Jolicoeur P, Lamontagne L
Département des Sciences Biologiques, Université du Québec à Montréal, Canada.
Adv Exp Med Biol. 1995;380:193-5. doi: 10.1007/978-1-4615-1899-0_33.
Mouse hepatitis virus type 3 (MHV3) appears to be an excellent model for the study of the relationship between viral-induced immunodeficiency and the development of chronic disease. Animal surviving acute hepatitis develop a chronic disease characterized by viral persistency in various organs, by a humoral immunodeficiency, and eventually die within the next three months postinfection. To verify if B cell immunodeficiency occurs during the chronic disease, percentage and absolute number of bone marrow B lineage cell subpopulations were recorded at various times postinfection (p.i.) in pathogenic L2-MHV3-infected (C57BL/6 x A/J) F1 mice. Absolute numbers of B (cmu+smu+) cells decreased as early as three days p.i. up to 15 days p.i., and then gradually returned toward normal values in L2-MHV3-infected mice during the chronic disease. In contrast, pre-B (cmu+smu-) cells were less significantly decrease during the chronic disease. In addition, abnormally enlarged cells (> 13 microns) were detected either in bone marrow pre-B or B cells from L2-MHV3-infected mice.
3型小鼠肝炎病毒（MHV3）似乎是研究病毒诱导的免疫缺陷与慢性疾病发展之间关系的理想模型。在急性肝炎中存活下来的动物会发展成一种慢性病，其特征是病毒在各个器官中持续存在、体液免疫缺陷，最终在感染后的接下来三个月内死亡。为了验证在慢性疾病期间是否发生B细胞免疫缺陷，在感染致病性L2-MHV3的（C57BL/6×A/J）F1小鼠感染后的不同时间记录骨髓B谱系细胞亚群的百分比和绝对数量。在感染后3天至15天，B（cmu+smu+）细胞的绝对数量最早开始减少，然后在慢性疾病期间，L2-MHV3感染小鼠中的B（cmu+smu+）细胞数量逐渐恢复到正常值。相比之下，在前B（cmu+smu-）细胞在慢性疾病期间减少不太明显。此外，在L2-MHV3感染小鼠的骨髓前B细胞或B细胞中检测到异常增大的细胞（>13微米）。
