SummaryThe discovery of T helper type 1 (Th1) and T helper type 2 (Th2) phenotypes within the CD4+T-lymphocyte population has allowed for further elucidation of the roles the T cells play in regulation of humoral and cellular immunity. It is suggested that differential activation of the CD4+subsets, particularly up-regulation of the Th2 cell and down-regulation of the Th1 cell, may be associated with diseases as diverse as AIDS and asthma. We report herein that by using the polymerase chain reaction to analyze the kinetics of in vivo cytokine- and virus-specific gene expression, we can show that mice infected with the molecularly cloned MAIDS defective virus 1/27/A BM5 exhibit an alteration in cytokine gene expression that closely parallels an increase in spleen cell numbers, an increase in IgM production, a decrease in the stimulation index, and an increase in defective-virus gene expression in these mice. As has been suggested to be true for human AIDS, the observed alteration of cytokine gene expression suggests that a pattern of expression similar to that produced by Th2 cells may also have a role in the development of MAIDS.