Quist C F, Howerth E W, Bounous D I, Stallknecht D E
Southeastern Cooperative Wildlife Disease Study, Athens, GA 30602, USA.
Vet Immunol Immunopathol. 1997 May;56(3-4):283-97. doi: 10.1016/s0165-2427(96)05747-9.
Hemorrhagic disease, caused by various serotypes of two closely related orbivirus serogroups, the epizootic hemorrhagic disease viruses (EHDV) and the bluetongue viruses (BTV), is a major cause of morbidity and mortality in white-tailed deer (WTD) in the United States. Despite the 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 related orbiviruses, as can occur under natural conditions. Initial experimental data from our laboratory showed WTD infected with EHDV serotype 2 (EHDV-2) had responded serologically but often became lymphopenic and had a reduced lymphocyte proliferative response in vitro to T-cell 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-mediated response was evaluated via in vitro lymphocyte proliferation and interleukin-2 (IL-2) production assays, and in vivo delayed type hypersensitivity tests. Deer infected with either EHDV-2 or BTV-10 responded similarly in all assays. Infected deer had decreased lymphocyte counts between post-infection days (PID) 6 and 10, with concurrent diminished lymphocytic response to concanavalin A in lymphocyte proliferation assays and phytohemagglutinin in delayed, type hypersensitivity tests. However, IL-2 production by peripheral blood lymphocytes of infected deer was comparable with that of non-infected control deer as measured using a IL-2-dependent bovine cell line (BT2). This suppression of T-cell proliferation, but not IL-2 production suggests selective inhibition of T-cells probably via altered signal transduction for either expression of the IL-2 receptor or for IL-2 receptor signal-induced T-cell proliferation.
出血性疾病由两种密切相关的环状病毒血清群的各种血清型引起，即流行性出血性疾病病毒（EHDV）和蓝舌病毒（BTV），是美国白尾鹿（WTD）发病和死亡的主要原因。尽管出血性疾病在白尾鹿中很重要，但对于由任何一种致病病毒感染引发的宿主防御机制，或者在自然条件下可能发生的与密切相关的环状病毒的挑战如何调节免疫反应，人们了解甚少。我们实验室的初步实验数据表明，感染EHDV血清型2（EHDV-2）的白尾鹿有血清学反应，但通常会出现淋巴细胞减少，并且在体外对T细胞有丝分裂原的淋巴细胞增殖反应降低，这表明细胞介导的免疫可能受到抑制。本研究的主要目的是更密切地研究白尾鹿在实验性感染EHDV-2并随后用BTV血清型10（BTV-10）攻击时的细胞介导免疫。通过体外淋巴细胞增殖和白细胞介素-2（IL-2）产生试验以及体内迟发型超敏反应试验来评估细胞介导的反应。感染EHDV-2或BTV-10的鹿在所有试验中的反应相似。感染的鹿在感染后天数（PID）6至10之间淋巴细胞计数减少，同时在淋巴细胞增殖试验中对伴刀豆球蛋白A的淋巴细胞反应以及在迟发型超敏反应试验中对植物血凝素的反应减弱。然而，使用依赖IL-2的牛细胞系（BT2）测量时，感染鹿外周血淋巴细胞产生的IL-2与未感染的对照鹿相当。T细胞增殖的这种抑制，但不是IL-2的产生，表明可能通过改变IL-2受体表达或IL-2受体信号诱导的T细胞增殖的信号转导来选择性抑制T细胞。
