Persistent infection with bovine herpesvirus type 1: rabbit model

Rock, Daniel L.; Reed, David E.

doi:10.1128/iai.35.1.371-373.1982

Cited by 43 publications

(28 citation statements)

References 10 publications

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“…BHV-1 DNA was not detected in TG of latently infected calves by in situ hybridization, which is consistent with other studies (4,15,23,26). Thus, it was expected that in situ hybridization would not detect viral DNA in tonsils of latently FIG.…”

Section: Discussionsupporting

confidence: 90%

Persistence and Reactivation of Bovine Herpesvirus 1 in the Tonsils of Latently Infected Calves

Winkler¹,

Doster²,

Jones³

2000

J. Virol.

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Bovine herpesvirus 1 (BHV-1), like other members of the Alphaherpesvirinae subfamily, establishes latent infection in sensory neurons. Reactivation from latency can occur after natural or corticosteroid-induced stress culminating 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 infection (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 tonsils of latently infected calves for the presence of viral DNA and gene expression. BHV-1 DNA was consistently detected in the tonsils of latently infected calves. Detection of the latency-related transcript (LRT) in tonsils of latently infected calves required nested reverse transcription-PCR (RT-PCR) suggesting that only a few cells contained viral DNA or that LRT is not an abundant transcript. bICP0 (immediate-early and early transcripts), ribonucleotide reductase (early transcript), and glycoprotein C (late transcript) were not detected by RT-PCR in latently infected calves. When reactivation was initiated by dexamethasone, bICP0 and ribonucleotide reductase transcripts were detected.Following dexamethasone treatment, viral nucleic acid was detected simultaneously in trigeminal ganglionic neurons and lymphoid follicles of tonsil. LRT was detected at 6 and 24 h after dexamethasone treatment but not at 48 h. Dexamethasone-induced reactivation led to apoptosis 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 that the shedding of virus from the tonsil during reactivation plays a role in virus transmission.

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Section: Discussionsupporting

confidence: 90%

Persistence and Reactivation of Bovine Herpesvirus 1 in the Tonsils of Latently Infected Calves

Winkler¹,

Doster²,

Jones³

2000

J. Virol.

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“…Cells and viruses. Bovine lung and bovine turbinate cells were used throughout the experiments and maintained as described previously (16). The Cooper strain of BHV-1, obtained from the National Veterinary Services Laboratory, Animal and Plant Health Inspection Service, Ames, Iowa, was used at passage 10.…”

Section: Methodsmentioning

confidence: 99%

Analysis of the transcriptional promoter which regulates the latency-related transcript of bovine herpesvirus 1

Jones

Delhon

Bratanich

et al. 1990

J Virol

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As a transcriptional promoter in primary cultures of sensory ganglionic neurons, DNA sequences near the 5' terminus of the latency-related (LR) gene of bovine herpesvirus 1 were at least 10 times more efficient than the simian virus 40 early promoter-enhancer. In contrast, as a promoter in bovine, rodent, or monkey cells, the LR promoter was approximately six times less efficient than the simian virus 40 early promoter-enhancer. The LR promoter had strict orientation preferences in neurons and all other mammalian cell lines tested. Removal of a 146-base-pair XhoI fragment from the LR promoter resulted in stimulation of LR promoter activity in bovine cells but not rabbit neurons, monkey fibroblasts, or rodent cells. LR promoter activity in bovine cells is stimulated by bovine herpesvirus 1 lytic infection, suggesting that viral gene products or virus-induced factors positively regulate the expression of the LR gene. A synthetic glucocorticoid, dexamethasone, repressed LR promoter activity in bovine cells. These results imply that a variety of factors can influence the expression of the LR gene during latent infections of neurons as well as during the lytic infection cycle.

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“…Administration of dexamethasone to latently infected animals shows gan glia to be the first tissue affected/infected during reexpression (166). This suggests that the neuron is a site of latency (165,195). Supporting this is the observation that BHV-1 has been isolated from trigeminal ganglia by cocultivation with sus ceptible cells of explanted ganglia from a dairy herd where 45% of die animals tested BHV-1 antibody positive (90).…”

Section: Latencymentioning

confidence: 97%

“…There is a large body of information on the molecular biology of HSV-1 productive and latent infections. While there is less known about the molecular biology of BHV-1, especially the IE stage of productive infection, the study of BHV-1 latency is worth pursuing because the latent virus can be studied in its natural host (Bovidae) and in a laboratory model system-the rabbit (127,195). The study of HSV-1 latency in its natural host must remain indirect (205).…”

Section: Projectmentioning

confidence: 99%

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Identification of the immediate-early products of bovine herpesvirus-1

Hulce

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Persistent infection with bovine herpesvirus type 1: rabbit model

Cited by 43 publications

References 10 publications

Persistence and Reactivation of Bovine Herpesvirus 1 in the Tonsils of Latently Infected Calves

Persistence and Reactivation of Bovine Herpesvirus 1 in the Tonsils of Latently Infected Calves

Analysis of the transcriptional promoter which regulates the latency-related transcript of bovine herpesvirus 1

Identification of the immediate-early products of bovine herpesvirus-1

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