Retrovirus-induced immunodeficiency in the mouse, MAIDS, is caused by a replication defective MuLV (BM5def) that expresses only an unususal Gag gene in contrast to the HIV lentivirus responsible for AIDS. MAIDS thus clearly differs from AIDS in pathogenesis, but may shed light on how retroviruses can disrupt the immune system and how retroviruses interact with cellular components. We have studied the interaction of HIV and BM5def Gag proteins with a common cellular proteins using the yeast two hybrid system initially and more recently in human and mouse cells. If these interactions prove important in virion formation, they may point to novel approaches for inhibition of HIV production. In addition, we have followed up on an unusual aspect of MAIDS, the production of wild type levels of IgE in the absence of IL-4. We have discovered that MAIDS develops normally in mice lacking STAT6, an important signaling molecule for IgE expression. We have also covered an unusual form of interferon signaling protein, PKR, expressed in cells of mice with this disease. Recent studies have tied induction of PKR activity to IgE switching as a possible cause for allergic responses to certain molecules.
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