[1] The mutation causing SCIDs in mice was discovered by Melvin and Gayle Bosma in 1983[1] in the CB/17 mouse line.
This has implications for B and T cell receptor development, which is dependent upon such double-stranded breaks and subsequent repairs in order to rearrange V, D, J or V and J segments.
[3][4] Studies such as those conducted by Ito et al. have found that non-obese diabetic (NOD) SCID IL2Rγ mice are even better suited as models for tissue transplants from non-self organisms due to their lower rate of rejection of human cells.
For example, they have been used to study Dengue virus and malaria, as well as to assess the efficacy of drugs that target these diseases.
[3] It is important to note that the use of SCID mice has been questioned as a model for studying the human immune system.
Some studies have suggested that after a period of time, human T cells in the immunocompromised mice become anergic, meaning that they no longer respond to stimuli.
[9] These mice are then infected with the virus and researchers are able to study how HIV attacks the human lymphocytes and causes acquired immunodeficiency syndrome (AIDS) over time.