CELL-MEDIATED IMMUNE-RESPONSE AND IL-2 PRODUCTION IN WHITE-TAILED DEER EXPERIMENTALLY INFECTED WITH HEMORRHAGIC-DISEASE VIRUSES

Hemorrhagic disease, caused by various serotypes of two closely relate d orbivirus serogroups, the epizootic hemorrhagic disease viruses (EHD V) and the bluetongue viruses (BTV), is a major cause of morbidity and mortality in white-tailed deer (WTD) in the United States. Despite th e importance of hemorrhagic disease in WTD, little is known about host defense mechanisms triggered by infection with either causative virus or how that immune response is modulated by challenge with closely re lated orbiviruses, as can occur under natural conditions. Initial expe rimental data from our laboratory showed WTD infected with EHDV seroty pe 2 (EHDV-2) had responded serologically but often became lymphopenic and had a reduced lymphocyte proliferative response in vitro to T-cel l mitogens, suggesting possible suppression of cell-mediated immunity. The primary objective of this study was to more closely examine cell- mediated immunity of WTD when experimentally infected with EHDV-2 and subsequently challenged with BTV serotype 10 (BTV-10). The cell-mediat ed response was evaluated via in vitro lymphocyte proliferation and in terleukin-2 (IL-2) production assays, and in vivo delayed type hyperse nsitivity tests. Deer infected with either EHDV-2 or BTV-IO responded similarly in all assays. Infected deer had decreased lymphocyte counts between post-infection days (PID) 6 and 10, with concurrent diminishe d lymphocytic response to concanavalin A in lymphocyte proliferation a ssays and phytonemagglutinin in delayed type hypersensitivity tests. H owever, IL-2 production by peripheral blood lymphocytes of infected de er was comparable with that of non-infected control deer as measured u sing a IL-2-dependent bovine cell line (BT2). This suppression of T-ce ll proliferation, but not IL-2 production suggests selective inhibitio n of T-cells probably via altered signal transduction for either expre ssion of the IL-2 receptor or for IL-2 receptor signal-induced T-cell proliferation. (C) 1997 Elsevier Science B.V.