PhronesisHIV infection is typically characterized by declining CD4+ T cell counts and rising viral load. We apply the displacement framework to HIV/AIDS pathophysiology, identifying the intact immune ground state () and tracing three compounding displacement mechanisms that together produce AIDS: (1) GALT displacement --- HIV preferentially depletes CD4+ T cells in the gut-associated lymphoid tissue (GALT) within weeks of infection, disrupting gut barrier integrity and producing systemic immune activation; (2) selenium depletion --- HIV encodes a functional selenoprotein that competes with host glutathione peroxidase for selenium, producing oxidative immune displacement; (3) the ART gap --- antiretroviral therapy (ART) suppresses viral replication and reduces ongoing displacement, but does not restore the immune ground state in patients with advanced depletion.
We show that the ART gap --- the residual distance from after viral suppression --- is itself a displacement that requires specific intervention. The framework identifies selenium supplementation and gut barrier restoration as the most tractable routes to closing the ART gap.