The LP-BM5 mixture of murine retroviruses elicits a disease in mice re
ferred to as murine immunodeficiency syndrome (MAIDS) that is consider
ed by some to be an animal homologue of human AIDS. In this article, w
e present and discuss some recent findings on the pathogenesis of the
murine disease and their implications for the proposed homology betwee
n murine and human syndromes. The murine disease seems to display as m
any similarities to as it does differences from human AIDS. Among the
latter are: definitive and exclusive viral etiology, a strong genetic
effect on susceptibility to infection, expansion of the CD4+ cell popu
lation in spleen and peripheral blood, consistent transmissibility by
a single transfusion of the minute amounts of blood or plasma from inf
ected donors, and striking similarity between virus-induced alteration
of the in vitro spleen cell proliferation and those caused by treatme
nt with a protein kinase inhibitor K252a. With this in mind, the use o
f the noncommittal term retrovirus-induced murine lymphoproliferative
disease instead of MAIDS appears to be more appropriate at this time.