感染致细胞病变型牛病毒性腹泻病毒的巨噬细胞释放一种（或多种）因子，该因子能够使未感染的巨噬细胞致敏，从而引发激活诱导的细胞凋亡。
Macrophages infected with cytopathic bovine viral diarrhea virus release a factor(s) capable of priming uninfected macrophages for activation-induced apoptosis.
作者信息
Adler B, Adler H, Pfister H, Jungi T W, Peterhans E
机构信息
Institute of Veterinary Virology, University of Bern, Switzerland.
出版信息
J Virol. 1997 Apr;71(4):3255-8. doi: 10.1128/JVI.71.4.3255-3258.1997.
Abstract
Bovine bone marrow-derived macrophages infected with the cytopathic biotype of bovine viral diarrhea virus released an antiviral activity into the supernatant which was tentatively characterized as type I interferon because of its physicochemical properties. Such supernatants primed both infected and uninfected macrophages for decreased nitric oxide production and apoptosis in response to lipopolysaccharide. This finding strongly suggests a role of this pathway in the pathogenesis of mucosal disease, a lethal form of infection with cytopathic bovine viral diarrhea virus in which the principal lesions are located in the oral cavity and the gastrointestinal tract, which are known to contain a high concentration of endotoxin.
摘要
感染牛病毒性腹泻病毒细胞病变生物型的牛骨髓来源巨噬细胞将一种抗病毒活性释放到上清液中，由于其物理化学性质，该活性初步被鉴定为I型干扰素。这种上清液使感染和未感染的巨噬细胞对脂多糖刺激产生的一氧化氮生成减少和凋亡受到抑制。这一发现有力地表明该途径在黏膜病发病机制中发挥作用，黏膜病是一种由细胞病变性牛病毒性腹泻病毒引起的致死性感染形式，其主要病变位于口腔和胃肠道，而这些部位已知含有高浓度的内毒素。
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