Murine Acquired Immune Deficiency Syndrome (MAIDS) is a highly contagious and debilitating immunodeficiency disorder caused by the infection of certain strains of retroviruses in laboratory mice. This syndrome is characterized by a rapid and progressive breakdown of the immune system, rendering the affected mice more susceptible to various opportunistic infections and tumors.
This acquired immune deficiency syndrome is similar to the human immunodeficiency virus (HIV) and simian immunodeficiency virus (SIV) infections in humans and non-human primates, respectively. However, the etiology, pathogenesis, and clinical manifestations of MAIDS are specific to mice and are distinct from those observed in HIV/AIDS.
The main causative agents of MAIDS are the murine leukemia virus (MuLV) and the murine acquired immunodeficiency syndrome virus (MAIDSV). These retroviruses infect and target specific immune cells, such as T cells and macrophages, leading to their dysfunction and depletion.
Clinical signs of MAIDS include weight loss, lymphadenopathy, splenomegaly, pneumonia, anemia, and increased susceptibility to other infections. The severity of the disease varies greatly depending on the viral strain and host susceptibility factors.
MAIDS poses a significant challenge in laboratory mouse research, as it can compromise the validity and reproducibility of experimental results. Thus, it is essential to implement stringent biosecurity measures to prevent the transmission and dissemination of MAIDS within mouse colonies. Additionally, understanding the immunopathogenesis of MAIDS can provide valuable insights into the study of retroviral infections and immunodeficiency disorders in both animals and humans.
