Abstract
During latency, the bovine herpesvirus 1 (BHV-1) latency-related (LR) RNA is abundantly expressed in neurons within trigeminal ganglia (TG). A LR mutant virus that does not express two LR proteins is unable to reactivate from latency following dexamethasone treatment. Increased infiltration of inflammatory cells occurs in TG of calves acutely infected with the LR mutant virus. Throughout acute infection, wild-type BHV-1 DNA is detected in neurons surrounded by mononuclear infiltrates and in non-neuronal cells comprising the infiltrate. Conversely, LR mutant DNA is only detected in neurons near the end of acute infection, suggesting LR gene products promote virus spread in TG.
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