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Related Concept Videos

Rab Proteins01:14

Rab Proteins

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Rab proteins constitute the largest family of monomeric GTPases, of which 70 members are present in humans. Rab proteins and their effectors regulate consecutive stages of vesicle transport such as vesicle transport, docking, and fusion to the correct recipient membrane.
Rab proteins switch between a cytosolic, GDP-bound inactive state and a membrane-anchored, GTP-bound active state. By themselves, Rabs show slow rates of GDP/GTP exchange and GTP hydrolysis. Thus, Rab proteins are considered...
5.3K

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Related Experiment Video

Updated: Feb 28, 2026

Author Spotlight: Rabies-Specific Antibody Isotypes Detection in Sera or Cerebral Spinal Fluid Using an IFA Test
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Ifit2 Is a Restriction Factor in Rabies Virus Pathogenicity.

Benjamin M Davis1, Volker Fensterl2, Tessa M Lawrence1

  • 1Department of Microbiology and Immunology, Sidney Kimmel Medical College, Thomas Jefferson University, Philadelphia, Pennsylvania, USA.

Journal of Virology
|June 23, 2017
PubMed
Summary
This summary is machine-generated.

Interferon-induced protein with tetratricopeptide repeats 2 (Ifit2) restricts rabies virus (RABV) replication. Depleting Ifit2 in cells and mice increased RABV severity, highlighting Ifit2 as a potential therapeutic target for rabies.

Keywords:
innate immunityneurotropic virusesneurovirulencerabiesrhabdovirus

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Area of Science:

  • Virology
  • Immunology
  • Molecular Biology

Background:

  • Rabies virus (RABV) poses a significant global health threat, causing fatal zoonotic disease.
  • Understanding host-pathogen interactions is crucial for developing effective rabies therapies.
  • Interferon-stimulated genes (ISGs) play a role in antiviral defense.

Purpose of the Study:

  • To investigate the role of interferon-induced protein with tetratricopeptide repeats 2 (Ifit2) in restricting RABV infection.
  • To determine the impact of Ifit2 on RABV replication and pathogenesis in vitro and in vivo.

Main Methods:

  • In vitro experiments using mouse neuroblastoma cells with and without Ifit2.
  • In vivo studies involving Ifit2 knockout mice and wild-type mice infected with RABV intranasally.
  • Quantification of RABV mRNA, live viral load, and disease severity.

Main Results:

  • Depletion of Ifit2 led to increased RABV replication in cell culture.
  • Ifit2 knockout mice exhibited more severe disease, higher viral loads, and accelerated spread in the brain.
  • Ifit2 appears to restrict RABV primarily at the replication stage.

Conclusions:

  • Ifit2 is a critical host restriction factor against RABV infection.
  • Ifit2's antiviral activity is mainly associated with inhibiting viral replication.
  • Targeting the Ifit2 pathway could offer a novel therapeutic strategy for rabies.