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Analysis of genetic mutations in the 7a7b open reading frame of coronavirus of cheetahs (Acinonyx jubatus)

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  • 1 Department of Comparative Medicine, College of Veterinary Medicine, University of Tennessee, Knoxville, TN 37996-4543.
  • | 2 Department of Comparative Medicine, College of Veterinary Medicine, University of Tennessee, Knoxville, TN 37996-4543.
  • | 3 Department of Comparative Medicine, College of Veterinary Medicine, University of Tennessee, Knoxville, TN 37996-4543.
  • | 4 White Oak Conservation Center, 726 Owens Rd, Yulee, FL 32097.
  • | 5 Department of Comparative Medicine, College of Veterinary Medicine, University of Tennessee, Knoxville, TN 37996-4543.

Abstract

Objective—To analyze the 7a7b genes of the feline coronavirus (FCoV) of cheetahs, which are believed to play a role in virulence of this virus.

Sample Population—Biologic samples collected during a 4-year period from 5 cheetahs at the same institution and at 1 time point from 4 cheetahs at different institutions.

Procedures—Samples were first screened for FCoV via a reverse transcription-PCR procedure involving primers that encompassed the 3′-untranslated region. Samples that yielded positive assay results were analyzed by use of primers that targeted the 7a7b open reading frames. The nucleotide sequences of the 7a7b amplification products were determined and analyzed.

Results—In most isolates, substantial deletional mutations in the 7a gene were detected that would result in aberrant or no expression of the 7a product because of altered reading frames. Although the 7b gene was also found to contain mutations, these were primarily point mutations resulting in minor amino acid changes. The coronavirus associated with 1 cheetah with feline infectious peritonitis had intact 7a and 7b genes.

Conclusions and Clinical Relevance—The data suggest that mutations arise readily in the 7a region and may remain stable in FCoV of cheetahs. In contrast, an intact 7b gene may be necessary for in vivo virus infection and replication. Persistent infection with FCoV in a cheetah population results in continued virus circulation and may lead to a quasispecies of virus variants.

Contributor Notes

Supported by the Morris Animal Foundation.

Presented as a poster presentation at the Conference for Research Workers in Animal Disease, Chicago, November 2002.

The authors thank Drs. Melvin Shaw, Mark Campbell, Ray Wack, and Clayton Hilton and Lisa Cree, Marcie Oliva, Cyd Shields, Michele Wiggs, and Karen Ziegler for technical assistance.

Dr. Kennedy.