PMID- 15635000
OWN - NLM
STAT- MEDLINE
DCOM- 20050301
LR  - 20181113
IS  - 0095-1137 (Print)
IS  - 1098-660X (Electronic)
IS  - 0095-1137 (Linking)
VI  - 43
IP  - 1
DP  - 2005 Jan
TI  - Latency-related gene encoded by bovine herpesvirus 1 promotes virus growth and 
      reactivation from latency in tonsils of infected calves.
PG  - 393-401
AB  - Infection of calves with bovine herpesvirus 1 (BHV-1) results in transient 
      immunosuppression that may lead to bacterium-induced pneumonia and, occasionally, 
      death. Although sensory neurons in the trigeminal ganglia (TG) are the primary 
      site of BHV-1 latency, viral genomes are detected in the tonsils of latently 
      infected calves. Dexamethasone (DEX) consistently induces reactivation from 
      latency, and viral gene expression is detected in TG and tonsils. In sensory 
      neurons of latently infected calves, the latency-related (LR) gene is abundantly 
      expressed and is required for reactivation from latency. In the present study, we 
      compared the abilities of wild-type (wt) BHV-1 and a strain with a mutation in 
      the LR gene (the LR mutant strain) to grow in the tonsils of infected calves and 
      reactivate from latency. Lower levels of the LR mutant virus were detected in the 
      tonsils of acutely infected calves. LR mutant viral DNA was consistently detected 
      by PCR in the tonsils of latently infected calves, suggesting that the 
      establishment of a latent or persistent infection occurred. Although the LR 
      mutant did not reactivate from latency in vivo after DEX treatment, explantation 
      of tonsil tissue from calves latently infected with the LR mutant yielded 
      infectious virus. Relative to wt BHV-1, the LR mutant did not induce 
      explant-induced reactivation as efficiently. These studies indicate that the LR 
      gene promotes virus shedding from tonsil tissue during acute infection and 
      reactivation from latency in tonsil tissue in vivo. We suggest that incorporation 
      of the LR gene mutation into existing modified live vaccines would prevent 
      reactivation from latency in neural and nonneural sites and would thus prevent 
      transmission to other animals.
FAU - Perez, Sandra
AU  - Perez S
AD  - Department of Veterinary and Biomedical Sciences, University of Nebraska, 
      Lincoln, Fair Street at East Campus Loop, Lincoln, NE 68583-0905, USA.
FAU - Inman, Melissa
AU  - Inman M
FAU - Doster, Alan
AU  - Doster A
FAU - Jones, Clinton
AU  - Jones C
LA  - eng
GR  - P20 RR015635/RR/NCRR NIH HHS/United States
GR  - 1P20RR15635/RR/NCRR NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Clin Microbiol
JT  - Journal of clinical microbiology
JID - 7505564
RN  - 0 (DNA, Viral)
RN  - 0 (Viral Proteins)
RN  - 0 (latency-related protein, Bovine herpesvirus 1)
SB  - IM
MH  - Acute Disease
MH  - Animals
MH  - Apoptosis
MH  - Cattle
MH  - Cattle Diseases/pathology/*virology
MH  - DNA, Viral/analysis
MH  - *Gene Expression Regulation, Viral
MH  - Herpesviridae Infections/pathology/*veterinary/virology
MH  - Herpesvirus 1, Bovine/genetics/*growth & development/physiology
MH  - Mutation
MH  - Palatine Tonsil/pathology/*virology
MH  - Viral Proteins/*genetics/metabolism
MH  - *Virus Activation
MH  - Virus Latency
PMC - PMC540132
EDAT- 2005/01/07 09:00
MHDA- 2005/03/02 09:00
PMCR- 2005/01/01
CRDT- 2005/01/07 09:00
PHST- 2005/01/07 09:00 [pubmed]
PHST- 2005/03/02 09:00 [medline]
PHST- 2005/01/07 09:00 [entrez]
PHST- 2005/01/01 00:00 [pmc-release]
AID - 43/1/393 [pii]
AID - 0986-04 [pii]
AID - 10.1128/JCM.43.1.393-401.2005 [doi]
PST - ppublish
SO  - J Clin Microbiol. 2005 Jan;43(1):393-401. doi: 10.1128/JCM.43.1.393-401.2005.