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Porcine reproductive and respiratory syndrome virus enters cells through a low pH-dependent endocytic pathway

L C Kreutz1, M R Ackermann

  • 1Virology Swine Research Unit, National Animal Disease Center, USDA, Agricultural Research Service, Ames, Iowa 50010, USA.

Virus Research
|June 1, 1996
PubMed

Insights

Porcine reproductive and respiratory syndrome virus (PRRSV) enters cells via endocytosis, requiring a low pH for uncoating. This study reveals key mechanisms of PRRSV cell entry.

Area of Science:

  • Virology
  • Cell Biology
  • Molecular Biology

Background:

  • Porcine reproductive and respiratory syndrome virus (PRRSV) is a significant pathogen affecting the swine industry.
  • Understanding the cellular entry mechanisms of PRRSV is crucial for developing effective control strategies.

Purpose of the Study:

  • To investigate the entry pathway of PRRSV into host cells (MARC-145).
  • To determine the role of intracellular vesicle pH and cellular machinery in PRRSV infection.

Main Methods:

  • Utilized drugs that alter intracellular vesicle pH (chloroquine, ammonium chloride, bafilomycin A1).
  • Assessed viral RNA replication and infectious virus production.
  • Employed electron microscopy to visualize virus particles.
  • Investigated the role of microfilaments using cytochalasin B and phenylarsine oxide.

Main Results:

  • pH-interfering drugs inhibited PRRSV replication in a dose-dependent manner, indicating a low pH requirement for entry.
  • Inhibition was observed when drugs were added before, during, or shortly after infection.
  • Chloroquine's effect was reversible under acidic conditions.
  • Electron microscopy showed PRRSV particles associated with clathrin-like structures.
  • Cytochalasin B and phenylarsine oxide reduced PRRSV infection, suggesting microfilament involvement.

Conclusions:

  • PRRSV entry into MARC-145 cells is an endocytic process dependent on microfilaments.
  • A low pH environment within vesicles is essential for PRRSV uncoating and subsequent infection.

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