|Knowles, Donald - Don|
Submitted to: Veterinary Microbiology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 4/19/2012
Publication Date: 8/31/2012
Publication URL: http://dx.doi.org/10.1016/j.vetmic.2012.04.021
Citation: Cunha, C.W., Gailbreath, K.L., O'Toole, D., Knowles Jr, D.P., Schneider, D.A., White, S.N., Taus, N.S., Davis, C.J., Davis, W.C., Li, H. 2012. Ovine herpesvirus 2 infection in american bison: virus and host dynamics in the development of sheep-associated malignant catarrhal fever. Veterinary Microbiology. 159:307-319. Interpretive Summary: Ovine herpesvirus 2 (OvHV-2) is a virus carried asymptomatically by sheep that can cause sheep associated malignant catarrhal fever (SA-MCF). SA-MCF is a severe and often fatal disease in ruminants and has been considered one of the major concerns for farmed bison in the United States. The events that lead to disease are not clear. Understanding the interactions between the virus and the host is a critical step in the development of vaccines to prevent or limit SA-MCF in predisposed animals. Thus, the goal of this work was to monitor the development of disease following experimental OvHV-2 in bison and investigate the linkage between viral products released during virus replication (e.g., transcripts of viral genes and viral DNA) and the host immune response and lesion development. The results obtained demonstrate only a subtle bison immune response to the initial viral infection and a relationship between severity of SA-MCF lesions in tissues and the levels of a viral gene (ORF 25) expressed when the virus replicates. The study suggests that viral replication may play a role in the development of SA-MCF in bison. Such information is important in guiding research toward the development of a vaccine to control SA-MCF.
Technical Abstract: Ovine herpesvirus 2 (OvHV-2) is a gammaherpesvirus that causes sheep-associated malignant catarrhal fever (SA-MCF), a frequently fatal disease mainly of ruminants. This study was designed to define virus-host dynamics following experimental OvHV-2 infection in bison. A transient peak in viral DNA accompanied by the presence of OvHV-2 ORF25, ORF50 and ORF73 transcripts was observed in lungs only from 9 to 12 days post-inoculation (DPI), suggesting occurrence of viral replication. This initial viral replication was associated with only a subtle increase in transcription of inflammation related genes in lungs and tracheal bronchial lymph nodes, while the level of expression of the majority of immune genes measured remained comparable to uninfected animals. Increasing viral load was observed in the blood and peripheral tissues at 16 and 21 DPI, respectively, indicating systemic viral dissemination. Clinical signs of MCF were observed between 28 and 35 DPI and the severity of lesions increased as disease progressed. Lesion scores were positively correlated with expression levels of ORF25, suggesting a contribution of viral replication in the pathogenesis of SA-MCF. Viral transcripts were observed in all tissues examined from 23 DPI to the end of the experiment at 35 DPI and expression levels of ORF25 were significantly higher in clinically infected animals as compared to pre-clinical stage. The data from this study provide a predictable viral-host interaction time course to test hypotheses concerning disease pathogenesis as well as mitigation of SA-MCF in susceptible species.