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Updated: Apr 18, 2026

An Ex Vivo Chicken Primary Bursal-cell Culture Model to Study Infectious Bursal Disease Virus Pathogenesis
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An Ex Vivo Chicken Primary Bursal-cell Culture Model to Study Infectious Bursal Disease Virus Pathogenesis

Published on: October 4, 2018

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Infectious bursal disease virus uptake involves macropinocytosis and trafficking to early endosomes in a

María C Gimenez1,2, José F Rodríguez Aguirre3, María I Colombo1,2

  • 1Facultad de Farmacia y Bioquímica, Universidad Juan Agustín Maza, Mendoza, Argentina.

Cellular Microbiology
|January 8, 2015
PubMed

Insights

Infectious bursal disease virus (IBDV) primarily enters cells via macropinocytosis, independent of clathrin and dynamin. This virus requires early endosomal trafficking and low pH for successful replication.

Area of Science:

  • * Virology
  • * Cell Biology
  • * Molecular Biology

Background:

  • * The cellular entry mechanisms of Infectious Bursal Disease Virus (IBDV) remain poorly understood.
  • * Elucidating IBDV internalization pathways is crucial for understanding viral pathogenesis and developing control strategies.

Purpose of the Study:

  • * To characterize the cell biological features and molecular pathways involved in IBDV endocytosis.
  • * To identify the specific endocytic mechanism utilized by IBDV for cellular entry.

Main Methods:

  • * Employed pharmacological inhibitors and dominant-negative mutants to perturb endocytic pathways.
  • * Quantified viral internalization using immunofluorescence and Western blot for viral proteins VP3 and VP2.
  • * Conducted ultrastructural studies to analyze viral internalization kinetics.
  • * Compared IBDV uptake with known ligands (transferrin, cholera-toxin B, dextran) using defined endocytic pathways.

Main Results:

  • * IBDV internalization is independent of clathrin and dynamin.
  • * Macropinocytosis was identified as the primary entry mechanism for IBDV.
  • * Post-uptake, IBDV traffics to early endosomes and requires low endocytic pH for replication.
  • * The GTPase Rab5 is essential for IBDV entry, indicating involvement of the early endosomal pathway.

Conclusions:

  • * IBDV utilizes macropinocytosis for cellular entry, a pathway distinct from clathrin-mediated endocytosis.
  • * Successful IBDV replication is dependent on early endosomal trafficking and acidic pH conditions.
  • * Rab5 GTPase plays a critical role in facilitating IBDV internalization and subsequent infection.

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