Interacting positive and negative feedback loops promote and control chronic activation in HIV-1–infected lymph nodes. T cells are specifically activated by HIV and other microbial antigens, and nonspecifically, as bystanders, by cytokines and other factors associated with inflammation, including Toll-like receptor (TLR) agonists. Such activation leads to proliferation, differentiation, and cytokine secretion; the latter contribute to inflammation and bystander activation (positive feedback). Different effector cells secrete inhibitory cytokines and apoptosis-inducing factors that may affect T cells and dendritic cells (negative feedback). Also depicted are ongoing cycles of infection that connect to both feedback loops.