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Title: THE EFFECTS OF LENTIVIRUS AND DRUG-INDUCED IMMUNOSUPPRESSION ON BLUETONGUE VIRUS PATHOGENESIS.

Author
item BRODIE, SCOTT - USDA-ARS-ABADRL
item BARDSLEY, K. - USDA-ARS-ABADRL
item THOMPSON, L. - USDA-ARS-ABADRL
item PEARSON, L. - COLORADO STATE UNIVERSITY
item Wilson, William

Submitted to: Research Workers in Animal Diseases Conference Proceedings
Publication Type: Abstract Only
Publication Acceptance Date: 11/13/1995
Publication Date: N/A
Citation: N/A

Interpretive Summary:

Technical Abstract: The effects of natural and artificially-induced immunosuppression on bluetongue virus (BTV) pathogenesis was investigated, including mechanisms of trafficking and distribution of virus in the experimentally-infected host. Three groups of age- and breed- matched sheep were assembled in the USDA-ARS-ABADRL biocontainment level 3 animal facility. The first group was chronically infected with ovine lentivirus, a common infection of sheep and an immunosuppressive agent. The second group was treated with immunosuppressive drugs prior to infection and subsequently shown to be immunosuppressed (lymphocyte blastogenesis, IL-2R). The third group was untreated. Half of the animals in each group were infected with BTV serotype 3, a Central American isolate, and half with North American serotype 11. Animals infected with BTV-3 developed mild dermatitis, interstitial pneumonia, and pulmonary and cerebral hemorrhage. Lesions associated with BTV-11 were less severe. Inflammatory infiltrates consisted mainly of CD8+ and CD11b/CD14+ cells which also demonstrated a high level of TCR-1 and class-II antigen expression, respectively. These findings correlated with the host immune status and with development of serum antibodies. Antibody production was not influenced by the infecting virus serotype; however, antibodies to BTV outer membrane proteins were delayed by several days in immunosuppressed sheep. Thus, immunosuppression may predispose animals to bluetongue- mediated diseases and may provide a mechanism for virus persistence in nature.