The murine acquired immunodeficiency syndrome (MAIDS) is caused in sus
ceptible C57BL/6 (B6) mice by a defective murine leukemia virus (MuLV)
and resembles human AIDS in several respects. The disease is characte
rized by hypergammaglobulinemia, polyclonal B cell activation, lymphad
enopathy, and generalized immunosuppression within 5-8 weeks postinfec
tion. The virus has been shown to infect B cells and macrophages and b
oth T and B cells are required for MAIDS development. The manner in wh
ich T cells contribute to the disease process is not known. We report
here that this retroviral infection leads to induction of a Thy-CD4(+)
T cell subpopulation capable of transferring all the symptoms of MAID
S disease to normal B6 and B6 nu/nu. Essentially 100% of T cells recov
ered from B6 nu/nu mice, injected with CD4(+) T cells from B6 MAIDS an
imal, is of the Thy-CD4(+) phenotype. The proliferation of these T cel
ls in culture and their ability to cause MAIDS in SCID mice is totally
dependent on the presence of B cells. These T cells do not exhibit si
gnificant V beta restriction of their T cell receptors (TCR) and, by P
CR analysis, have defective virus-specific sequences in the cellular g
enome. By several criteria, however, these cells do not produce the in
fectious virus. These results suggest that a B-cell-dependent populati
on of CD4(+) T cells from MAIDS animals, in the absence of detectable
infectious virus production, has the ability to transfer MAIDS-like di
sease. (C) 1994 Academic Press, Inc.