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Persistent equine arteritis virus infection in HeLa cells.

Jianqiang Zhang1, Peter J Timoney, N James MacLachlan

  • 1Department of Veterinary Science, Maxwell H Gluck Equine Research Center, University of Kentucky, Lexington, Kentucky 40546-0099, USA.

Journal of Virology
|June 27, 2008
PubMed
Summary

Equine arteritis virus (EAV) persistence was established in human cervix cells. Viral structural protein mutations, not replicase changes, enabled this persistent infection in vitro.

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Area of Science:

  • Virology
  • Cell Biology
  • Molecular Biology

Background:

  • Equine arteritis virus (EAV) causes significant disease in horses.
  • Persistent viral infections are challenging to model and study.
  • Understanding EAV adaptation and persistence is crucial for disease control.

Purpose of the Study:

  • To establish an in vitro model for studying EAV persistence.
  • To identify viral genetic factors responsible for EAV persistence in human cells.
  • To investigate virus-host cell interactions during persistent EAV infection.

Main Methods:

  • Adaptation of virulent Bucyrus (VB) strain of EAV to high-passage human cervix cells (HeLa-H).
  • Comparative genomic sequencing of EAV strains.
  • Reverse genetics to assess the role of specific viral protein substitutions.

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Main Results:

  • EAV established persistent infection in high-passage HeLa-H cells but not low-passage HeLa-L cells.
  • Virus adapted to HeLa-H cells (HeLa-H-EAVP80) could infect HeLa-L cells persistently.
  • 16 amino acid substitutions were identified, with structural protein mutations being key for persistence in HeLa-L cells.

Conclusions:

  • An in vitro model for EAV persistence was successfully established.
  • Mutations in EAV structural proteins, particularly E, GP2, GP3, GP4, and GP5, are critical for establishing persistent infection in human cervix cells.
  • This model system offers a valuable tool for studying EAV-host cell interactions and viral receptor binding.