Mouse adenovirus infection in SCID mice

小鼠腺病毒K87（Mouse adenovirus K87， MAV）在普通小鼠肠道内复制，感染后3周，由于肠道内局部中和性IgA类抗体的作用，在粪便中完全无法检测到。在先天性胸腺缺陷裸鼠中，从粪便中检测到病毒持续到感染后约6周，远远晚于正常小鼠。表现为可检测病毒消失的耐药是暂时的，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，尽管环磷酰胺已被证明可以完全消除耐药。在MAV感染的严重联合免疫缺陷（SCID）小鼠中，由于缺乏功能性T细胞和B细胞，无法产生中和抗体，一些小鼠表现出明确的持续感染，而另一些小鼠则经历反复的病毒复制和耐药性，类似于裸鼠的感染过程。目前，正在进行的研究正在测试这样一种假设，即在一些SCID小鼠中表现出的维持病毒抗性的因素与在裸鼠中发现的因素相似。

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.