Mouse adenovirus infection in SCID mice

SCID 小鼠中的小鼠腺病毒感染

• 批准号: 03670236
• 负责人: SHIMIZU Keiko
• 金额: $ 0.32万
• 依托单位: School of Medicine, Tokai University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for General Scientific Research (C)
• 财政年份: 1991
• 资助国家: 日本
• 起止时间: 1991 至 1992
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-03670236/
• 关键词: SCID mouse; Mouse adenovirus; Immunodeficiency; Virus persistent infection

Mouse adenovirus K87(MAV) replicate within the intestinal tract of ordinary mice, becoming completely undetectable in feces 3 weeks after infection due to the action of localized neutralizing IgA class antibodies in the intestinal tract. In congenitally athymic nude mice, detection of virus from feces continues up to about 6 weeks after infection, far later than in normal mice. The resistance manifested as disappearance of detectable virus is temporary, and implications of interferon, natural killer cell activation, and macrophage involvement are negative, although cyclophosphamide administration has been demonstrated to eliminate the resistance altogether. Neutralizing anti-bodies are not produced in MAV infected severe combined immunodeficiency (SCID) mice, lacking functional T and B cells, and some mice exhibit definite sustained infections, while others undergo repeated periods of viral replication and resistance, similar to the course of infection in nude mice. And presently, studies are underway to test the assumption that the factor upholding the resistance to virus exhibited by some of the SCID mice is akin to that found in nude mice.

小鼠腺病毒K87（MAV）在普通小鼠的肠道内复制，由于肠道中局部中和伊加类抗体的作用，感染后3周在粪便中变得完全检测不到。在先天无胸腺裸鼠中，从粪便中检测到病毒持续到感染后约6周，远晚于正常小鼠。表现为可检测病毒消失的耐药性是暂时的，干扰素、自然杀伤细胞活化和巨噬细胞参与的影响是阴性的，尽管环磷酰胺给药已被证明完全消除耐药性。在MAV感染的严重联合免疫缺陷（SCID）小鼠中不产生中和抗体，缺乏功能性T和B细胞，并且一些小鼠表现出明确的持续感染，而另一些小鼠经历重复的病毒复制和抗性期，类似于裸鼠中的感染过程。目前，研究正在进行中，以测试这样一种假设，即一些SCID小鼠表现出的维持对病毒的抵抗力的因素与裸鼠中发现的相似。