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Related Concept Videos

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...
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Viral replication and dissemination rely on efficient mechanisms for host cell entry, genome replication, assembly, and release. Influenza viruses, such as types A and B, are negative-sense single-stranded RNA viruses with a segmented genome, that depend on two critical surface glycoproteins to carry out these processes: hemagglutinin (HA) and neuraminidase (NA). HA initiates infection by binding to sialic acid residues on the surface of host epithelial cells, facilitating receptor-mediated...
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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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Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
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Related Experiment Video

Updated: Jun 11, 2026

A High Resolution Method to Monitor Phosphorylation-dependent Activation of IRF3
11:44

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Published on: January 24, 2016

Fish virus-induced interferon exerts antiviral function through Stat1 pathway.

Fei-Fei Yu1, Yi-Bing Zhang, Ting-Kai Liu

  • 1State Key Laboratory of Freshwater Ecology and Biotechnology, Institute of Hydrobiology, Chinese Academy of Sciences, Graduate School of the Chinese Academy of Sciences, Wuhan 430072, China.

Molecular Immunology
|July 15, 2010
PubMed
Summary

Fish interferons (IFNs) show antiviral activity and utilize the Stat1 pathway, similar to mammals. This study reveals a conserved signaling mechanism and a positive feedback loop for fish IFN regulation.

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10:00

High-throughput Quantitative Real-time RT-PCR Assay for Determining Expression Profiles of Types I and III Interferon Subtypes

Published on: March 24, 2015

Area of Science:

  • Immunology
  • Virology
  • Fish Biology

Background:

  • Virus-induced interferons (IFNs) are crucial for antiviral defense in fish, analogous to mammalian type I IFNs.
  • The specific signaling pathways mediating fish IFN antiviral responses remain largely uncharacterized.

Purpose of the Study:

  • To investigate the antiviral activity and signaling pathway of crucian carp interferon (IFN).
  • To determine the role of the Stat1 pathway in fish IFN-mediated antiviral responses and gene expression.

Main Methods:

  • Transient transfection and recombinant protein expression in fish cells.
  • Assessing antiviral activity against grass carp hemorrhagic virus (GCHV) and Poly I:C stimulation.
  • Analyzing the impact of wild-type and mutant Stat1 (Stat1-Delta C) on IFN-stimulated genes (ISGs) and viral inhibition.
  • Investigating IFN self-regulation using Stat1 knockdown and overexpression.

Main Results:

  • Crucian carp IFN demonstrated significant antiviral activity against GCHV and Poly I:C-induced responses.
  • Overexpression of wild-type Stat1 enhanced IFN's antiviral effects and ISG induction, while Stat1-Delta C inhibited them.
  • Fish IFN exhibited self-upregulation, forming a positive feedback loop dependent on Stat1.

Conclusions:

  • Fish IFN utilizes an evolutionarily conserved Stat1 signaling pathway, similar to mammals, for antiviral defense.
  • The Stat1 pathway is essential for fish IFN-induced antiviral responses and ISG expression.
  • A Stat1-dependent positive feedback loop regulates fish IFN production.