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Region-Specific Apoptosis-Related Gene Expression Is Uncoupled from Viral RNA Load in Canine Distemper
Bruno Benetti Junta Torres1, Bernardo De Caro Martins2, Luana de Sousa Ribeiro3
1Escola de Veterinária e Zootecnia, Universidade Federal de Goiás, Goiânia 74691-835, Goiás, Brazil.
Viruses
|July 28, 2026
Summary
Canine distemper virus causes neurodegeneration by altering apoptosis gene expression differently across brain regions. Viral RNA load did not correlate with these region-specific changes in dogs.
Area of Science:
- Veterinary Neurology
- Molecular Virology
- Neuroscience
Background:
- Canine distemper virus (CDV) is a significant cause of neurological disease in dogs.
- Apoptosis plays a role in CDV-induced neurodegeneration, but its regional transcriptional patterns are unclear.
- Understanding these patterns is crucial for deciphering CDV neuropathogenesis.
Purpose of the Study:
- To quantify CDV RNA load and apoptosis-related gene expression in distinct brain regions of infected dogs.
- To investigate the relationship between viral RNA levels and apoptotic gene responses.
- To elucidate the region-specific nature of CDV neuroinflammation.
Main Methods:
- Quantitative reverse transcription PCR (qRT-PCR) was used to measure CDV RNA and gene expression.
- Apoptosis markers (Bax, Bcl-2, caspase-3, caspase-8) were analyzed in the frontal cortex, hippocampus, and cerebellum.
- 21 CDV-infected dogs and 4 control dogs were included.
Main Results:
- CDV RNA was detected in all brain regions with no significant regional variation.
- Apoptosis gene expression varied by region: hippocampus and cerebellum showed significant upregulation of pro-apoptotic markers.
- No significant correlation was found between viral RNA load and apoptosis gene expression in any brain region.
Conclusions:
- CDV-associated apoptosis responses in the canine central nervous system are region-dependent.
- These responses are not directly correlated with local viral RNA concentration.
- Findings highlight the importance of regional brain susceptibility in CDV encephalitis and neuropathogenesis.
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