PMID- 18218160
OWN - NLM
STAT- MEDLINE
DCOM- 20080331
LR  - 20220330
IS  - 1466-2523 (Print)
IS  - 1466-2523 (Linking)
VI  - 8
IP  - 2
DP  - 2007 Dec
TI  - A review of the biology of bovine herpesvirus type 1 (BHV-1), its role as a 
      cofactor in the bovine respiratory disease complex and development of improved 
      vaccines.
PG  - 187-205
LID - 10.1017/S146625230700134X [doi]
AB  - Infection of cattle by bovine herpesvirus type 1 (BHV-1) can lead to upper 
      respiratory tract disorders, conjunctivitis, genital disorders and immune 
      suppression. BHV-1-induced immune suppression initiates bovine respiratory 
      disease complex (BRDC), which costs the US cattle industry approximately 3 
      billion dollars annually. BHV-1 encodes at least three proteins that can inhibit 
      specific arms of the immune system: (i) bICP0 inhibits interferon-dependent 
      transcription, (ii) the UL41.5 protein inhibits CD8+ T-cell recognition of 
      infected cells by preventing trafficking of viral peptides to the surface of the 
      cells and (iii) glycoprotein G is a chemokine-binding protein that prevents 
      homing of lymphocytes to sights of infection. Following acute infection of 
      calves, BHV-1 can also infect and induce high levels of apoptosis of CD4+ 
      T-cells. Consequently, the ability of BHV-1 to impair the immune response can 
      lead to BRDC. Following acute infection, BHV-1 establishes latency in sensory 
      neurons of trigeminal ganglia (TG) and germinal centers of pharyngeal tonsil. 
      Periodically BHV-1 reactivates from latency, virus is shed, and consequently 
      virus transmission occurs. Two viral genes, the latency related gene and ORF-E 
      are abundantly expressed during latency, suggesting that they regulate the 
      latency-reactivation cycle. The ability of BHV-1 to enter permissive cells, 
      infect sensory neurons and promote virus spread from sensory neurons to mucosal 
      surfaces following reactivation from latency is also regulated by several viral 
      glycoproteins. The focus of this review is to summarize the biology of BHV-1 and 
      how this relates to BRDC.
FAU - Jones, Clinton
AU  - Jones C
AD  - Department of Veterinary and Biomedical Sciences, University of Nebraska, 
      Lincoln, Fair Street at East Campus Loop, Lincoln, NE 68583-0905, USA. 
      cjones@unlnotes.unl.edu
FAU - Chowdhury, Shafiqul
AU  - Chowdhury S
LA  - eng
GR  - 1P20RR15635/RR/NCRR NIH HHS/United States
GR  - R21AI069176/AI/NIAID NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Review
PL  - England
TA  - Anim Health Res Rev
JT  - Animal health research reviews
JID - 101083072
RN  - 0 (Herpesvirus Vaccines)
RN  - 0 (Viral Proteins)
SB  - IM
MH  - Animals
MH  - Apoptosis
MH  - Bovine Respiratory Disease Complex/immunology/virology
MH  - Cattle
MH  - Cattle Diseases/*immunology/*virology
MH  - Herpesviridae Infections/immunology/*veterinary/virology
MH  - Herpesvirus 1, Bovine/genetics/*immunology/*pathogenicity
MH  - Herpesvirus Vaccines
MH  - Mutation
MH  - Trigeminal Ganglion/virology
MH  - Viral Proteins/metabolism
MH  - Virus Activation
MH  - Virus Latency
RF  - 166
EDAT- 2008/01/26 09:00
MHDA- 2008/04/01 09:00
CRDT- 2008/01/26 09:00
PHST- 2008/01/26 09:00 [pubmed]
PHST- 2008/04/01 09:00 [medline]
PHST- 2008/01/26 09:00 [entrez]
AID - S146625230700134X [pii]
AID - 10.1017/S146625230700134X [doi]
PST - ppublish
SO  - Anim Health Res Rev. 2007 Dec;8(2):187-205. doi: 10.1017/S146625230700134X.