Ivanyi J, Morris R
Clin Exp Immunol. 1976 Jan;23(1):154-65.
Chickens inoculated orally with infectious bursal disease virus (IBDV) 1 day after hatching subsequently showed a 50% incidence of immunodeficiency but little mortality. Antibody responses against IBDV and to immunization with sheep red blood cells (SRBC) or human serum albumin (HSA) were suppressed. Serum IgG concentration was decreased while IgM occurred exclusively in its 7S monomeric form (mIgM). An allotypic marker of chicken IgM (Mla) was lacking in mIgM derived from IBDV-infected birds. The loss of Mla occurred gradually in several birds between 3 and 12 weeks after perinatal infection. Inoculation of IBDV into chickens 3 weeks after hatching resulted in 50% mortality level but little immunodeficiency. Paradoxically, the serum IgG concentration was elevated, in comparison with normal birds. Histology of the bursa showed permanent hypo- or aplasia of follicles irrespective of the age of infection. The results suggest that bursal but not peripheral B cells are targets for IBDV, and immunodeficiency results from impaired peripheral seeding of B cells in infected juvenile chickens.
孵化后1天经口接种传染性法氏囊病病毒（IBDV）的鸡，随后出现50%的免疫缺陷发生率，但死亡率很低。针对IBDV以及用绵羊红细胞（SRBC）或人血清白蛋白（HSA）免疫的抗体反应受到抑制。血清IgG浓度降低，而IgM仅以其7S单体形式（mIgM）出现。来自IBDV感染鸡的mIgM缺乏鸡IgM的一种同种异型标记（Mla）。在围产期感染后的3至12周内，几只鸡的Mla逐渐丧失。孵化后3周给鸡接种IBDV导致50%的死亡率，但免疫缺陷很少。矛盾的是，与正常鸡相比，血清IgG浓度升高。无论感染年龄如何，法氏囊的组织学检查显示滤泡永久性发育不全或发育不全。结果表明，法氏囊而非外周B细胞是IBDV的靶标，免疫缺陷是由于受感染幼鸡外周B细胞播种受损所致。
