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Development and Validation of a Quantitative PCR Method for Equid Herpesvirus-2 Diagnostics in Respiratory Fluids
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Equine Influenza Culture Methods.

Thomas M Chambers1, Stephanie E Reedy2

  • 1Maxwell H. Gluck Equine Research Center, Department of Veterinary Science, University of Kentucky, Lexington, KY, USA. tmcham1@uky.edu.

Methods in Molecular Biology (Clifton, N.J.)
|March 15, 2020
PubMed
Summary
This summary is machine-generated.

Equine influenza viruses are cultured in chicken eggs or canine kidney cells. Equine-1 viruses kill chicken embryos, while equine-2 viruses do not, indicating different host adaptations.

Keywords:
Embryonated eggsMDCKMammalian influenzaPlaque assayTCID assay

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Area of Science:

  • Virology
  • Animal Health

Background:

  • Equine influenza viruses (EIVs) are significant pathogens in horses.
  • Standard culture methods for influenza A viruses, including EIVs, involve embryonated chicken eggs or mammalian cell lines like Madin-Darby canine kidney (MDCK) cells.
  • Mutations influencing host adaptation can arise during in vitro culture.

Purpose of the Study:

  • To compare the replication and effects of equine-1 (H7N7) and equine-2 (H3N8) influenza viruses in embryonated chicken eggs.
  • To investigate differences in host adaptation between EIV subtypes during in vitro culture.

Main Methods:

  • Culturing of equine-1 (H7N7) and equine-2 (H3N8) influenza viruses.
  • Inoculation of 11-day-old embryonated chicken eggs with both EIV subtypes.
  • Observation and recording of viral replication and embryo viability.

Main Results:

  • Both equine-1 H7N7 and equine-2 H3N8 viruses replicated efficiently in 11-day-old embryonated chicken eggs.
  • Equine-1 H7N7 viruses caused embryo death.
  • Equine-2 H3N8 viruses replicated without causing embryo death.

Conclusions:

  • Embryonated chicken eggs are a suitable host for culturing both equine-1 and equine-2 influenza viruses.
  • Equine-1 and equine-2 influenza viruses exhibit distinct pathogenic effects on chicken embryos, suggesting differential host adaptation mechanisms.