The control mechanisms that maintain a steady-state viral load during chronic HIV-1 infection are critical to understanding the pathophysiology of HIV disease. This paper compares the conceptual features of the two alternative models of viral control, target cell limitation and immune control, with available data on the viral and cellular dynamics of HIV-1 infection and the pattern of changes induced by effective antiretroviral drug therapy. These data suggest that an antigen-driven immune response is the primary control mechanism for in vivo viral growth.
