This study demonstrates that several CCchemokines, including those that inhibit entry and replication of macrophage-tropic strains of HIV, increase the replication of T cell (T)-tropic strains in CD4 ؉ T cells. Enhancement of T-tropic HIV replication is observed at early stages of replication, requires signaling through inhibitory guanine nucleotide-binding regulatory (G i ) proteins, and is associated with increased cell surface colocalization of CD4 and the T-tropic HIV coreceptor CXCR4. These findings may further our understanding of the factors that inf luence the replication and spread of T-tropic strains of HIV in vivo and suggest that the use of cell signaling CC-chemokines as therapeutic agents for the purpose of limiting HIV replication in vivo should be approached with caution.

It is well known that the immune response declines with senescence and it is suggested that these changes render an individual susceptible to infection, autoimmune phenomena and cancer. Bacterial and viral infections are a major cause of illness and death amongst aged subjects, and once infection is established, the elderly also have a diminished capacity to prevent its spread (1). The cellular and molecular basis for this age-related decline in immunocompetence are still unknown and, possibly, are related to an alteration in cell transduction mechanisms (2).

In summary, these studies demonstrated that HIV-infected hemophiliac bone marrowderived nonadherent CD34 + SC were capable of differentiating and/or maturing into T cells when cocultured in a normal allogeneic thymic environment. Furthermore, the T cells derived from derived CD34 + SC were capable of differentiating into T cells when cocultured in a normal allogeneic thymic environment, proliferated maximally with APCs from the stem cell donor and were tolerant of thymic HLA class II antigens, and to a lesser degree to stem cell donor B cell HLA antigens.