TY - JOUR
T1 - Analysis of bovine trigeminal ganglia following infection with bovine herpesvirus 1
AU - Winkler, M. T.C.
AU - Doster, A.
AU - Sur, J. H.
AU - Jones, C.
N1 - Funding Information:
This research was supported by grants from the USDA (9802064 and 2000-02060). We thank S.I. Chowdhury for the gC plasmid (Department of Diagnostic Medicine and Pathobiology, College of Veterinary Medicine, Kansas State University). At the Department of Veterinary and Biomedical Sciences, University of Nebraska, Lincoln we are grateful to S. Srikumaran for the monoclonal antibody directed against BHV-1 gD and T. Holt for technical assistance. We would also like to thank B. Clowser, J. Wilkinson and T. Green for assistance with cattle experiments. Finally, we thank R. Olmscheid and V. Johns for assistance with histological preparations.
PY - 2002/4/22
Y1 - 2002/4/22
N2 - Following primary infection of the eye, oral cavity, and/or nasal cavity, bovine herpesvirus 1 (BHV-1) establishes latency in trigeminal ganglionic (TG) neurons. Virus reactivation and spread to other susceptible animals occur after natural or corticosteroid-induced stress. Infection of calves with BHV-1 leads to infiltration of lymphocytes in TG and expression of IFN-γ (interferon-gamma), even in latently infected calves. During latency, virus antigen and nucleic acid positive non-neural cells were occasionally detected in TG suggesting there is a low level of spontaneous reactivation. Since we could not detect virus in ocular or nasal swabs, these rare cells do not support high levels of productive infection and virus release or they do not support virus production at all. Dexamethasone (DEX) was used to initiate reactivation in latently infected calves. Foci of mononuclear or satellite cells undergoing apoptosis were detected 6 h after DEX treatment, as judged by the appearance of TUNEL+ cells (terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling). BHV-1 antigen expression was initially detected in lymphocytes and other non-neural cells in latently infected calves following DEX treatment. At 24 h after DEX treatment, viral antigen expression and nucleic acid were readily detected in neurons. Our data suggest that persistent lymphocyte infiltration and cytokine expression occur during latency because a low number of cells in TG express BHV-1 proteins. Induction of apoptosis and changes in cytokine expression following DEX treatment correlates with reactivation from latency. We hypothesize that inflammatory infiltration of lymphoid cells in TG plays a role in regulating latency.
AB - Following primary infection of the eye, oral cavity, and/or nasal cavity, bovine herpesvirus 1 (BHV-1) establishes latency in trigeminal ganglionic (TG) neurons. Virus reactivation and spread to other susceptible animals occur after natural or corticosteroid-induced stress. Infection of calves with BHV-1 leads to infiltration of lymphocytes in TG and expression of IFN-γ (interferon-gamma), even in latently infected calves. During latency, virus antigen and nucleic acid positive non-neural cells were occasionally detected in TG suggesting there is a low level of spontaneous reactivation. Since we could not detect virus in ocular or nasal swabs, these rare cells do not support high levels of productive infection and virus release or they do not support virus production at all. Dexamethasone (DEX) was used to initiate reactivation in latently infected calves. Foci of mononuclear or satellite cells undergoing apoptosis were detected 6 h after DEX treatment, as judged by the appearance of TUNEL+ cells (terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling). BHV-1 antigen expression was initially detected in lymphocytes and other non-neural cells in latently infected calves following DEX treatment. At 24 h after DEX treatment, viral antigen expression and nucleic acid were readily detected in neurons. Our data suggest that persistent lymphocyte infiltration and cytokine expression occur during latency because a low number of cells in TG express BHV-1 proteins. Induction of apoptosis and changes in cytokine expression following DEX treatment correlates with reactivation from latency. We hypothesize that inflammatory infiltration of lymphoid cells in TG plays a role in regulating latency.
KW - Apoptosis
KW - Bovine herpesvirus type 1
KW - Latency
KW - Neuroimmunology
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U2 - 10.1016/S0378-1135(01)00498-9
DO - 10.1016/S0378-1135(01)00498-9
M3 - Article
C2 - 11888697
AN - SCOPUS:0037156221
SN - 0378-1135
VL - 86
SP - 139
EP - 155
JO - Veterinary Microbiology
JF - Veterinary Microbiology
IS - 1-2
ER -