Persistence and reactivation of bovine herpesvirus 1 in the tonsils of latently infected calves

Bovine herpesvirus 1 (BHV-1), like other members of the Alphaherpesvirinae subfamily, establishes latent infection in sensory neurons. Reactivation fr om latency can occur after natural or corticosteroid-induced stress culmina ting in recurrent disease and/or virus transmission to uninfected animals. Our previous results concluded that CD4(+) T cells in the tonsil and other adjacent lymph nodes are infected and undergo apoptosis during acute infect ion (M. T. Winkler, A. Doster, and C. Jones, J. Virol. 73:8657-8668, 1999). To test whether BHV-1 persisted in lymphoreticular tissue, we analyzed ton sils of latently infected calves for the presence of viral DNA and gene exp ression. BHV-1 DNA was consistently detected in the tonsils of latently inf ected calves, Detection of the latency-related transcript (LRT) in tonsils of latently infected calves required nested reverse transcription-PCR (RT-P CR) suggesting that only a few cells contained viral DNA or that LRT is not an abundant transcript. bICP0 (immediate-early and early transcripts), rib onucleotide reductase (early transcript), and glycoprotein C (late transcri pt) were not detected by RT-PCR in latently infected calves, When reactivat ion was initiated by dexamethasone, bICP0 and ribonucleotide reductase tran scripts were detected, Following dexamethasone treatment, viral nucleic aci d was detected simultaneously in trigeminal ganglionic neurons and lymphoid follicles of tonsil, LRT was detected at 6 and 24 h after dexamethasone tr eatment but not at 48 h, Dexamethasone-induced reactivation led to apoptosi s that was localized to tonsillar lymphoid follicles, Taken together, these findings suggest that the tonsil is a site for persistence or latency from which virus can be reactivated by dexamethasone. We further hypothesize th at the shedding of virus from the tonsil during reactivation plays a role i n virus transmission.