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Characterization of ovine herpesvirus 2-induced malignant catarrhal fever in rabbits

Li, Hong, Cunha, Cristina W., Gailbreath, Katherine L., O’Toole, Donal, White, Stephen N., Vanderplasschen, Alain, Dewals, Benjamin, Knowles, Donald. P., Taus, Naomi S.
Veterinary microbiology 2011 v.150 no.3-4 pp. 270
Alcelaphine herpesvirus 1, B-lymphocytes, DNA, Ovine herpesvirus 2, T-lymphocytes, atomization, gene expression, incubation period, lymphocyte proliferation, malignant catarrhal fever, pathogenesis, rabbit diseases, rabbits, secretion, sheep, virus replication, viruses, wildebeest
Malignant catarrhal fever (MCF) is a frequently fatal lymphoproliferative disease syndrome primarily of ruminant species, caused by gammaherpesviruses in the genus Macavirus. Ovine herpesvirus 2 (OvHV-2), carried by sheep, causes sheep-associated MCF worldwide, while Alcelaphine herpesvirus 1 (AlHV-1), carried by wildebeest, causes wildebeest-associated MCF, mainly in Africa. Diseases in rabbits can be induced by both viruses, which are clinically and pathologically similar; however, recent studies revealed different expression of viral genes associated with latency or lytic replication during clinical disease between the two viruses. In this study, we further characterized experimentally induced MCF in rabbits by nebulization with OvHV-2 from sheep nasal secretions to elucidate the course of viral replication, along with in vivo incorporation of 5- Bromo-20-Deoxyuridine (BrdU), to evaluate lymphoproliferation. All six rabbits nebulized with OvHV-2 developed MCF between 24 and 29 days post infection. OvHV-2 DNA levels in peripheral blood leukocytes (PBL) remained undetectable during the incubation period and increased dramatically a few days before onset of clinical signs. During the clinical stage, we found that predominantly lytic gene expression was detected in PBL and tissues, and both T and B cells were proliferating. The data showed that the viral gene expression profile and lymphoproliferation in rabbits with OvHV-2 induced MCF were different from that in rabbits with AlHV-1 induced MCF, suggesting that OvHV-2 and AlHV-1 may play a different role in MCF pathogenesis.