased inflammatory cytokine secretion.
  • Monocytes from Dengue patients exhibit high RTN3 expression correlating with CD16+ subset expansion and vesicle machinery gene enrichment.

Conclusions:

  • DENV hijacks RTN3S to promote the formation of infectious exosomes, facilitating viral spread and immune evasion.
  • RTN3S is a critical host factor in DENV pathogenesis and a potential target for host-directed antiviral strategies.