As with other alphaherpesviruses, the molecular mechanisms that underlie bovine herpesvirus type 1 (BHV-1) latency and reactivation are poorly understood. Restricted transcription of the BHV-1 genome has been described in latently infected neurons of the natural host and in the rabbit latency model. BHV-1 latency-associated transcription (LAT) is predominantly nuclear, approximately 1.0 to 1.2 kb in size, and anti-parallel to and overlapping an immediate-early gene. Down-regulation of LAT expression observed in ganglia during dexamethasone-induced viral reactivation, together with altered reactivation characteristics of a LAT-promoter deletion mutant suggests that expression and/or proper regulation of LAT is necessary for efficient viral reactivation.
- Latency-associated transcripts
- Latent infection
- Viral reactivation
- Virus-neuron interaction
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