Pathogenesis of virus-induced osteopetrosis in the chicken.
Pathogenesis of virus-induced osteopetrosis in the chicken.
复制标题
病毒诱导的鸡骨硬化症的发病机制。
作者：
R. Smith;J. Ivanyi
用无缺陷禽白血病病毒MAV-2(0)感染鸡胚，可在孵化后2至3周内诱导骨增生，并严重抑制法氏囊和胸腺淋巴样细胞的发育。胚胎期感染性的时间过程研究表明，在孵化和孵化的第10天之间，易感性逐渐丧失。这一发现提示胚胎干细胞在植入骨和原发性淋巴器官之前或之后早期是一种病毒易感靶细胞。法氏囊的组织学观察显示，在第一周只有轻微的损伤，在随后几周的发育中，滤泡淋巴样细胞的增殖严重受损。因此，病毒感染对淋巴样靶细胞产生细胞抑制作用而不是细胞溶解作用。干细胞是淋巴样细胞和骨破骨细胞的祖细胞，其感染与该病的表现是一致的。提出了一种骨和淋巴组织细胞紊乱的模型。将MAV-2(0)免疫的成年鸡的淋巴样细胞过继移植到组织相容性病毒感染的幼年受者体内，消除了骨质疏松的表现。被动注射含有病毒中和抗体的抗血清也有效。接受免疫细胞的过继保护鸡血清中抗gp85病毒表面糖蛋白结合抗体均为细胞供体IgG异型。
Infection of chicken embryos with a nondefective avian leukosis virus MAV-2(0) induced bone hyperplasia and profound suppression of bursal and thymic lymphoid cell development within 2- to 3 weeks after hatching. A time-course study of infectivity during embryonal life showed a gradual loss of susceptibility between the 10th day of incubation and hatching. This finding suggests that an embryonal stem cell either before or early after seeding into the bone and primary lymphoid organs is a virus-susceptible target cell. Histologic observations of the bursa indicated only mild damage during the 1st week and severely impaired proliferation of follicular lymphoid cells during subsequent weeks of development. Thus, viral infection conferred a cytostatic rather than a cytolytic effect upon the lymphoid target cell. Infection of stem cells, which are progenitors of lymphoid cells as well as of bone osteoclasts, is compatible with the manifestations of the disease. A model of cellular disorders of the bone and lymphoid tissues is proposed. Adoptive transfer of lymphoid cells from adult MAV-2(0)-immunized chickens into histocompatible virus-infected juvenile recipients abrogated the manifestation of osteopetrosis. Passive injection of antiserum containing virus-neutralizing antibodies was also effective. Anti-gp85 viral surface glycoprotein-binding antibodies in sera from adoptively protected chickens receiving immune cells were exclusively of cell donor IgG allotype.