T-HELPER CELL ACTIVATION AND HUMAN RETROVIRAL PATHOGENESIS

T helper (Th) cells are of central importance in regulating many criti cal immune effector mechanisms. The profile of cytokines produced by T h cells correlates with the type of effector cells induced during the immune response to foreign antigen. Th1 cells induce the cell-mediated immune response, while Th2 cells drive antibody production. Th cells are the preferential targets of human retroviruses. Infections with hu man T-cell leukemia virus (HTLV) or human immunodeficiency virus (HIV) result in the expansion of Th cells by the action of HTLV (adult T-ce ll leukemia) or the progressive loss of T cells by the action of HIV ( AIDS). Both retrovirus infections impart a high-level activation state in the host immune cells as well as systemically. However, diverging responses to this activation state have contrasting effects on the Th- cell population. In HIV infection, Th-cell loss has been attributed to several mechanisms, including a selective elimination of cells by apo ptosis. The induction of apoptosis in HIV infection is complex, with m any different pathways able to induce cell death. In contrast, infecti on of Th cells with HTLV-1 affords the cell a protective advantage aga inst apoptosis. The advantage may allow the cell to escape immune surv eillance, providing the opportunity for the development of Th-cell can cer. In this review, we will discuss the impact of Th-cell activation and general immune activation on human retrovirus expression with a fo cus upon Th-cell function and the progression to disease.